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Brochures for Primary Care Physicians, to increase awareness of Cushing’s syndrome. In English and Spanish

2012-02-15T10:44:00.001-05:00

Brochures for Primary Care Physicians, to increase awareness of Cushing's syndrome. In English and Spanish

These were sent to me by a Facebook friend who wrote:

it's Vida A, I have writen in the facebook group that I would like to upload some information that I think it's very useful. Most of it is in Spanish but maybe someone is able to understand it.

I've found it in: www.ciberer.es

then you go to enfermedades raras > divulgación social > boletin social and then it's in Boletin Social number 3 (dedicated to Cushing)

I think it may be very useful

Thanks very much

Núria (Vida A)

GUIA_CUSHING_completa.pdf Download this file

Brochure_for_Primary_Care_physicians_-_final_version.pdf Download this file

Making sense of your child's health numbers

2012-02-15T10:43:00.001-05:00

Excerpt from: http://thechart.blogs.cnn.com/2012/02/14/
making-sense-of-your-childs-health-numbers/

"...Unfortunately, as obesity becomes more common among children, diseases once thought to be primarily a problem of adulthood are showing up in kids. For this reason, children should be screened for medical complications of obesity, such as diabetes, high blood pressure and high cholesterol.

Not everyone agrees when you should start screening your children, but the latest recommendation is to test cholesterol between 9 and 11 years old and then again between 17 and 21. Ask your pediatrician for his or her opinion based on your child’s BMI. Blood pressure can be measured with a cuff at the doctor’s office, and diabetes and high cholesterol can be checked with simple blood tests.

These tests may include blood sugar, hemoglobin A1c and insulin levels for diabetes; a lipid panel (such as cholesterol and triglycerides) which, along with blood pressure, is a marker for heart disease; and tests for liver problems that can occur with obesity.

In some situations it might be important to rule out medical causes of obesity. For example, patients who have a higher concentration of fat in the neck and head region could have Cushing's syndrome, and those who are relatively short for their weight and age and have other symptoms might have low thyroid function..."

Read the entire article at http://thechart.blogs.cnn.com/2012/02/14/
making-sense-of-your-childs-health-numbers/

Clinical relevance of cardiac structure and function abnormalities in patients with Cushing's syndrome before and after cure

2012-02-15T10:24:00.001-05:00

Authors: Toja, Paola M.1; Branzi, Giovanna2; Ciambellotti, Francesca2; Radaelli, Piero3; De Martin, Martina1; Lonati, Laura Maria2; Scacchi, Massimo; Parati, Gianfranco; Cavagnini, Francesco1; Giraldi, Francesca Pecori

Source: Clinical Endocrinology, Volume 76, Number 3, 1 March 2012 , pp. 332-338(7)

Publisher: Wiley-Blackwell

Abstract:

Objectives Sustained hypercortisolism impacts cardiac function, and, indeed, cardiac disease is one of the major determinants of mortality in patients with Cushing's syndrome. The aim of this study was to assess the clinical relevance of cardiac structure and function alterations by echocardiography in patients with active Cushing's syndrome and after disease remission.

Study design Seventy-one patients (61 women, 10 men) with Cushing's syndrome and 70 age-, sex- and blood pressure-matched controls were enrolled. Echocardiography was performed in 49 patients with active disease and at several time points after remission in 44 patients (median follow-up 46·4 months), and prevalence of abnormal left ventricular mass measurements and systolic and diastolic functions indices was compared between patients with active disease, after remission and controls. Twenty-two patients were evaluated both before and after remission.

Results Up to 70% of patients with active Cushing's syndrome presented abnormal left ventricular mass parameters; 42% presented concentric hypertrophy and 23% concentric remodelling. Major indices of systolic and diastolic functions, i.e. ejection fraction and E/A ratio, respectively, were normal. Upon remission of hypercortisolism, left ventricular mass parameters ameliorated considerably, although abnormal values were still more frequent than in controls. Both cortisol excess and hypertension contribute to cardiac mass alterations and increase the prevalence of target organ damage.

Conclusions Cushing's syndrome is associated with an increased risk for abnormalities of cardiac mass, which ameliorates, but does not fully disappear after remission. Systolic and diastolic functions are largely within the normal range in these patients.

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1365-2265.2011.04206.x

Affiliations: 1: Ospedale San Luca, Neuroendocrinology Research Lab, Istituto Auxologico Italiano IRCCS 2: Department of Cardiology, Ospedale San Luca, Istituto Auxologico Italiano IRCCS 3: Department of Medical Sciences, University of Milan

Buy this article here: http://www.ingentaconnect.com/content/bsc/cend/2012/00000076/00000003/art00004

New Endocrinology App

2012-02-06T20:51:00.001-05:00

[prMac.com] South Dartmouth, Massachusetts - The Editors of Endotext and Thyroidmanager announce the release of their new medical app, "Endocrinology and Endo Emergency".

The app provides concise, practical information on endocrine emergencies, and provides the answers needed RIGHT NOW for their care. Each of the 36 topics covered includes the clinical recognition, pathophysiology, diagnosis, differential, treatment, and follow up. In addition, references to available Clinical Guidelines, and important literature citations are provided.

Focusing on the critical information needed at the point of care, the app includes topics such as Cushing's disease, diabetic ketoacidosis, managing acute type I and type II diabetes, hypercholesterolemia, adrenal insufficiency, hyperthyroidism, thyroid storm, and much more. Key facts are presented in tables and flow-charts to allow quick reference to crucial information.

The app is designed for physicians, nurses, emergency room caregivers, hospitalists, trainees, students, and any caregiver who needs to treat seriously ill patients.

The "Endocrinology and Endo Emergency" mobile application was created by the world-renowned endocrinologists who also brought you ENDOTEXT.ORG and THYROIDMANAGER.ORG, the most comprehensive and up-to-date web-based endocrine textbooks. Endocrinology and Endo Emergency is always updated with the latest information, and updates can be automatically downloaded by users.

To view or purchase the app in the Apple App store (also available for android) or go to endoemergencies website for information and to view a sample section. Qualified reviewers may contact us for promo codes.

* Covers endocrinology and endocrine emergencies

* Provides critical information needed at the point of care

* 36 topics covered

* written by expert endocrinologists from around the world

Device Requirements:
* iPhone 3GS, iPhone 4, iPhone 4S, iPod touch (3rd generation), iPod touch (4th generation) and iPad
* Requires iOS 5.0 or later
* 1.7 MB

Pricing and Availability:
Endocrinology & Endo Emergency 1.0 is $5.99 USD (or equivalent amount in other currencies) and available worldwide exclusively through the App Store in the Medical category.

Endocrine Emergencies
Thyroid Disease Manager
Endotext Web Book
Purchase and Download
Screenshot
App Icon

Produced and owned by Endocrine Education, Inc. and Mdtext.Com, Inc. Copyright (C) 2012 Endocrine Education, Inc. and Mdtext.Com, Inc. All Rights Reserved. Apple, the Apple logo, iPhone, iPod and iPad are registered trademarks of Apple Inc. in the U.S. and/or other countries.

From http://prmac.com/release-id-38000.htm

Pregnancy-induced Cushing’s Syndrome: A Case Report

2012-01-19T06:43:00.001-05:00

Cushing’s syndrome(CS) during pregnancy is a rare condition with fewer than 150 cases reported in the literature. Adrenal adenomas were found to be the commonest cause.The other causes include tumors in hypothalamus and pituitary. Ectopic ACTH secretion has been reported to cause CS.

There is a very rare condition. Cushing’s syndrome develops in pregnancy and resolving after delivery. The mechanisms underlying these conditions are poorly understood.

There are non-significant differences in the clinical features of pregnant and non-pregnant women with CS.The gestation dramatically affects the maternal hypothalamic-pituitary-adrenal axis, The normal gestational changes in the HPA axis alter these parameters and complicate the screening process for CS.

Comparing with non-pregnant women with CS, the treatment is different in Cushing’s syndrome during pregnancy.

We described here the case of a 25-year-old woman with CS during her forth [sic] pregnancy. Hypertension, diabetes, hypopotassaemia, purple striae and acne are present. Cushing’s syndrome in the patient resolved within four weeks of artificial termination. Eight months after artificial termination, the patient became pregnant again and rapidly developed Cushing’s syndrome with typical clinical symptoms and signs and laboratory results.

Title: Pregnancy-induced Cushing’s Syndrome: A Case Report

Category: Tumor Biology

Filename: Pregnancy-induced Cushing’s Syndrome: A Case Report.pdf

Pages: 101

Price: US$48.00

Buy this pater at http://www.tumorres.com/tumor-biology/25201.htm

Treatment Options in Cushing’s Disease

2012-01-19T06:20:00.001-05:00

Download PDF

Authors: Ahmed Rizk, Juergen Honegger, Monika Milian and Tsambika Psaras

Publication Date: 11 Jan 2012

Journal: Clinical Medicine Insights: Oncology

Citation: Clinical Medicine Insights: Oncology 2012:6 75-84

doi: 10.4137/CMO.S6198

Abstract

Endogenous Cushing’s syndrome is a grave disease that requires a multidisciplinary and individualized treatment approach for each patient. Approximately 80% of all patients harbour a corticotroph pituitary adenoma (Cushing’s disease) with excessive secretion of adrenocorticotropin-hormone (ACTH) and, consecutively, cortisol.

The goals of treatment include normalization of hormone excess, long-term disease control and the reversal of comorbidities caused by the underlying pathology. The treatment of choice is neurosurgical tumour removal of the pituitary adenoma. Second-line treatments include medical therapy, bilateral adrenalectomy and radiation therapy.

Drug treatment modalities target at the hypothalamic/pituitary level, the adrenal gland and at the glucocorticoid receptor level and are commonly used in patients in whom surgery has failed.

Bilateral adrenalectomy is the second-line treatment for persistent hypercortisolism that offers immediate control of hypercortisolism. However, this treatment option requires a careful individualized evaluation, since it has the disadvantage of permanent hypoadrenalism which requires lifelong glucocorticoid and mineralocorticoid replacement therapy and bears the risk of developing Nelson’s syndrome.

Although there are some very promising medical therapy options it clearly remains a second-line treatment option. However, there are numerous circumstances where medical management of CD is indicated.

Medical therapy is frequently used in cases with severe hypercortisolism before surgery in order to control the metabolic effects and help reduce the anestesiological risk. Additionally, it can help to bridge the time gap until radiotherapy takes effect.

The aim of this review is to analyze and present current treatment options in Cushing’s disease.

From http://www.la-press.com/treatment-options-in-cushings-disease-article-a2985

Healthy New Year Video Challenge

2012-01-19T05:52:00.001-05:00

$5,000 in prizes!

Let’s get the new year off to a healthy start! The Office of the National Coordinator for Health Information Technology (ONC) Healthy New Year Video Challenge (#HealthIT4U2012) invites you to create a short, compelling video (up to 2 minutes in length) sharing one New Year’s resolution for improving your health or the health of a loved one, and how you will use technology to achieve your resolution.

We encourage you to create videos that are creative, inspiring and instructive — share a resolution that others can relate to, and demonstrate how technology will make it easier to achieve. Your resolution can be anything health related, such as quitting smoking or drinking, eating healthier, losing weight, reducing stress, or managing a chronic condition. Videos must show how you will use information technology to achieve your resolution and how you plan to maintain it. Entries could include the following kinds of resolutions (these are just examples — be creative and craft your own resolution!):

I will set up an online personal health record for myself (or another family member) so I can have all of my health information conveniently stored in one place.
I will ask my doctor for a copy of my own health records — electronically if available — and help him or her to identify any important information that may be missing or need to be corrected.
I will find an online community that helps me figure out the best ways to manage my health condition (depression, cancer, diabetes, etc.)
I will use an electronic pedometer to help me track my physical activity and will try to take 10,000 steps per day.
I will find an app on my smartphone to help me track my food intake so I can lose 10 pounds by my high school reunion.
I will sign up for a text reminder program on my cell phone to help me stop smoking or remind me to take my medications on time.

The goal of the challenge is to make 2012 a healthier year by motivating and inspiring others to use health information technology to be more engaged in improving health and increasing adoption of consumer health technology.

Note: To participate, you must be a citizen or permanent resident of the United States. Team members must be at least 18, but your video can include minors under 18 as long as a parent or legal guardian signs their consent forms. For details on eligibility, review the Official Rules.

More at http://healthynewyea...v/details/about

(Adrenal Cushing's) Tumour behind 7-yr-old's weight gain, moustache

2012-01-10T14:21:00.001-05:00

By: Priyanka Vora Date: 2012-01-03 Place: Mumbai

Tanzania resident Mohammad Abdulrazaq Jussa recuperating after city doctors removed 7-cm tumour from his adrenaline [sic] gland, which was responsible for his 12-kg weight gain, growth of facial hair

Painful and embarrassing stories about one's childhood years, when inexplicable physical changes take place, are not uncommon. But for Mohammad Abdulrazaq Jussa, a resident of Tanzania, it wasn't just ordinarily painful. The seven-year-old was harbouring a tumour in his adrenaline [sic] gland, causing him to suddenly gain 12 kg in a year, and develop a pencil moustache, much to the amusement of his classmates.

Growing pains: Mohammad at age six weighed 25 kg but suddenly his
weight shot up to 37 kg without any explanation. Doctors are now hoping
that after the removal of the tumour, the physical changes will regress.

The tumour was discovered last year when the boy suddenly started becoming fatter and started growing facial hair. "We had to start buying bigger clothes for him. Initially, my son was thin and active but suddenly, he began growing at a considerable pace.

"He would keep complaining to me about stomach pains but I thought it was just an excuse to miss school and the taunts he received from his friends. Now I regret not paying heed to his cries for help," said Bilkis, Mohammad's mother.

When the weight gain did not stop and he had put on about 12 kg, Mohammad's family sensed something was amiss and took him to doctors in Tanzania.

"The doctors we consulted at first told us that we should restrict his diet but when we told them that there was no change in his diet, doctors started investigating further. We even went to Jerusalem where physicians finally diagnosed that he had a tumour in his adrenaline gland. Seeking treatment for our son, we finally reached Mumbai," added Bilkis.

What doctors found

After the family finally reached city shores a week back, doctors at Saifee Hospital started treatment.

According to Mohammad's doctors, a tumour had grown inside his left adrenaline gland, causing the excess release of hormones resulting in weight gain. Doctors say that Mohammad is suffering from Cushing's syndrome

Under the knife

On Thursday, Mohammad underwent a laparoscopic surgery to remove the tumour, which was seven-cm long and weighed approximately 450 g.

"Mohammad's case was a challenging surgery as he is just seven and at the same time the tumour was as big as his kidney. As we did the surgery laparoscopically, there was no blood loss, giving us excellent post-operative results," said Dr Anup Ramani, uro-oncological surgeon at Saifee Hospital.

'Hoping for normalcy'

Now recuperating at the hospital, Mohammad and his family hope the boy starts looking his age again. Commenting on the changes, Bilkis said, "He was really active before but once he started putting on weight, he started becoming introverted and his studies were also affected. I now pray that everything returns to normal."

When asked about the pace of growth, Dr Ramani said most physical changes would regress in a year's time. "We have put him on a dose of steroids to compensate for the growth spurts he has experienced and hope that all the changes regress."

Cushing's syndrome

Cushing's syndrome is a hormone disorder caused by high levels of cortisol in the blood. This can be caused by taking glucocorticoid drugs, or by tumours that produce cortisol. Cushing's disease refers to one specific cause of the syndrome: a tumour in the pituitary gland that elevates cortisol.

From http://www.mid-day.com/news/2012/jan/030112-Tumour-behind-7-yr-olds-weight-gain-moustache.htm

What is the best long-term management strategy for patients with primary adrenal insufficiency?

2012-01-04T20:15:00.001-05:00

Authors: Quinkler, Marcus¹; Hahner, Stefanie²

Source: Clinical Endocrinology, Volume 76, Number 1, 1 January 2012 , pp. 21-25(5)

Publisher: Wiley-Blackwell

Abstract Summary

Primary adrenal insufficiency is treated with glucocorticoid and mineralocorticoid replacement therapy. Recent data revealed that health-related quality of life in adrenal insufficiency is impaired in many patients and that patients with adrenal insufficiency are also threatened by an increased mortality and morbidity. This may be caused by inadequate glucocortiocid therapy and adrenal crisis. Therefore, the optimization of hormone replacement therapy remains one of the most challenging tasks in endocrinology because it is largely based on clinical grounds because of the lack of objective assessment tools.

This article provides answers to the important daily clinical questions, such as correct dose finding, dose adaptation in special situations, e g, pregnancy, improvement of quality of life and measures for protection from adrenal crisis. Other important aspects discussed are side effects of glucocortiocid replacement therapy and interactions with other drugs.

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1365-2265.2011.04103.x

Affiliations: 1: Clinical Endocrinology, Charité Campus Mitte, Charité University Medicine Berlin, Berlin 2: Department of Internal Medicine I, University Hospital, University of Wuerzburg, Wuerzburg, Germany

Publication date: 2012-01-01

From http://www.ingentaconnect.com/content/bsc/cend/2012/00000076/00000001/art00005

Synchronous bilateral adrenalectomy by midline incision: A reliable method for treatment of hypercortisolism

2012-01-04T19:59:00.001-05:00

Sayyed Abbas Tabatabaee, Sayyed Mozaffar Hashemi, Mohamadreza Fazel Najafabadi, Amirhossein Davarpanah Jazi

Abstract

Cushing syndrome is one of the diseases associated with adrenals secreting too much cortisol. The syndrome was first described by Harvey Cushing in 1932.¹ It can be caused either by a tumor originating from the corticotroph cells located in pituitary glands, called corticotroph adenoma, or primary adrenal hyperplasia. It can be also the consequence of some other rare conditions such as ectopic corticotropin-releasing hormone (CRH) causing increased adrenocorticotropic (ACTH) secretion and macronodular adrenal hyperplasia (a primary pigmented nodular adrenal disease).^2,3 To manage the situation, previous articles demonstrated some strategies including two main groups of surgical treatments and non-surgical procedures.
Surgical interventions are very important to completely cure this condition. Pituitary surgery, referred to as transsphenoidal operation, is the treatment of choice for patients with secondary disease.² However, in some situations, e.g. in patients with recurrent or persistent Cushing syndrome and those not responding to medical therapies after the surgery, the effectiveness of pituitary surgery is under question. Such patients are the best candidates for bilateral adrenalectomy. Some previous articles outlined this method.⁴ Laparoscopy is one of the methods recently used for adrenalectomy. During the surgery, some complications may occur which deteriorates patient's condition with noticeable rates of 9.5 to 12%. These complications are bleeding, organ damages, pain and deep vein thrombosis.^7,8
Although in recent years the experts have achieved great improvements in management and treatment of the patients suffering from Cushing syndrome, some controversies still exist. In this manuscript, we explained a new method to accomplish a reliable bilateral adrenalectomy to manage the disease and cure the condition completely.
After opening the abdomen, left adrenal gland is determined and adjacent vessels are ligated. Then, the enlarged adrenal gland would be entirely removed. However, adrenalectomy at the right side is not as simple as the left side. Renal vein detachment from the inferior vena cava can be a serious complication of right adrenalectomy if it is performed without enough exposure and experience. Massive bleeding in such clinical setting may significantly compromise patient's outcome. To avoid this complication during the procedure we can perform a new method explained below.
Access to the right gland cannot be obtained by conventional retraction of the liver and it is necessary to mobilize the right hepatic lobe by fully incising the falciform ligament, the right triangular ligament, and rotating the right lobe medially. In this procedure, the bare area of the liver is dissected from the diaphragm. Care must be taken to avoid twisting and occluding the vena cava during this maneuver. After medial rotation of the liver in the proper position, the right adrenal and inferior vena cava can be directly visualized. This excellent exposure makes adrenalectomy very simple and minimizes the risk for renal vein detachment as a significant complication.
This method was conducted on 6 cases admitted due to Cushing syndrome in Alzahra Hospital, Isfahan, Iran. While no major complications were observed, favorable outcomes were found in the 6-month follow-up period.
Based on our experience, bilateral adrenalectomy via a midline incision is a promising and acceptable technique for patients with Cushing syndrome. However, due to excess adipose tissue and lack of enough exposure, adrenalectomy by lumbotomy in such patients has prominent limitations. Therefore, midline incision provides feasible exposure for direct visualization of both adrenals.

Full Text: PDF
This work is licensed under a Creative Commons Attribution 3.0 License

This work is licensed under a Creative Commons Attribution 3.0 Unported License.

A New Link in the Stress Response Could Mean Better Treatment Soon

2012-01-02T19:07:00.001-05:00

Hoping to pave the way for improved treatment options, researchers have found that they can significantly reduce our response to stress.

A team at Tufts University appears to have found an important step in the body's stress reaction, and blocking this step from occurring can significantly reduce the response. The finding may pave the way for improved treatments for depression and anxiety.

The stress cascade is governed by the brain's hypothalamus, which communicates with the pituitary and adrenal glands, which in turn secrete stress hormones like cortisol. Disruptions in this pathway are also connected with problems like postpartum depression, obesity, Cushing's syndrome (hypercortisolism), premenstrual syndrome (PMS), epilepsy, and osteoporosis, according to the study's press release.

Using mice as their subjects, the researchers set out to fill in some of the blanks in the cascade of events that leads to the secretion of the stress hormone coriticosterone (the mouse equivalent to our cortisol). They used brain samples from mice, and tracked the activity of the brain cells that release corticotrophin-releasing hormone (CRH), which ultimately stimulates the secretion of stress hormones.

They discovered that specific "neurosteroids" are needed to bind to receptors on the CRH neurons to activate them, serving as an important early step in the stress response. The team reasoned that disrupting the synthesis of the neurosteroids should significantly reduce the stress response by stopping it almost before it begins.

This is just what they found. When they blocked the neurosteroids' synthesis in live mice, their coriticosterone levels were reduced after stressful situations compared to normal mice. Additionally, if neurosteroid synthesis was halted, the mice did not show anxiety-like behaviors after they had been stressed.

One of the authors, Jamie Maguire, said that the data "suggest that these receptors may be novel targets for control of the stress-control pathway. Our next work will focus on modulating these receptors to treat disorders associated with stress, including epilepsy and depression-like behaviors."

The study is published in The Journal of Neuroscience.

From http://www.theatlantic.com/health/archive/2012/01/a-new-link-in-the-stress-response-could-mean-better-treatment-soon/250570/

Disturbances of the hypothalamic-pituitary-adrenal axis and plasma electrolytes during experimental sepsis.

2012-01-02T18:57:00.001-05:00

Michael A Flierl, Daniel Rittirsch, Sebastian Weckbach, Markus Huber-Lang, Kyros Ipaktchi, Peter A Ward and Philip F Stahel

Annals of Intensive Care 2011, 1:53 doi:10.1186/2110-5820-1-53

Published: 30 December 2011

Background

Sepsis continues to be a poorly understood syndrome with a high mortality rate. While we are beginning to decipher the intricate interplay of the inflammatory response during sepsis, the precise regulation of the hypothalamic-pituitary-adrenal (HPA) axis and its impact on electrolyte homeostasis during sepsis remains incompletely understood.

Methods

Sepsis was induced in adult male Sprague-Dawley rats by cecal ligation and puncture (CLP). Plasma samples were obtained as a function of time (6-48 hrs) after CLP and compared to healthy animals (neg ctrl). Samples were analyzed for adrenocorticotropin (ACTH), corticosterone, and aldosterone levels as well as concentrations of sodium (Na+), potassium (K+), chloride (Cl-) and magnesium (Mg2+).

Results

ACTH levels were found to be significantly reduced 6-24 hrs after CLP in comparison to baseline levels and displayed gradual recovery during the later course (24-48 hrs) of sepsis. Plasma corticosterone concentrations exhibited a bell-shaped response, peaking between 6 and 12 hrs followed by rapid decline and concentrations below negative control levels 48 hrs after injury. Aldosterone levels in septic animals were continuously elevated between 6 and 48 hrs. While plasma Na+ levels were found to be persistently elevated following CLP, levels of K+, Cl- and Mg2+ were significantly reduced as a function of time and gradually recovered during the later course of sepsis.

Conclusion

CLP-induced sepsis resulted in dynamic changes of ACTH, corticosterone and aldosterone levels. In addition, electrolyte levels showed significant disturbances following CLP. These electrolyte perturbations might be evoked by a downstream effect or a dysfunctional HPA-axis response during sepsis and contribute to severe complications during sepsis.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

From http://www.annalsofintensivecare.com/content/1/1/53/abstract

We have been Nominated for a Health Activist Hero 2011!

2012-01-02T18:36:00.001-05:00

We were nominated for a wego Health Activist Hero 2011 award!

Our Health Activist Awards program will award Health Activists for their outstanding achievements in online health leadership and advocacy in 2011.

Health Activist Hero 2011

Who has changed your life? There are some people who can truly change your entire outlook on life just with their story, their dedication, their words, and their encouragement. Who is your Health Activist Hero? Who would you like to thank and why? For so many Health Activists, impacting the life of just one reader is worth more than 1,000s of page views. This award is an emotional one but will yield some incredible stories.

Do you know a Health Activist who has changed your life, your condition, or your Health Activism? Thank them by recognizing them as a Health Activist Hero!

Vote for us here: http://info.wegohealth.com/hero-2011

Our nominating post:

Award: Health Activist Hero (http://info.wegohealth.com/hero-2011)

Link: https://www.facebook.com/mary.oconnor

Reason: If it wasn't for MaryO's hard work in creating an online community I don't know if I'd have made it through all these years. She's a behind the scenes kind of person, she doesn't ask for much and often winds up on the periphery but despite her own health challenges she gives and gives and gives and has helped thousands of people.

Red alert: Hypertension on the prowl

2012-01-01T16:15:00.001-05:00

The family of Mr. Adulphus Opara of Umunokwu in Okwuato, Aboh Mbaise Local Government Area of Imo State was shocked to its nerves as the man slumped from the chair on which he was sitting and cuddling his little daughter who was just less than five months. Scampering and running up and down, all efforts by family members to revive their breadwinner were too little and too late as he died that sunny Saturday afternoon. It was later revealed by doctors at a private hospital that Adolphus died of hypertension attack.

The case of Adolphus is just one out of the numerous complaints of the havocs wreaked by untreated or unchecked hypertension. Medical experts say it has sent so many victims to their untimely grave.

Dr. Francis Duru, a physician and senior lecturer in Human Anatomy, College of Medicine, University of Lagos Teaching Hospital (LUTH), Idi Araba, described hypertension as a silent killer and the major cause of most sudden deaths in Nigeria. He said high blood pressure is when one’s BP is consistently above 140/90 mmHg.

According to him, “Normal blood pressure is when your blood pressure is measured at 120/80 mmHg most of the time. If your blood pressure is consistently above 140/90, then the person has hypertension or is hypertensive. Untreated hypertension can lead to many health complications and the worst of all is sudden death.”

MedicinePlus, a medical publication, defines hypertension or high blood pressure as a cardiac chronic medical condition in which the systemic arterial blood pressure is elevated. What that means is that the heart is having to work harder than it should to pump blood around the body. Blood pressure involves two measurements, systolic and diastolic. Normal blood pressure is 120/80 mm/Hg.

The first figure is the systolic blood pressure, the pressure there is in the arteries when your heart is contracting. The second, or lower figure, is the diastolic blood pressure, which is the pressure in your arteries between heartbeats. High blood pressure is anything above 140/90 mm/Hg. Hypertension is the opposite of hypotension. Hypertension is classified as either primary (essential) hypertension or secondary hypertension; about 90–95% of cases are categorised as “primary hypertension,” which means high blood pressure with no obvious medical cause.

The remaining 5–10% of cases (secondary hypertension) are caused by other conditions that affect the kidneys, arteries, heart or endocrine system. MedicinePlus added: “Persistent hypertension is one of the risk factors for stroke, myocardial infarction, heart failure and arterial aneurysm, and is a leading cause of chronic kidney failure. Moderate elevation of arterial blood pressure leads to shortened life expectancy. Dietary and lifestyle changes can improve blood pressure control and decrease the risk of associated health complications, although drug treatment may prove necessary in patients for whom lifestyle changes prove ineffective or insufficient.”

The American Heart Association, in one of its recent reports, made it known that the World Health Organisation (WHO) attributes hypertension, or high blood pressure, as the leading cause of cardiovascular mortality. The World Hypertension League (WHL), an umbrella organisation of 85 national hypertension societies and leagues, recognised that more than 50% of the hypertensive population worldwide are unaware of their condition. To address this problem, the WHL initiated a global awareness campaign on hypertension in 2005 and dedicated May 17 of each year as World Hypertension Day (WHD). Over the past three years, more national societies have been engaging in WHD and have been innovative in their activities to get the message to the public. In 2007, there was record participation from 47 member countries of the WHL. During the week of WHD, all these countries – in partnership with their local governments, professional societies, nongovernmental organisations and private industries – promoted hypertension awareness among the public through several media and public rallies.

Causes and risk factors

Although Duru noted that there were several causes of hypertension, he still insisted that there were instances when it had no direct link or cause. He said: “Medically, we have causes, incidences and risk factors that are associated with hypertension. I am talking about factors that can cause or lead to hypertension. In this case we have issues like the level of water or salt in a person’s body; ability or inability of some organs like the kidneys or blood vessels to function at optimum levels; life history, that is, does hypertension run in your family? lifestyle, that is, the type of food you eat; lack of exercises and always being in a noisy place or being in a state of anxiety all the time. Let me also quickly add that excessive smoking and over-indulgence in alcohol can lead to hypertension.”

He added: ‘“You can easily become hypertensive when you reach the stage of adult age because one’s blood vessels are stiffer as one reaches old age. This leads to HBP. I can also tell you that high blood pressure increases your chances of having a stroke, heart attack, heart failure, kidney disease, and early death. I must also state it here that there are some conditions of health one will find oneself and one will surely expect to be hypertensive. For instance, some pregnant women are usually hypertensive especially from the sixth month until they put to birth. Diabetic patients are sometimes hypertensive although there is no causal relationship between hypertension and diabetes.

People who are obsessed are at risk of suffering from hypertension just as chronic kidney diseases and poor conditions or disorders of the adrenal glands can as well lead to hypertension.” The LUTH medical expert revealed that wrong or too much application of some drugs could also lead to hypertension. “Wrong application or continuous administration of some medications such as birth control pills, diet control pills, cold medications, etc are other ways by which hypertension can hit at a person”, he warned. Meanwhile, Duru noted that there were some instances when hypertension had no cause or trace and it is described as essential hypertension.

Symptoms

Most medical experts agree that hypertension, in most cases, has no external symptoms. To this effect, Duru said: “You can now see why we call hypertension a silent killer. It is a silent killer because it gives no sign, no symptom and no warning before it strikes. I must comment here that most Nigerians are suffering from hypertension without knowing it. This is why we also recommend that people should go for BP check regularly to confirm their status. Based on these facts, so many Nigerians develop sicknesses like heart diseases, kidney failures and other complications without any prior knowledge that all their problems started from untreated or unchecked hypertension.

It is also important to note that a hypertensive patient can live his normal life if he abides by medical advice and that means taking his drugs.” ADAM Medical Encyclopedia listed certain conditions as symptoms of hypertension. According to its report, “If you have a severe headache, nausea or vomiting, bad headache, confusion, changes in your vision, or nosebleeds you may have a severe and dangerous form of high blood pressure called malignant hypertension.” The publication recommended that there should be several checks before it could be ascertained that one has hypertension. It noted that: “Your health care provider will check your blood pressure several times before diagnosing you with high blood pressure. It is normal for your blood pressure to be different depending on the time of day. Blood pressure readings taken at home may be a better measure of your current blood pressure than those taken at your doctor’s office.”

Among the tests to be taken to confirm whether or not one has hypertension, according to Duru, are physical examinations to look for bad conditions of the heart or diseases severely affecting it, poor state or damage of the eyes, as well as other bad physical changes in your body. In this case, tests that enable doctors to handle the situation well include: cholesterol level; level of heart disease like echocardiogram or electrocardiogram; level of metabolic panel/ urinalysis or ultrasound of the kidney and this is when the case has become a chronic one.

Types

A widely posted medical material stated: “A blood pressure is usually classified based on the systolic and diastolic blood pressures. Systolic blood pressure is the blood pressure in vessels during a heartbeat. Diastolic blood pressure is the pressure between heartbeats. A systolic or the diastolic blood pressure measurement higher than the accepted normal values for the age of the individual is classified as pre hypertension or hypertension. Hypertension has several sub-classifications, including hypertension stage I, hypertension stage II, and isolated systolic hypertension. Isolated systolic hypertension refers to elevated systolic pressure with normal diastolic pressure and is common in the elderly.

These classifications are made after averaging a patient’s resting blood pressure readings taken on two or more office visits. Individuals older than 50 years are classified as having hypertension if their blood pressure is consistently at least 140 mmHg systolic or 90 mmHg diastolic. Hypertension is also classified as resistant if medications do not reduce blood pressure to normal levels.”

Accelerated hypertension – this is associated with headache, drowsiness, confusion, vision disorders, nausea, and vomiting. These symptoms are collectively called hypertensive encephalopathy. Hypertensive encephalopathy is caused by severe small blood vessel congestion and brain swelling, which is reversible if blood pressure is lowered.

Secondary hypertension– some additional signs and symptoms suggest that the hypertension is caused by disorders in hormone regulation. Hypertension combined with obesity distributed on the trunk of the body, accumulated fat on the back of the neck (“buffalo hump”), wide purple marks on the abdomen (abdominal striae), or the recent onset of diabetes suggests that an individual has a hormone disorder known as Cushing’s syndrome. Hypertension caused by other hormone disorders such as hyperthyroidism, hypothyroidism, or growth hormone excess will be accompanied by additional symptoms specific to these disorders. For example, hyperthyroidism can cause weight loss, tremors, heart rate abnormalities, reddening of the palms, and increased sweating.

In pregnancy–Hypertension in pregnant women is one symptom of pre-eclampsia. Pre-eclampsia can progress to a life-threatening condition called eclampsia, which is the development of protein in the urine, generalised swelling, and severe seizures. Other symptoms indicating that brain function is becoming impaired may precede these seizures such as nausea, vomiting, headaches, and vision loss.

In children –Some signs and symptoms are especially important in newborns and infants such as failure to thrive, seizures, irritability, lack of energy, and difficulty breathing. In children, hypertension can cause headache, fatigue, blurred vision, nosebleeds, and facial paralysis. Even with the above clinical symptoms, the true incidence of paediatric hypertension is not known. In adults, hypertension has been defined due to the adverse effects caused by hypertension. However, in children, similar studies have not been performed thoroughly to link any adverse effects with the increase in blood pressure. Therefore, the prevalence of paediatric hypertension remains unknown due to the lack of scientific knowledge.

Essential hypertension– this is the most prevalent hypertension type, affecting 90–95% of hypertensive patients. Although no direct cause has been identified, there are many factors such as sedentary lifestyle smoking, stress, visceral obesity, potassium deficiency (hypokalemia), obesity (more than 85% of cases occur in those with a body mass index greater than, salt (sodium) sensitivity, alcohol intake, and vitamin D deficiency that increase the risk of developing hypertension. Risk also increases with aging, some inherited genetic mutations, and having a family history of hypertension. An elevated level of rennin, a hormone secreted by the kidney, is another risk factor, as is sympathetic nervous system over activity.

Secondary hypertension–By definition, this results from an identifiable cause. This type is important to recognise since it’s treated differently to essential hypertension, by treating the underlying cause of the elevated blood pressure. Hypertension results in the compromise or imbalance of the path physiological mechanisms, such as the hormone-regulating endocrine system, that regulates blood plasma volume and heart function.

Treatment

According to an ADAM Medical Encyclopedia research work, “The goal of treatment is to reduce blood pressure so that you have a lower risk of complications. You and your health care provider should set a blood pressure goal for you. If you have pre-hypertension, your health care provider will recommend lifestyle changes to bring your blood pressure down to a normal range. Medicines are rarely used for pre-hypertension. You can do many things to help control your blood pressure, including: Eat a heart-healthy diet, including potassium and fibre, and drink plenty of water.

Exercise regularly — at least 30 minutes of aerobic exercise a day. If you smoke, quit – find a programme that will help you stop. Limit how much alcohol you drink — one drink a day for women, two a day for men. Limit the amount of sodium (salt) you eat — aim for less than 1,500 mg per day Reduce stress — try to avoid things that cause you stress. You can also try meditation or yoga. Stay at a healthy body weight — find a weight-loss program to help you, if you need it.

There are many different medicines that can be used to treat high blood pressure but must be prescribed by well-qualified physician. Often, a single blood pressure drug may not be enough to control your blood pressure, and you may need to take two or more drugs. It is very important that you take the medications prescribed to you. If you have side effects, your health care provider can substitute a different medication. Most of the time, high blood pressure can be controlled with medicine and lifestyle changes.

Effects

It has been gathered through various medical work that a patient is at risk and may likely suffer from complications when BP is not treated or controlled. The ADAM Medical publication warned that the following poor conditions of health might result as an evidence of poor treatment: Bleeding from the aorta, the large blood vessel that supplies blood to the abdomen, pelvis, and legs. Chronic kidney disease, heart attack and heart failure, poor blood supply to the legs, stroke and problems with the vision.

Here Duru was of the view that most of the sudden death now recorded in Nigeria was as a result of untreated hypertension. ‘ I have explained earlier that most Nigerians are hypertensive without knowing it. In other words, they carry on their daily activities or life style without undergoing the tests and living the medically prescribed way a hypertension victim suppose to observe’. ‘ The effect’, he explained, ‘is that the patient might likely be attacked or hit by stroke, kidney failure or heart attack which leads to instant death. You know I described it as a silent killer and this is exactly what I mean.

So many Nigerians have been killed by heart failure resulting from hypertension. In some instances the person slumps at home, on the road, in the office or anywhere as the case might be. At some other time, the victim goes to bed and does not wake up. When we experience such situations, some us, in the usual Nigerian way, blame it on the wicked landlord, the envious next door neighbour or a witch or wizard in the village.’

Prevention

Doctors have unanimously agreed that hypertension has no permanent cure. At best, it can be managed or controlled. Duru explains further. He said: ‘first, for now, there is no permanent cure for hypertension, medically speaking. As a Christian, I believe in miracles but in medical terms, it is yet to be proved that hypertension has any known permanent cure. If you a victim, it means that you have to be on drugs all the days of your life. And such a patient must be ready to go for BP check regularly. He has to abstain from certain behaviour like too much salt in-take, smoking, taking more than two bottles of beer daily and he must watch his weight and do regular exercises.

I am aware the trado-medicine people usually come up with so many claims but they are also not bold enough to submit their claims to empirical proves or thorough laboratory tests.’ A medical sponsored by the American National Heart, Lung and Blood Institute reported that the prevention depends on so many factors: It wrote thus: ‘ The degree to which hypertension can be prevented depends on a number of features including current blood pressure level, sodium/potassium balance, detection and omission of environmental toxins, changes in end/target organs (retina, kidney, heart, among others), risk factors for cardiovascular diseases and the age at diagnosis of pre hypertension or at risk for hypertension.

A prolonged assessment that involves repeated blood pressure measurements provides the most accurate blood pressure level assessment. Following this, lifestyle changes are recommended to lower blood pressure, before the initiation of prescription drug therapy. According to the British Hypertension Society, the process of managing pre hypertension includes lifestyle changes such as the following: Weight reduction and regular aerobic exercise (e.g., walking): Regular exercise improves blood flow and helps to reduce the resting heart rate and blood pressure. Reduce sodium (salt) in the body by disuse of condiment sodium and the adoption of a high potassium diet, which rids the renal system of excess sodium.

Many people use potassium chloride salt substitute to reduce their salt intake.’ In 2003 the American Heart Association recommended the following drugs for the treatment of hypertension: Potassium - is essential for the proper functioning of the heart, kidneys, muscles, nerves, and digestive system. Usually the food you eat supplies all of the potassium you need.

Bosentan - is used to treat Pulmonary Arterial Hypertension (PAH, high blood pressure in the vessels that carry blood to the lungs). Bosentan may improve the ability to exercise and slow the worsening of symptoms in patients with PAH. Tadalafil (Cialis) is used to treat erectile dysfunction (impotence; inability to get or keep an erection) in men. Tadalafil (Adcirca) is used to improve the ability to exercise in people with pulmonary arterial hypertension (PAH; high blood pressure in the vessels carrying blood to the lungs, causing shortness of breath, dizziness, and tiredness.

From http://www.sunnewsonline.com/webpages/features/icon/2012/jan/01/icon-01-10-2012-003.html

FDA Rare Disease Patient Advocacy Day

2011-12-31T08:44:00.001-05:00

On March 01, 2012, the Food and Drug Administration (FDA) will celebrate the fifth annual Rare Disease Day by hosting a "FDA Rare Disease Patient Advocacy Day" to engage and educate the rare disease community on regulatory processes related to rare diseases.

This meeting is intended to enhance the awareness of the rare disease community as to FDA’s roles and responsibilities in the development of products (drugs, biological products and devices) for the diagnosis, prevention, and/or treatment of rare diseases or conditions.

This educational meeting will consist of live and interactive simultaneous webcast of presentations provided by FDA experts from various Centers and Offices, as well as from outside experts. The interactive meeting will include two general panel discussion sessions, as well as afternoon breakout sessions for more in-depth information on the roles of FDA. In addition, on-site attendees will have an opportunity during lunch to engage with FDA and outside experts in a small group setting.

Registration:

While attendance is free, registration is required to attend the event.

Register for FDA Rare Disease Patient Advocacy Day

If you need sign language interpretation during this meeting, please contact Megan McNamee at mmcnamee@icfi.com by February 15, 2012.

Location and Directions:

White Oak Campus
10903 New Hampshire Ave
Silver Spring, MD, 20993

Location, directions, and other information about White Oak

Date:

March 01, 2012

Agenda:

Event agenda is in preparation and will be posted prior to the meeting

Webcast:

To connect to the live webcast of the meeting please follow the Connect Pro instructions.

Sponsors:

The FDA Rare Disease Patient Advocacy Day is supported by the Food and Drug Administration (FDA), the National Institutes of Health (NIH), the National Organization for Rare Disorders (NORD), and the Genetic Alliance.

The FDA encourages all attendees to also plan on attending the National Institutes of Health (NIH) Rare Disease Day day-long celebration on February 29, 2012.

Rare Disease Day at NIH

2011-12-31T07:29:00.001-05:00

Rare Disease Day at NIH (RDD@NIH)

On February 29, 2012, the National Institutes of Health (NIH) will celebrate the fifth annual Rare Disease Day with a day-long celebration and recognition of the various rare diseases research activities supported by the NIH Office of Rare Diseases Research, the NIH Clinical Center, other NIH Institutes and Centers; the Food and Drug Administration’s Office of Orphan Product Development; the National Organization for Rare Disorders; and the Genetic Alliance. Rare Disease Day at NIH (RDD@NIH) will be held in the Clinical Center’s Masur Auditorium (Building 10) from 8:30 a.m. to 5:00 p.m. Attendance is free and open to the public.

In addition to the various scheduled talks, we expect to have posters and exhibits from many groups relevant to the rare diseases research community. In association with the Global Genes Project, we again encourage all attendees to wear their favorite pair of jeans.

While attendance is free, we would like to know how many people are planning to attend to prepare accordingly. If you would like to display a poster or exhibit, please include that information on your registration form. You can contact Dr. David J. Eckstein at eckstein@od.nih.gov for more information.

The NIH Office of Rare Diseases Research encourages all attendees to also plan on attending the Food and Drug Administration’s Rare Disease Day activities on March 1, 2012.

Visit the NIH Visitors and Security website for the latest instructions and updates. Please allow 30 minutes to move through security.

Sign language interpreters will be provided. Individuals with disabilities who need reasonable accommodation to participate in this event should contact Kimberly Potter at kpotter@icfi.com or 301-251-4962.

About Rare Disease Day

Rare Disease Day was established to raise awareness with the public about rare diseases, the challenges encountered by those affected, the importance of research to develop diagnostics and treatments, and the impact of these diseases on patients' lives. The focus of Rare Disease Day 2010 was 'Patients and Researchers, Partners for Life!' and is aligned with ORDR's philosophy that researchers need to work closely with patients and patient advocacy groups to maximize chances for success. This philosophy has been put into practice in our very successful Rare Diseases Clinical Research Network.

There are about 7000 rare diseases identified in the United States. About 80 percent of rare diseases are genetic in origin and it is estimated that about half of all rare diseases affect children. Rare diseases can be chronic, progressive, debilitating, disabling, severe and life-threatening. Information is often scarce and research is usually insufficient. People affected face challenges such as delays in obtaining a diagnosis, misdiagnosis, psychological burden and lack of support services for the patient and family. The goals remain for rare disease patients to obtain the highest attainable standard of health and to be provided the resources required to overcome common obstacles in their lives.

By highlighting these issues, the NIH Office of Rare Diseases Research hopes to

Raise awareness of rare diseases
Strengthen the voice of patients and patient advocacy groups
Give hope and information to patients
Bring stakeholders closer together
Coordinate policy actions within the United States and with other countries
Inspire continued growth of the awareness of rare diseases
Emphasize rare disease research and the search for new therapeutics
Get equality in access to care and treatment

The first Rare Disease Day sponsored by EURORDIS was held in Europe on February 29, 2008. February 29th was chosen since it is a rare day and it is symbolic of rare diseases. 2009 was the first time that Rare Disease Day was observed in the U.S. In addition to 17 European countries participating in Rare Disease Day 2009, the United States was joined by Argentina, Australia, Canada, China, Colombia, and Taiwan in celebrating the first global Rare Disease Day. The National Organization for Rare Disorders serves as the coordinator of this activity in the United States.

The Global Genes Project

A video developed by a rare disease parent advocate circulated on YouTube as part of World Rare Disease Day 2009, making a connection between jeans and genes. This video inspired a group of individuals and rare disease organizations to take this connection to the next level by creating the Global Genes Project, a grassroots effort to use jeans to raise awareness for rare genetic disorders.

This group has grown and continues to add individuals and organizations that want to be involved. The hope is that the rare disease community as a whole will view this initiative as an opportunity to build unity around this important cause. The goal is to create a platform for collaboration, while building awareness about the prevalence of rare diseases, educating the public about genes and the impact they play in rare diseases, and engaging support from the general public.

There are numerous organizations that are working to help some of the individual diseases. They are funding much needed research, helping drive policy and develop educational programs, all in an effort to bring hope to this underserved community. The Global Genes Project encourages those who are concerned and compelled to join the cause to help both individual rare disease organizations, children and their families affected, as well as the community as a whole.

More information: http://rarediseases.info.nih.gov/RareDiseaseDay.aspx

Subclinical Cushings syndrome: definition and management

2011-12-22T22:16:00.001-05:00

Subclinical Cushing's syndrome is an ill-defined endocrine disorder that may be observed in patients bearing an incidentally found adrenal adenoma. The concept of subclinical Cushing's syndrome stands on the presence of ACTH-independent cortisol secretion by an adrenal adenoma, that is not fully restrained by pituitary feed-back. A hypercortisolemic state of usually minimal intensity may ensue and eventually cause harm to the patients in terms of metabolic and vascular diseases, and bone fractures.

However, the natural history of subclinical Cushing's syndrome remains largely unknown. The present review illustrates the currently used methods to ascertain the presence of subclinical Cushing's syndrome and the surrounding controversy. The management of subclinical Cushing's syndrome, that remains a highly debated issue, is also addressed and discussed.

Most of the recommendations made in this chapter reflects the view and the clinical experience of the Authors and are not based on solid evidence.

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1365-2265.2011.04253.x

Affiliations: 1: Internal Medicine I, San Luigi Gonzaga Hospital, University of Turin, Orbassano, Italy

Buy the article at http://www.ingentaconnect.com/content/bsc/cend/2012/00000076/00000001/art00003

Investigational drugs may expand medical treatment of Cushing’s syndrome

2011-12-22T20:26:00.001-05:00

Endocrinologists face many challenges when treating patients with Cushing’s syndrome. Diagnosis can be difficult because many of the disease’s characteristics, such as obesity, depression and hypertension, are also common in the general population.

Treating the disease presents hurdles as well. With its potential for total cure, transsphenoidal surgery remains the first-line treatment. However, the problems of achieving permanent remission in all cases demonstrate the need for medical therapies for this condition.

Currently, endocrinologists use several medical therapies to treat hypercortisolism, although none have FDA approval for that particular indication. Two new investigational drugs — mifepristone (Korlym, Corcept Therapeutics) and pasireotide (SOM230, Novartis) — have the potential to meet those unmet needs, according to experts interviewed by Endocrine Today.

“Recently completed research studies, which involved innovative medical therapeutic strategies that target the corticotroph adenoma itself or block the effects of cortisol in the periphery, should bring new treatment options in the future,” Maria Fleseriu, MD, associate professor, director of the Northwest Pituitary Center at Oregon Health & Science University, said in an interview.

Manufacturers of both new medications have submitted new drug applications to the FDA. Corcept expects to hear from the FDA on Feb. 17, according to a spokesperson for the company.

Mifepristone has a unique mode of action in that it blocks the cortisol receptor, Robert L. Roe, MD, president of Corcept Therapeutics, said in an interview.

“With that receptor blocked, many of the problems associated with Cushing’s syndrome can be greatly improved, including: obesity, diabetes, insulin resistance, high blood pressure, quality of life and depression,” Roe said.

The SEISMIC trial, a 24-week, multicenter, open-label study, included 50 patients with persistent or recurring Cushing’s disease, metastatic adrenal cortical carcinoma or ectopic adrenocorticotropic hormone (ACTH) syndrome that was not amenable to surgery, according to Fleseriu, who was an investigator on the study. There were two primary endpoints: blood sugar improvement in patients with glucose intolerance and an improvement in BP in patients with a diagnosis of hypertension but without abnormal blood sugar levels. The key secondary endpoint looked for global clinical improvement as determined by a three-member independent data review board.

Results from the phase 3 study showed that, overall, mifepristone yielded significant clinical and metabolic improvement in patients with refractory Cushing’s syndrome, Fleseriu said. Of the glucose-intolerant patients, 60% responded, and BP improved in 38% of patients. The global clinical endpoint was positive in 87% of patients, Roe said.

Maria Fleseriu

“In addition, out of 34 patients who completed the main study, 30 elected to continue in the long-term extension study,” Fleseriu said.

She said mifepristone “offers a new approach for the treatment of Cushing’s syndrome that [has] failed other therapies. Keeping in mind that biochemical parameters will not be available for monitoring these patients, close clinical observation is recommended.”

Yet, there are aspects of mifepristone that are still unknown.

“There will be a learning curve with this drug on how to dose it and use it properly to get a good response,” said James Findling, MD, professor of medicine, Endocrinology Center and Clinics, Medical College of Wisconsin, Milwaukee, who was the principal investigator of the study.

James Findling

Also on the horizon is the investigational agent pasireotide, a multiligand somatostatin analogue with a high affinity for the somatostatin receptor type 5, which is often expressed by corticotroph adenomas in Cushing’s disease. Pasireotide blocks the secretions from ACTH-secreting pituitary tumors.

“Pasireotide works by attacking the pituitary tumor to reduce the ACTH level,” according to Laurence Katznelson, MD, professor of medicine and neurosurgery at Stanford University and medical director of the pituitary program at Stanford Hospital and Clinics. “Possibly, this drug could prevent tumor growth or lead to tumor shrinkage, although we await data to support that.”

Results of the multicenter, phase 3 PASPORT-CUSHINGS trial, presented at the Endocrine Society’s 93rd Annual Meeting & Expo in June, included 162 patients with persistent/recurrent or newly diagnosed Cushing’s disease who were ineligible for surgery. Researchers randomly assigned participants to receive twice-daily subcutaneous pasireotide injections of 600 mcg or 900 mcg. The primary endpoint was urinary-free cortisol levels at 6 months without dose up-titration.

Of the patients in the 900-mcg dose group, 26.3% had normal urinary-free cortisol levels at 6 months; at 12 months, 25% maintained normal levels. The median reduction from baseline in urine-free cortisol after 6 months of treatment was 47.9% for both dose groups.

The researchers noted significant clinical benefit in most patients, including lower BP and total cholesterol, as well as weight loss, Fleseriu said.

“It is noteworthy that while urinary-free cortisol normalization was seen in just a subset of patients, the rate of normalization was higher in patients with lower baseline urinary-free cortisol, making it, in my opinion, an attractive treatment for patients with mild elevations in urinary-free cortisol,” Fleseriu, who was also an investigator for this trial, told Endocrine Today.

Pasireotide was well tolerated in the studies, she added.

“Adverse events were comparable to the other somatostatin analogues, with the exception of a much higher incidence of hyperglycemia,” Fleseriu said. “Patients treated with this drug will require strict monitoring and prompt treatment of hyperglycemia.” The reasons for hyperglycemia are related to inhibition of insulin release from the pancreas by this multiligand somatostatin analogue. The type 5 receptor is abundant on pancreatic insulin secreting cells of the pancreas.

Timely diagnosis, treatment critical

Cushing’s syndrome is the result of chronic exposure to high levels of cortisol. Cortisol, typically released in stressful situations, controls how the body uses carbohydrates, fats and proteins. In addition, it helps decrease the immune system’s response to inflammation.

Untreated, Cushing’s syndrome can have serious consequences, including significant mortality and morbidity. Timely diagnosis and appropriate treatment are critical for this rare disorder, according to Fleseriu, who is also associate professor of medicine/endocrinology and neurological surgery at Oregon Health & Science University.

The endocrinologist uses the following tests to diagnose the disorder: 24-hour urinary-free cortisol levels; late-night salivary cortisol measurements; and low-dose dexamethasone suppression test.

After making the diagnosis of hypercortisolism, the next step is to determine the cause of excess cortisol secretion. There are several tests available for this purpose: corticotropin-releasing hormone (CRH) simulation test; direct radiologic visualization of the pituitary and adrenal glands; and inferior petrosal sinus sampling for ACTH.

The most common cause is long-term synthetic steroid use to treat inflammatory illnesses such as asthma or rheumatoid arthritis, according to Katznelson. In these cases, gradually reduction of the glucocorticoid will reverse the disorder.

Another cause is an ACTH-secreting pituitary adenoma. The excess stimulates the adrenals to produce and secrete excess cortisol release, Katznelson said. This is also known as Cushing’s disease.

Pituitary adenomas are responsible for 70% of Cushing’s syndrome cases, according to information from the National Institute of Diabetes and Digestive and Kidney Diseases.

Surgery is first-line treatment

John Carmichael

First-line therapy for Cushing’s disease is transsphenoidal adenomectomy, in which the surgeon approaches the pituitary through the nose and, using either a microscope or endoscope by trained neurosurgeons, according to John Carmichael, MD, assistant professor of medicine, The Pituitary Center, Cedars-Sinai Medical Center, Los Angeles.

The procedure boasts an excellent cure rate.

“In good hands, with a small tumor, you can get cure rates of about 85%,” Carmichael said. “It depends on a number of factors: the skill of the surgeon, the size of the tumor and the level of invasiveness.”

If surgery is curative, the patient will require cortisol replacement.

“Once you remove the tumor, the normal tissue has been suppressed by the activity of the tumor for so long that it takes a long time for patients to recover and start making cortisol on their own,” Carmichael said. “It can take as long as 6 to 12 months for patients to completely recover their normal cortisol secretion once they’ve been cured.”

David M. Cook

However, the surgery is associated with risks, including bleeding and infection, although they are “pretty rare,” according to Carmichael. One of the most common risks is a pituitary injury that can cause diabetes insipidus, which is almost always transient. Other postoperative problems include possible cerebrospinal fluid leaks and the possibility of recurrence, said David M. Cook, MD, an endocrinologist in the department of medicine, Oregon Health & Sciences University.

Sometimes the tumor is hard to find during the first surgery, Katznelson said.

“The problem is, in 40% to 50% of patients who have Cushing’s disease, the tumor is very small, if not almost invisible, on the MRI scan,” he said. As a result, the surgeon may remove normal gland or possibly the entire pituitary, resulting in hypopituitarism. The patient would require hormone replacement and would still have Cushing’s syndrome.

Radiation is a possible treatment for these cases.

“The role of radiation is in the patient who has already had surgery for Cushing’s syndrome. The tumor is visible but cannot be completely removed. Radiation is most useful when there is a target to irradiate,” Katznelson said, adding that even in these cases, radiation cannot promise 100% efficacy.

Unfortunately, radiation takes a significant amount of time to work.

“People are a little reluctant to use radiation because it takes years to help,” Cook said. “It is not curative and patients can relapse from radiation also; it is not foolproof.”

Ectopic ACTH syndrome

Sometimes, tumors located outside the pituitary can produce ACTH, resulting in the ectopic ACTH syndrome. The tumors are usually malignant. In more than half of the cases, the tumors are found in the lungs, according to information from the NIDDK.

“You would need surgery in that location to get rid of the tumor,” Carmichael said.

If an adrenal tumor is stimulating an overabundance of cortisol, the definitive cure is adrenalectomy.

“If we do adrenalectomy, all of the [symptoms of] Cushing’s syndrome go away, but the primary pituitary tumor, which may have been microscopic, can start to become more aggressive and grow and become more difficult to treat in the long run,” Katznelson said. “That is Nelson’s syndrome.”

The adrenal insufficiency that follows adrenalectomy is serious, Cook said.

“It is dangerous to not have your adrenals; it is the most dangerous disease that endocrinologists treat,” he said. “A number of sudden deaths have been reported in patients without adrenals.”

Katznelson also said that managing these patients can be challenging.

“Management of primary adrenal insufficiency is sometimes difficult, because not only does the patient lack cortisol, but will also lack aldosterone, which is important for maintaining electrolytes and volume status,” he said. “Patients often find it quite challenging to manage primary adrenal insufficiency.”

Medical therapies for Cushing’s syndrome

Besides surgery and radiation, endocrinologists can use several medical therapies to treat Cushing’s syndrome; however, to date, none has obtained FDA approval to treat the disorder.

The medical treatment used most often in the United States is ketoconazole, an antifungal agent that blocks the enzymes in the adrenal glands that produce steroids, Findling told Endocrine Today.

Ketoconazole, administered two to three times daily, is generally successful.

“It is an effective therapy,” Findling said. “Probably 50% to 70% of patients will have a response.”

However, this drug is not the optimal choice for long-term use.

“Ketoconazole has been associated with some toxicity; liver function abnormalities can occur and, in fact, liver failure can occur,” he said.

Another medical treatment option is mitotane (Lysodren, Bristol-Myers Squibb), which blocks adrenal steroid enzymes, Findling said. This toxic agent takes considerable time to work; in fact, it may require roughly 3 or 4 months for cortisol levels to normalize. It is used rarely in the United States.

“Mitotane has a limited future as a therapy for Cushing’s syndrome, except for in patients who have adrenal cancer, at least in the US,” Findling said.

Metyrapone (Metopirone, Novartis), another agent, effectively blocks adrenal steroid enzymes; however, it is not commercially available in the United States, Findling said.

Etomidate is an anesthetic agent that also inhibits adrenal steroidogenesis and is employed successfully in patients with very severe hypercortisolism who are not ready for surgery.

“If etomidate were available in a pill, it would be an excellent medical treatment for Cushing’s syndrome,” Findling said. “With subhypnotic doses, etomidate lowers the cortisol level smoothly down into the normal range. … It is well tolerated, but has to be given as a continuous IV infusion, so it is not practical.”

All of these medications have severe adverse effect profiles, according to Carmichael.

No replacement for surgery … yet

Although mifepristone and pasireotide show some promise as treatments for Cushing’s syndrome, it is not time to put the scalpels in storage, the experts said.

“Neither of these drugs, at least for the foreseeable future, will replace surgical treatment of Cushing’s syndrome,” Findling said. “Like most disorders, if you have a surgical procedure that will resolve the endocrinopathy and restore normal hormonal function, it is usually the treatment of choice.”

However, these medications are a welcome addition to the armamentarium, Carmichael said.

“It remains to be seen exactly what their place will be and how they will be best used. But, certainly, in cases where surgery is not an option or where you need to control the disease in someone who has very severe disease, they would have a role,” he said. Currently, Carmichael sees medical therapy as an adjuvant treatment, which would follow surgery if it was not curative. Also, endocrinologists may use them in place of surgery if surgery was not an option.

“There is a lot more room for work,” Carmichael said. “The ideal paradigm of having a medication that is safe and controls the disease and in a sense would replace surgery would be an ideal goal, but we are certainly not there yet.”– by Colleen Owens

For more information:

Colao A. OR09-6. Presented at: The Endocrine Society 93rd Annual Meeting & Expo; June 4-7, 2011; Boston.

Fleseriu M. [OR09-5] Mifepristone, a glucocorticoid receptor antagonist, produces clinical and metabolic benefits in patients with refractory Cushing syndrome: results from the Study of the Efficacy and Safety of Mifepristone in the Treatment of Endogenous Cushing Syndrome (SEISMIC). Presented at: The Endocrine Society 93rd Annual Meeting & Expo; June 4-7, 2011; Boston.

Gross BA. Neurosurg Focus. 2007;23:E10.

National Institute of Neurological Disorders and Stroke. NINDS Cushing’s syndrome information page. Available at: www.ninds.nih.gov/disorders/cushings/cushings.htm.

National Endocrine and Metabolic Diseases Information Service. Cushing’s syndrome. Available at: www.endocrine.niddk.nih.gov/pubs/cushings/cushings.aspx#causes.

Disclosures: Dr. Fleseriu is principal investigator in multiple Cushing’s trials and past consultant for Novartis; she is also the principal investigator on Corcept Cushing’s trials. Dr. Findling is a paid consultant for Corcept Therapeutics. The other doctors in this article did not report any relevant financial disclosures.

Which is the most reliable screening method for Cushing’s syndrome?

Tests are equally accurate, but have limitations

The diagnosis of Cushing’s syndrome is problematic. It is one of the most difficult endocrine diseases to diagnose. Diagnosis includes assessing the symptoms and signs of Cushing’s syndrome because the symptoms and signs overlap with common disorders, including obesity, depression and polycystic ovary syndrome. Many patients consult websites in an attempt to find an explanation for their weight gain, fatigue, depression and other symptoms. They ask frequently after a Web search if their symptoms could be Cushing’s syndrome.

Screening tests for Cushing’s syndrome include three different tests: an 11 p.m. or midnight salivary cortisol level; a 24-hour urine free cortisol level; and an 8 a.m. cortisol level after ingestion of 1 mg of dexamethasone at midnight the previous night. How reliable are these tests? They are equally accurate — approximately 90% to 92% reliable, which is actually good for screening tests.

However, all three tests have limitations. Results of the nighttime salivary cortisol test are affected by laboratory accuracy (not all laboratories are equally reliable) and sleep patterns. In severe depression cases, the results may be falsely elevated. The 24-hour urine free cortisol test is an indicator of overall cortisol production. The most accurate method of measurement — tandem mass spectrometry with concomitant measurement of urine volume and urine creatinine — provides a good measure. It may take several 24-hour urine collections to confirm hypercortisolism. The 1-mg overnight dexamethasone suppression test is reliable, but with several caveats. The test is standardized according to administering dexamethasone at midnight and measurement of serum cortisol promptly at 8 a.m. the following day. However, while the patient may have gone to the lab at 8 a.m., the blood sample may have been obtained later, which invalidates the test. Additionally, if the patient is taking medications that alter dexamethasone metabolism, the results may not be valid. The endocrinologist must measure a serum dexamethasone level to confirm the validity of the test.

The diagnosis of Cushing’s syndrome is dependent upon confirming consistent overproduction of cortisol. The diagnosis may require repeated testing and this should be done in any patient in which there is a suspicion of Cushing’s syndrome.

Mary Lee Vance, MD, is professor of medicine and neurosurgery at University of Virginia Health System, Charlottesville, Va.

Disclosure: Dr. Vance reports no relevant financial disclosures.

Late-night salivary cortisol is best initial test

Ty Carroll

No test is perfect for all patients. In addition, it is important to remember that some patients will require multiple, different tests to confirm or exclude Cushing’s syndrome. However, that being said, late-night salivary cortisol is the best initial screening for most patients with suspected Cushing’s syndrome.

Late-night salivary cortisol is the most specific test for Cushing’s syndrome. The sensitivity and specificity are very good. Multiple studies have examined late night salivary cortisol testing, and the majority of those studies show sensitivity of more than 95% and a specificity in the range of 90% to 100%. That is comparable to — or better than — other methods to diagnose Cushing’s syndrome.

Also important to note: It is easy for patients to perform late-night salivary testing. Patients are able to do the collection at home and mail in the completed samples to a reference lab, whereas urinary free cortisol and dexamethasone suppression testing can be difficult for some patients to complete. In addition, for the most part, late-night salivary cortisol is not affected by other medications that patients take, unlike dexamethasone suppression testing, which can be affected by several medications that patients often take to treat other conditions.

Ty Carroll, MD, is assistant professor of medicine at Endocrinology Center and Clinics, Menomonee Falls, Wisc.

Disclosure: Dr. Carroll is an investigator in Corcept’s clinical trials of mifepristone.

From http://www.endocrinetoday.com/view.aspx?rid=90578

A Pill That Stops Stress In Your Brain Before You Feel It

2011-12-16T11:02:00.001-05:00

Stress makes many of us miserable — but it can also kill you. Besides just causing horrible anxiety and depression, the physiological basis for stress has also been linked to diseases as varied as obesity, postpartum depression, Cushing's syndrome, epilepsy, and osteoporosis. But what if we could just turn your brain's stress response off?

Now, researchers from Tufts claim to have pinpointed the way that stress hormones hit specific receptors in your brain — and they've even been able to block them. This could lead to the next great psychopharmaceutical breakthrough.

The Tufts researchers discovered that stress pathways are activated by neurosteroids acting on corticotrophin-releasing hormone neurons in what's known as the Hypothalamus-Pituitary-Adrenal axis. By blocking the synthesis of the neurosteroids, they stopped the elevation of corticosterone, and prevented anxiety in mice.

"We have identified a novel mechanism regulating the body's response to stress by determining that neurosteroids are required to mount the physiological response to stress. Moreover, we were able to completely block the physiological response to stress as well as prevent stress-induced anxiety," said author Jamie Maguire, PhD.

Now the team is focusing on modulating the neuroreceptors to treat some of the diseases that accompany stress — be they depression, anxiety, or epilepsy.

From http://io9.com/5867762/a-pill-that-stops-stress-in-your-brain-before-you-feel-it

P36 - Severe Osteoporosis in Cushing’s Syndrome

2011-12-14T22:06:00.001-05:00

Clin Cases Miner Bone Metab. 2010 Sep-Dec; 7(3): 240.

PMCID: PMC3213844

M.C. Caffetti

Specialist Rehabilitation Unit, Hospital of Voghera, Voghera, Italy

Abstract

Cushing’s syndrome is characterised by a series of clinical manifestations due to hypersecretion of cortisol. These include: arterial hypertension, diabetes mellitus (DM), asthenia, amenorrhea, osteoporosis and pathological fractures. We describe the case of a 70-year-old woman with Cushing’s syndrome with right adrenal adenoma, vertebral compression fractures (VCFs) and severe secondary osteoporosis. This patient had been diagnosed with Cushing’s syndrome in May 2008, three years after the onset of arterial hypertension and type II DM, treated with insulin; in July 2008, she underwent right adrenalectomy and replacement therapy with cortisone acetate, 37.5 mg/day, in association with a multiple drug regimen for hypertension and DM; she also had an at least 10-year history of dorso-lumbar pain with multiple disc protrusions. As part of a series of investigations for Cushing’s syndrome the patient underwent femoral bone mineral densitometry, recording a T-score <−3, radiographic examination of the dorso-lumbar spine, which revealed collapse of the superior endplate of D7 and a wedge fracture of D8. At the endocrinology centre of reference for Cushing’s syndrome, she began treatment with alendronate 70 mg/day without undergoing blood chemistry tests of bone metabolism and without calcium and vitamin D supplementation. At the end of August 2009, she experienced worsening spinal pain due to a new severe fracture of D9, which was confirmed on MRI as a recent fracture. At the end of December 2009 she received kyphoplasty of D9, antiresorptive therapy and a CAMP-C35 brace.

In January 2010 she was admitted to the specialist rehabilitation unit for functional recovery, in view of her comorbidities, and bone disease investigation, with collection of history relating to osteoporosis risk factors. First- and second-level blood chemistry analyses revealed the presence of iron-deficiency anaemia, mild chronic renal insufficiency, and secondary hyerparathyroidism (PTH 101ng/ml); spinal radiography revealed severe VCFs of D7, D8 and D9, treated with kyphoplasty; the patient was also assessed using the VAS for pain, the FIM to evaluate independence in activities of daily living, and the SF-36 to investigate quality of life. The alendronate treatment was suspended and the patient was given cholecalciferol 300,000 IU, administered as an oral bolus, followed by a maintenance dose of 800 IU/day. When PTH values had returned to normal, she began treatment with teriparatide 20 mcg/day s.c. (therapeutic plan in compliance with Note 79 issued by the AIFA - Italian Drug Agency).

In conclusion, this case underlines the importance of a correct diagnostic and therapeutic approach in patients with severe osteoporosis. Over time, we will evaluate the efficacy of the treatment in preventing new fractures and the whether the use of a bone anabolic agent might be the correct choice also in order to control pain and improve quality of life. There are no reports in the literature of patients with Cushing’s syndrome treated with teriparatide.

Cushing’s Syndrome Clinical Analysis of 77 Cases

2011-12-10T14:16:00.001-05:00

OBJECTIVE To analyze the cause of Cushing’s syndrome classification, the major clinical manifestations and laboratory features of frequency of occurrence, and the efficiency of various diagnostic methods to evaluate the clinical doctors to improve diagnosis and treatment of disease, improve patient prognosis.

METHODS from 2004 to 2009 in our hospital by clinical or pathological diagnosis of Cushing’s syndrome in patients with clinical data, of which 57 cases of females, 20 males. For the 77 cases of clinical manifestations, laboratory examination, imaging studies, clinical diagnostic tests, pathological characteristics and with the results of literature analysis and summary of them were analyzed retrospectively.

RESULTS 1. From 2004 to 2009 were diagnosed 77 cases of Cushing’s syndrome, of which 20 males, female 57 cases, male: female = 2:2.85, adrenal adenoma 80% of female patients of childbearing age women.

2. In Cushing’s disease causes the most common (35 cases), followed by adrenal cortical adenoma (30 cases, the left side of 21 cases), there is a growing trend in the latter. Cushing’s disease course and age of onset of adrenal adenomas were higher than those, the difference was statistically significant (P <0.05), the shortest duration of adrenal carcinoma.

3. Clinical performance, the performance of the diversity of its starter, Hypertension and central obesity were the most frequently occur in 75%, and 79.22% suffering from hypertension, Hypertension 1 11.48%, Hypertension 2 62.30%, Hypertension 3 grade 26.23%, and the incidence of abnormal glucose metabolism and hyperlipidemia, respectively 41% and 68%, of which the proportion of diabetes by 30%, 65% of patients had hypokalemia, mostly mild to moderate, adrenal cortex carcinoma 100% of patients with a low potassium, and is of moderate to severe hypokalemia. Cushing’s disease and adrenal adenoma in serum potassium, blood pressure and gender showed no significant difference.

4. In the diagnosis of Cushing’s syndrome test, blood cortisol circadian rhythm disappeared (98.65%), elevated midnight serum cortisol (98.55%), 4Pm serum cortisol increased (97.14%), low-dose dexamethasone suppression test (94.59%), 24hUFC increased (91.22%), morning serum cortisol increased (71.62%). Low-dose dexamethasone suppression of serum cortisol in the morning the next day the basis of 8:00 of serum cortisol of 50% and 275,200,138,50 nmol/Lthe sensitivity of the cut-off point were 94.6%, 95.9%, 97.3% , 97.3% and 100%.

5. Patients with Cushing’s syndrome in the differential diagnosis, 80% of Cushing’s patients can be high-dose dexamethasone suppression, while more than 95% of patients with adrenal cortical adenoma can not be high-dose dexamethasone suppression. Cushing’s patients compared with blood cortisol and ACTH levels were significantly higher in patients with adrenal tumors, while the latter’s rhythmic performance is worse, the differences were statistically significant (P<0.05). Both urinary free cortisol showed no significant difference.6. imaging examination, pituitary MRI can detect 88% of Cushing’s disease there is pituitary adenoma, while the adrenal CT 100% can find out the adrenal tumors, adrenal CT of adrenal tumors and hyperplasia pathology consistent rate of 97.5%.

CONCLUSION 1. The present study in Cushing’s disease and adrenal cortical adenoma is still the most common cause of this group a high proportion of cases of adrenal adenoma, left more common. Cushing’s syndrome more common in women of childbearing age women, more common adrenal adenoma, Hypertension is the most common symptoms, mostly moderate to severe hypertension, diabetes, low potassium, high incidence of dyslipidemia.

2. Diagnostic tests in the CS, the morning cortisol increase the sensitivity of the worst, and serum cortisol circadian rhythm disappeared, midnight serum cortisol increased, 4PM cortisol rise, low-dose dexamethasone suppression test, 24hUFC elevated. There was no significant difference。

3. Patients with Cushing’s disease course, age of onset, blood cortisol and ACTH levels were higher than the adrenal adenoma, the latter comparison rhythm of blood cortisol rhythm performance is worse. The serum potassium, blood pressure and no significant difference in gender.

4. High-dose dexamethasone suppression test is to identify Cushing’s disease and adrenal cortical adenoma of the most appropriate method, CT of the adrenal lesion positive rate and help confirm the diagnosis and localization, B super-positive rate was significantly lower than CT, head MRI in Cushing’s disease positive rate.

From http://www.tumorres.com/tumor-metastasis/15968.htm

Adrenal glands: The reserve tank for stress?

2011-12-09T14:14:00.001-05:00

Have you ever noticed that when you are "stressed" you can feel either emotionally/physically depleted or energized? When our body is under stress the brain responds by producing epheniphrine (aka adrenaline), sending signals to our adrenal glands, increasing the rate at which our heart beats while releasing oxygen to our muscles. The long term response to this process produces cortisol (aka the stress hormone) facilitating the release of energy throughout our body. However, when our body isn't properly balanced these hormones can wreak havoc on our wellness possibly resulting in one of three conditions: Cushing's syndrome, Cushing's disease or Addison's disease.

The actual Adrenal glands sit physically atop both kidneys, taking on a triangular shape and a roundish rectangular type shape. These glands are responsible for our sex hormones and cortisol, helping us respond to stress amongst other functions. When our body is under stress, physically and/or nutritionally, it responds one of two ways: Produces too much or too little of the cortisol hormone. Our Adrenal glands also contribute to regulating our blood sugar, blood pressure, salt and water.

Adrenal disorders can cause our body to make too much or not enough of these hormones, bringing about adrenal gland related syndromes and disease. Cushing's syndrome results from our body making too much versus Addison's disease produces too little.

Cushing's syndrome vs Cushing's disease

Glucocorticoids (naturally produced in our body or received through medicine) are groups of corticosteroids (cortisol or dexamethasone) involved in metabolizing our carbohydrates and proteins. When taken synthetically (i.e. treatment of allergies, skin problems, and respiratory problems) or over-produced naturally, the side effects can result in "Cushing's syndrome".

Cushing's syndrome can occur one of two ways: Endogenous or Exogenous. Endogenous is caused by the body (usually through tumors). Exogenous is caused by medication. In both cases, the body produces too much cortisol.

Symptoms: Severe fatigue/muscle weakness, high blood sugar and high blood pressure, upper body obesity, thin arms/legs, bruising easily.

Treatment: The cure and treatment for Cushing's Syndrome and disease can come through medicine, surgery, or by lowering the dosage of your current synthetic hormone treatment and can likely be cured.

Cushing's disease is the most common form of endogenous Cushing's syndrome and is likely treatable. Caused by a tumor in the pituitary gland secreting too much Adrenocorticotropic hormone (ACTH), this type of tumor does not spread and can be removed through surgery.

Nutrition: See a nutritionist or dietician for your condition. Mostly, avoid excess sodium. High blood sugar (hyperglycemia) and high blood pressure can easily occur with this condition. Bone loss density is common with this condition, so be extra aware of your calcium (800 – 1200 mg per day, based upon age) and Vitamin D intake (5mcg from age 0-50, increasing up to 10 mcg 50-71, and 15 mcg after 71). Eating healthy, balanced and whole food (versus processed) is extremely important. (Resource: http://www.aboutcushings.com/understanding-cushings-disease/causes-and-differences.jsp)

Addison's disease Opposite from Cushing's syndrome, Addison's disease doesn't make “enough” of the sex hormones and cortisol. The result of this disease causes our immune system to attack our tissue, damaging our adrenal glands.

Symptoms: Weight loss, muscle weakness, increasingly worse fatigue, low blood pressure and patchy or dark skin.

Treatment: If left untreated, the condition can be fatal. Lifetime hormone treatment is usually required. Addison disease patients should always carry medical/emergency ID on them, listing their medication, dosage and disease

Lab tests can confirm that you have Addison's disease. If you don't treat it, it can be fatal. Very likely, you will need to take hormone pills for the rest of your life. If you have Addison's disease, you should carry an emergency ID. It should say that you have the disease, list your medicines and say how much you need in an emergency.

(Ref: http://www.nlm.nih.gov/medlineplus/cushingssyndrome.html, NIH: National Institute of Neurological Disorders and Stroke)

If all of this sounds a little overwhelming there is hope. Learning how to balance our stress-filled lives is extremely important to our overall health. Healthy nutrition always contributes benefits to our overall wellness. We can overwhelm our endocrine system by simply not eating nutritionally. Understanding that “Food is a drug” is vitally important to how we help our body naturally heal itself. The above conditions are the result of our body not handling the stress we are putting it through, causing our body to producing too much or too little of the sex hormones and cortisol.

Unless we first address what we can do naturally through nutrition, the medicine we consume will only do so much in helping our body heal completely. You simply cannot continue doing the same thing over and over again, expecting the medicine to do all the work. Some diseases are brought upon us through our environment (emotionally as well as physically) as well as our diet/nutrition. Reviewing our entire wellness is always wisdom whenever we're diagnosed with anything.

Certainly listen to your doctor and their advice. But also ask your doctor to refer you to a nutritionist or clinical/registered dietician for a complete evaluation that includes a review of your nutritional diet/wellness. Too often we reach for a pill or a procedure to “fix” our health problems, ignoring what we should be doing on our own to help our body heal. Medical intervention is "sometimes" the result of providing our body with what it cannot produce on its own. Nutrition should always be the “natural” medicine we take, as well as what we might need through prescribed medication.

Quick Tips for Wellness: Living “well” requires living nutritionally balanced.

Adapted From http://hamptonroads.com/2011/12/adrenal-glands-reserve-tank-stress

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2011-12-08T11:49:00.001-05:00

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The Message Boards will be Down

2011-11-30T23:55:00.001-05:00

The boards will be down for a few days for an upgrade and move to a new server.

For more information, please see this post.

After the upgrade, there will be a learning curve for everyone, so please be patient!

Endocrine disorders & female infertility

2011-11-30T13:48:00.001-05:00

David Unuane, MD (Doctor), Department of Endocrinology, Universitair Ziekenhuis Brussel, UZ Brussel, Vrije Universiteit Brussel, Brussels, Belgium, Herman Tournaye, MD, PhD (Professor, Doctor), Brigitte Velkeniers, MD, PhD (Professor, Doctor), Kris Poppe, MD, PhD (Professor, Doctor)

Female infertility occurs in about 37% of all infertile couples and ovulatory disorders account for more than half of these. The ovaries are in continuous interaction with the other endocrine organs. The interplay may account for infertility occurring at different levels and may render the diagnosis of infertility a difficult exercise for the involved physician. A hypothalamic cause of female infertility should be considered in an appropriate clinical context, with tests pointing to a hypogonadotropic hypogonadism. It can be functional, physiological or related to organic causes. Hyperprolactinemia has well characterized effects on the normal gonadal function and treatment is well established.

Acromegaly and Cushing’s disease may impair fertility at different levels, mechanisms involved however remain ill defined. Thyroid disorders, both hyperthyroidism and hypothyroidism, can interact with the ovaries, through a direct effect on ovarian function, but autoimmunity may be involved, as well as alterations of the sex hormone binding protein levels. Primary ovarian disorders, such as the polycystic ovary syndrome and primary ovarian insufficiency are frequent diseases, for which novel treatments are currently being developed and discussed.

We will propose an algorithm for the diagnosis and approach of the female patient presenting with infertility on the basis of the available evidence in literature.

Keywords: female infertility, pituitary, adrenal, ovarian, thyroid

From http://www.bprcem.com/article/PIIS1521690X1100087X/abstract?rss=yes

Not the Usual Suspects: Animal Study Finds Surprising Clues to Obesity-Induced Infertility

2011-11-18T11:37:00.001-05:00

Source: Johns Hopkins Medicine

FOR IMMEDIATE RELEASE

Newswise — Infertility is common among obese women, but the reasons remain poorly understood and few treatments exist. Now a team of Johns Hopkins Children's Center scientists, conducting experiments in mice, has uncovered what they consider surprising evidence that insulin resistance, long considered a prime suspect, has little to do with infertility in women with type-2 diabetes, polycystic ovary syndrome (PCOS) and metabolic syndrome, all obesity-related conditions in which the body becomes desensitized to insulin and loses the ability to regulate blood sugar.

In a report, published online Nov.10 in the journal Diabetes, the Johns Hopkins scientists say the real culprit appears to be insulin sensitivity in the ovaries and the pituitary.

The Johns Hopkins team said its findings show that these organs escape insulin resistance and, awash with high levels of circulating insulin common in obesity, develop abnormal cell signaling that disrupts ovulation and eventually leads to infertility.

"Our findings suggest that the focus should shift from treating insulin resistance in peripheral tissue to taming insulin sensitivity in the pituitary and ovaries," says lead investigator Sheng Wu, Ph.D., of the Johns Hopkins Children's Center. Scientists traditionally have treated obesity-induced infertility by lowering blood insulin to counter the effects of insulin resistance.

A 2010 study by the same team discovered that the pituitary gland, insensitive to insulin in lean mice, became sensitive to elevated levels of insulin seen in human and rodent obesity. By knocking out the insulin receptors in the pituitary glands of obese mice, the researchers were able to partially restore fertility, thus proving that abnormal insulin signaling in the pituitary was only part of the story.

"In the original study, disrupting insulin signaling in the pituitary restored 50 percent of fertility in obese mice, but the search was on for the accomplice," says senior investigator Andrew Wolfe, Ph.D., an endocrinologist at the Johns Hopkins Children's Center. "Our new findings point to the ovaries."

In the pituitary, faulty insulin signaling stimulates increased secretion of luteinizing hormone, the researchers say. In the ovary, it puts testosterone production into overdrive. Both disrupt ovulation, the researchers explain.

In the latest study, lean mice and mice made obese on a three-month high-fat diet received injections of progressively higher doses of insulin to mimic the effects of high circulating insulin seen in obesity, diabetes and PCOS. In lean mice, the ovaries and pituitaries were insensitive to the hormone at low-dose injections, and responded only when injected with higher doses of insulin. The "trigger" doses corresponded to insulin levels typically seen in obesity. Obese mice with naturally elevated insulin levels exhibited high levels of insulin signaling in their pituitary and ovarian cells. When injected with insulin, the livers and muscles of obese mice showed greatly reduced response to insulin -- or insulin resistance. Their ovaries and pituitary glands, however, responded to insulin injections, confirming that in obese mice, these reproductive organs escape the insulin resistance seen in other organs.

To determine insulin sensitivity, the researchers focused on two signaling proteins, IRS-1 and IRS-2, regulators of cell-insulin communication involved in the development of insulin resistance in liver and muscle tissue. The scientists hypothesized that in the pituitary and ovaries, these messenger proteins would remain dormant under normal insulin levels, but would get activated once exposed to high levels of insulin. Indeed, the researchers found, the pituitary glands of obese mice showed higher IRS-2 signaling activity compared with lean mice, while the ovaries of obese mice had higher signaling activity in both IRS-1 and IRS-2 proteins, compared with lean mice.

In a follow-up study now under way, the Hopkins team is trying to determine whether knocking out the insulin receptors in both the ovaries and the pituitary would fully restore fertility in obese mice with high insulin levels.

Other co-investigators on the study included Sara Divall, M.D., and Fred Wondisford, M.D., both of the Johns Hopkins Children's Center.

The research was funded by the Endocrine Fellow Foundation, by The Eunice Kennedy Shriver National Institute of Child Health and Human Development, part of the National Institutes of Health, and by the Baltimore Diabetes Research and Training Center, which is supported by the National Institute for Diabetes and Digestive and Kidney Diseases.

Founded in 1912 as the children's hospital of the Johns Hopkins Medical Institutions, the Johns Hopkins Children's Center offers one of the most comprehensive pediatric medical programs in the country, treating more than 90,000 children each year. Hopkins Children's is consistently ranked among the top children's hospitals in the nation.
Hopkins Children's is Maryland's largest children's hospital and the only state-designated Trauma Service and Burn Unit for pediatric patients. It has recognized Centers of Excellence in dozens of pediatric subspecialties, including allergy, cardiology, cystic fibrosis, gastroenterology, nephrology, neurology, neurosurgery, oncology, pulmonary, and transplant. For more information, please visitwww.hopkinschildrens.org

From http://www.newswise.com/articles/not-the-usual-suspects-animal-study-finds-su.../articles/list&category=medicine&page=1&search%5Bstatus%5D=3&search%5Bsort%5D=date+desc&search%5Bsection%5D=10&search%5Bhas_multimedia%5D=

(Addison's Disease) Coma man defies odds to write book

2011-11-12T09:20:00.001-05:00

By Lisa Smyth

A Northern Ireland man has defied medical predictions and overcome the effects of a rare condition that left him in a coma for three months.

Jonathan Fisher is a survivor of an Addisonian crisis which affected him so badly doctors feared he would never recover.

His mother ignored medical advice to switch off his life-support system as doctors believed he was brain dead.

However, convinced he could recover after noticing that he was reacting to her with the occasional slight movement of his little finger she refused to give up on her son.

Now — against all the odds — he has made a remarkable recovery and has regained many of the skills lost as a result of his condition.

Addison’s disease is a rare disorder of the adrenal glands. It affects the production of two hormones — cortisol and aldosterone — which help to regulate blood pressure.

If left untreated, the amount of steroid hormones in the body will gradually fall and the symptoms of Addison’s disease will get progressively worse.

Eventually, this will cause an adrenal crisis — when the symptoms become very severe and blood pressure drops to a dangerously low level. An adrenal crisis can be fatal if it is not treated immediately.

Jonathan can now get around Lisburn in his electric wheelchair and has even managed to complete his first book, August Always — a triumph as he has considerable speech impairment and great difficulty using his hands to operate a keyboard.

The process has been long and laborious but Jonathan said he was determined to share his experience with others.

“There are moments in life that define us, like birth and death,” he said.

“Along the journey there will be crises of passion, of love, of faith and desire, but none so devastating as an Addisonian crisis. I am Jonathan Fisher, a survivor.

“August Always is my memoir. I believe in the incredible. I dream of a better future.”

Background

Addison’s disease is a rare disorder of the adrenal glands which are located on top of the kidneys. The condition affects the production of two hormones. Cortisol, which helps to regulate blood pressure, maintaining blood glucose and heart function. And aldosterone which also helps regulate blood pressure. Addison’s sufferers must get treatment if their blood pressure falls as it can be fatal.

From http://www.belfasttelegraph.co.uk/news/health/coma-man-defies-odds-to-write-book-16076458.html

Diabetes in Cushing syndrome: basic and clinical aspects

2011-11-10T14:11:00.001-05:00

Diabetes mellitus is a frequent complication of Cushing syndrome (CS) which is caused by chronic exposure to glucocorticoid excess, either endogenous or exogenous, and that is characterized by several clinical symptoms such as central obesity, purple striae, proximal muscle weakness, acne, hirsutism and neuropsychological disturbances.

Diabetes occurs as a consequence of an insulin-resistant state together with impaired insulin secretion which are induced by glucocorticoid excess. The management of patients with CS and diabetes mellitus includes the treatment of hyperglycemia and, when possible, the correction of glucocorticoid excess.

This review focuses on the disorders of glucose metabolism in patients exposed to glucocorticoid excess, addressing both the pathophysiological aspects and the clinical and therapeutic implications.

Read the entire article at http://www.cell.com/trends/endocrinology-metabolism/abstract/S1043-2760(11)00138-X

November Cushing's News

2011-11-10T14:00:00.001-05:00

Something new of interest to Cushies most every day. Please note that there is a current backlog of about three weeks for submitted bios to be added to the website.

November 10, 2011:

Three New Helpful Doctors added: Dr. Gordon Wotton (Atlanta, Georgia)
Dr. Amel Arnaout (Ottowa, Ontario, Canada)
Dr. Emilie Collins (Kent, Michigan) http://cushie.info
Korlym: Corcept Therapeutics Announces Third Quarter Results and Corporate and Development Update http://cushie.info
Google+ page for Cushings http://cushie.info
Patients Diagnosed With Severe Adult GH Deficiency Using The Insulin Tolerance Test, Arginine Or Glucagon Stimulation Tests Share Similar Clinical Features http://cushie.info
ACTH-secreting pituitary adenomas: size does not correlate with hormonal activity http://cushie.info
Diabetes in Cushing syndrome: basic and clinical aspects http://cushie.info
DuoCort Pharma's Orphan Drug Plenadren® Granted European Marketing Authorization for Adrenal Insufficiency http://cushie.info
Endoscopic bilateral adrenalectomy in patients with ectopic Cushing's syndrome http://cushie.info
Pituitary glands grown from mouse embryonic stem cells http://www.guardian.co.uk
Hot Topics: Cushings Disease and Acromegaly https://www.aace.com
Cushing's and Cancer Blog (Updated 11/10/11) http://www.cushingshelp.blogspot.com
Cushing's Help on Posterous Blog (Updated 11/10/11) http://cushings.posterous.com
The CushieWiki updated 11/10/2011. http://www.CushieWiki.com
Addison's Help Blog (Updated 11/10/11) http://www.addisonshelp.blogspot.com
Addison's and Cushing's Help and Support RSS Feed. Last updated 11/10/11. http://www.cushingsonline.com

November 5, 2011:

What Is the Best Approach for the Evaluation and Management of Endocrine Incidentalomas? http://cushie.info
Endoscopic endonasal compared with microscopic transsphenoidal and open transcranial resection of giant pituitary adenomas http://www.cushie.info
Where Does My Donation Go? Spreadsheet Updated 11/3/11 https://docs.google.com/a/cushings-help.org
Comment has been added: Discussion/debate topics http://cushie.info
The Cushing's Daily http://www.cushie.info
Addison's and Cushing's Help and Support RSS Feed. Last updated 11/5/11. http://www.cushingsonline.com
Our Locations (Updated 11/5/11) http://cushie.info
Lou, undiagnosed bio http://www.cushie.info
Caryn, undiagnosed bio http://www.cushie.info
Mallissa F, undiagnosed bio http://www.cushie.info

November 2, 2011:

The CushieWiki updated 11/2/2011. http://www.CushieWiki.com
New Comment added: Gail M W, undiagnosed bio http://cushie.info
Clinical trial: Effects of Hormone Stimulation on Brain Scans for Cushing's Disease http://cushings.posterous.com
New FAQ Question added http://www.cushie.info
Tweeting about Cushing's? Use this hashtag: #cushings
Where Does My Donation Go? Spreadsheet https://docs.google.com/a/cushings-help.org
Help Cushing's Help at No Cost to You http://www.cushie.info
Comment has been added: Discussion/debate topics http://cushie.info
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DuoCort Pharma's Orphan Drug Plenadren® Granted European Marketing Authorization for Adrenal Insufficiency

2011-11-10T13:58:00.001-05:00

HELSINGBORG, Sweden and EXTON, Pa., Nov. 7, 2011 /PRNewswire/ -- The Swedish specialty pharma company, DuoCort Pharma, announced today that the European Commission has granted a European Marketing Authorisation for Plenadren®(hydrocortisone, modified release tablet), an orphan drug for treatment of adrenal insufficiency in adults, bringing these patients their first pharmaceutical innovation in over 50 years.

Developed by DuoCort Pharma, Plenadren® is a dual release hydrocortisone replacement therapy designed to better mimic the normal physiological cortisol profile in order to improve outcomes for patients suffering from adrenal insufficiency. Plenadren® is given as an oral tablet once daily. It has an outer layer releasing hydrocortisone immediately and an inner core releasing the rest of the drug more slowly during the day.

Although glucocorticoid hormone replacement therapy for adrenal insufficiency has been available for decades, studies have recorded complications and comorbidities including premature death, impaired quality of life, increased risk of cardiovascular diseases, and decreased bone mineral density in treated patients, most likely because it is difficult to match the natural secretion pattern of cortisol.

Maria Forss, CEO of DuoCort Pharma, said: "The marketing authorization for Plenadren® in Europe is an important step towards addressing the unmet needs of these patients."

The approval of Plenadren® follows the positive opinion adopted by the Committee for Medicinal Products for Human Use (CHMP) in July 2011. Plenadren® is now approved for marketing in all countries of the European Union (EU) as well as in the European Economic Area (EEA), namely Iceland, Norway and Lichtenstein.

Professor Gudmundur Johannsson of the Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden, and Chief Medical Officer of DuoCort Pharma, said: "Plenadren® offers a welcome new treatment option to help patients suffering from adrenal insufficiency. Plenadren® can improve therapy for many of the almost 200,000 patients in Europe who suffer from this disease and who need life-long cortisol replacement therapy for their survival."

On October 26, 2011, ViroPharma Incorporated (NASDAQ: VPHM) signed a definitive agreement to acquire DuoCort Pharma AB. The companies expect to complete the acquisition in November 2011. On closing, ViroPharma will pay an upfront closing cost of 220 million Swedish kroner (SEK) or $33 million in US dollars (USD). Additionally, there are contingent milestone payments of up to 860 million SEK or $130 million USD associated with manufacturing, sales thresholds and territory expansion.

About Adrenal insufficiency

Adrenal insufficiency (cortisol deficiency) is a rare, life-threatening disease that affects patients in their active years. To survive, patients suffering from this disease need lifelong replacement therapy with hydrocortisone. Treatment of adrenal insufficiency involves replacing, or substituting, the hormones that the patient's own adrenal glands are not producing. Cortisol is replaced using hydrocortisone, the synthetic form of cortisol.

About Plenadren® (hydrocortisone, modified release tablet)

Plenadren is the first true innovation in over 50 years in the treatment of adrenal insufficiency.

Hypersensitivity to the active substance of Plenadren or to any of the excipients may occur. During acute adrenal insufficiency, parenteral administration of hydrocortisone in high doses, together with physiological sodium chloride solution for injection, must be given. Use of Plenadren with potent CYP 3A4 inducers and inhibitors may merit an adjustment of hydrocortisone dosage. High (supra-physiological) dosages of cortisone can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium. Long-term treatment with higher than physiological hydrocortisone doses can lead to clinical features resembling Cushing's syndrome with increased adiposity, abdominal obesity, hypertension and diabetes, and thus result in an increased risk of cardiovascular morbidity and mortality. All glucocorticoids increase calcium excretion and reduce the bone remodeling rate. Patients with adrenal insufficiency on long term glucocorticoid replacement therapy have been found to have reduced bone mineral density. Psychiatric adverse events may occur with systemic glucocorticoids.

The most common adverse reactions observed in clinical studies have been fatigue, gastroenteritis, upper respiratory tract infection, sedation, vertigo and dry eyes.

About ViroPharma Incorporated

ViroPharma Incorporated is an international biopharmaceutical company committed to developing and commercializing novel solutions for physician specialists to address unmet medical needs of patients living with diseases that have few if any clinical therapeutic options, including C1 esterase inhibitor deficiency, treatment of seizures in children and adolescents, and C. difficile infection (CDI). Our goal is to provide rewarding careers to employees, to create new standards of care in the way serious diseases are treated, and to build international partnerships with the patients, advocates, and health care professionals we serve. ViroPharma's commercial products address diseases including hereditary angioedema (HAE), seizures in children and adolescents, and CDI; for full U.S. prescribing information on our products, please download the package inserts athttp://www.viropharma.com/Products.aspx; the prescribing information for other countries can be found atwww.viropharma.com.

ViroPharma routinely posts information, including press releases, which may be important to investors in the investor relations and media sections of our company's web site, www.viropharma.com. The company encourages investors to consult these sections for more information on ViroPharma and our business.

About DuoCort Pharma

DuoCort Pharma is a drug development company focused on improving glucocorticoid therapy. The company has its origins among researchers at the Sahlgrenska Academy at Gothenburg University and at Uppsala University in Sweden. DuoCort Pharma has developed Plenadren®, an improved glucocorticoid replacement therapy for patients with adrenal insufficiency, which is a rare disease. DuoCort Pharma has orphan drug designations in EU, Switzerland and the USA for Plenadren®. Plenadren® is a once daily, dual-release hydrocortisone oral tablet. It has an outer layer that releases the drug immediately and an inner core that releases the drug over the day. The tablets come in both 5 mg and 20 mg strengths. For more information please visit www.duocort.com.

DuoCort Pharma is a project company of the life science incubator PULS. For more information visit www.pulsinvest.se.

Disclosure Notice

Certain statements in this press release contain forward-looking statements that involve a number of risks and uncertainties. Forward-looking statements provide our current expectations or forecasts of future events, including statements about the benefits of the business combination transaction involving ViroPharma and DuoCort Pharma, including, among others, future financial and operating results, enhanced revenues, ViroPharma's plans, objectives, expectations and intentions and other statements that are not historical facts. The following factors, among others, could cause actual results to differ from those set forth in the forward-looking statements: the ability to achieve the other conditions to closing on the proposed schedule; the risk that the business will not be integrated successfully; the risk that revenues following the acquisition will be lower than expected, including the successful commercialization of Plenadren; potential for disruption from the transaction making it more difficult to maintain relationships with manufacturers, employees or other suppliers; competition and its effect on pricing, spending, third-party relationships and revenues; our ability to achieve favorable pricing for Plenadren from European regulatory authorities; the risk that the safety and/or efficacy results of existing clinical trials for Plenadren will not be consistent with the results of additional clinical studies, including the required registry study, or with commercial usage; market acceptance of Plenadren; and our inability to maintain the orphan drug status associated with Plenadren. These factors, and other factors, including, but not limited to those described in our annual report on Form 10-K for the year ended December 31, 2010 and quarterly reports on Form 10-Q filed with the Securities and Exchange Commission, could cause future results to differ materially from the expectations expressed in this press release. The forward-looking statements contained in this press release are made as of the date hereof and may become outdated over time. ViroPharma does not assume any responsibility for updating any forward-looking statements. These forward looking statements should not be relied upon as representing our assessments as of any date subsequent to the date of this press release.

SOURCE DuoCort Pharma

From http://www.prnewswire.com/news-releases/duocort-pharmas-orphan-drug-plenadren-granted-european-marketing-authorization-for-adrenal-insufficiency-133348658.html

Endoscopic bilateral adrenalectomy (BLA) in patients with ectopic Cushing's syndrome

2011-11-10T13:42:00.001-05:00

Alberda WJ, van Eijck CH, Feelders RA, Kazemier G, de Herder WW, Burger JW; Surgical Endoscopy (Nov 2011)

BACKGROUND: Bilateral adrenalectomy (BLA) is a treatment option to alleviate symptoms in patients with ectopic Cushing's syndrome (ECS) for whom surgical treatment of the responsible nonpituitary tumor is not possible. ECS patients have an increased risk for complications, because of high cortisol levels, poor clinical condition, and metabolic disturbances. This study aims to evaluate the safety and long-term efficacy of endoscopic BLA for ECS.

METHODS: From 1990 to present, 38 patients were diagnosed and treated for ECS in the Erasmus University Medical Center, a tertiary referral center. Twenty-four patients were treated with BLA (21 endoscopic, 3 open), 9 patients were treated medically, and 5 patients could be cured by complete resection of the adrenocorticotropic hormone (ACTH)-producing tumor. The medical records were retrospectively reviewed and entered into a database. For evaluation of the efficacy of BLA, preoperative biochemical and physical symptoms were assessed and compared with postoperative data.

RESULTS: Endoscopic BLA was successfully completed in 20 of the 21 patients; one required conversion to open BLA. Intraoperative complications occurred in two (10%) patients, and postoperative complications occurred in three (14%) patients. Median hospitalization was 9 (2-95) days, and median operating time was 246 (205-347) min. Hypercortisolism was resolved in all patients. Improvements of hypertension, body weight, Cushingoid appearance, impaired muscle strength, and ankle edema were achieved in 87, 90, 65, 61, and 78% of the patients, respectively. Resolution of diabetes, hypokalemia, and metabolic alkalosis was achieved in 33, 89, and 80%, respectively.

CONCLUSION: Endoscopic BLA is a safe and effective treatment for patients with ectopic Cushing's syndrome.

From http://www.docguide.com/endoscopic-bilateral-adrenalectomy-patients-ectopic-cushings-syndrome?tsid=5

Corlux: Corcept Therapeutics Announces Third Quarter Results and Corporate and Development Update

2011-11-10T11:26:00.001-05:00

MENLO PARK, CA, Nov 07, 2011 (MARKETWIRE via COMTEX) -- Corcept Therapeutics IncorporatedCORT -1.58% , a pharmaceutical company engaged in the discovery, development and commercialization of drugs for the treatment of severe metabolic and psychiatric disorders, today reported financial results for the quarter ended September 30, 2011, and updated its corporate progress.

"Following the acceptance by the U.S. Food and Drug Administration (FDA) of our New Drug Application (NDA) for the use of our lead product candidate, Korlym(TM), in Cushing's Syndrome," said Joseph Belanoff, M.D., Chief Executive Officer of Corcept, "we continue to focus our efforts on building our commercial capabilities to support the launch of Korlym, if Korlym is approved by the FDA, in order to allow us to provide an important treatment option to patients suffering from Cushing's Syndrome."

Corporate and Development Highlights

--  Received notification in October 2011 that the FDA had accepted our proposed brand name, Korlym (formerly referred to as CORLUX(R)), for our lead product candidate in the treatment of endogenous Cushing's Syndrome.   --  Advanced our commercial launch preparations related to Korlym for the treatment of Cushing's Syndrome, including developing our internal infrastructure and engaging third-party vendors to provide market analytics and to support distribution and other logistical needs in the event Korlym is approved by the FDA.   --  Received notification in October 2011 that the European Commission had granted Korlym Orphan Designation for the treatment of endogenous Cushing's Syndrome (hypercortisolism) in the European Union (EU). Benefits of Orphan Drug Designation in the EU are similar to those in the U.S., but include ten years of marketing exclusivity in all 27 member states, free scientific advice during drug development, access to a centralized review process and a reduction or complete waiver of fees levied by the European Medicines Agency.   --  Enrolled additional patients in our double-blind placebo controlled Phase 3 trial of Korlym for the treatment of the psychotic features of psychotic depression.   --  Continued the clinical portion of our Phase 1b/2a multi-dose safety and proof of concept studies of CORT 108297, one of our selective GR-II antagonists.   --  Identified additional compounds from among our proprietary series of selective GR-II antagonists to advance toward an Investigational New Drug submission.

Third Quarter Financial Results

For the third quarter of 2011, Corcept reported a net loss of $6.4 million, or $0.08 per share, compared to a net loss of $7.1 million, or $0.10 per share, for the third quarter of 2010.

In the third quarter of 2011, research and development expenses decreased to $3.2 million from $5.2 million in the third quarter of 2010. This decrease in research and development expenses was due primarily to decreases in clinical trial costs related to drug-drug interaction and other NDA-supportive studies with Korlym, which were substantially completed in late 2010, and decreases in the clinical trial costs related to the Phase 1b/2a studies with CORT 108297. These decreases were partially offset by increased costs associated with the prosecution of our NDA for Korlym for the treatment of Cushing's Syndrome. General and administrative expenses increased to $3.2 million for the third quarter of 2011 from $1.9 million for the same period in 2010 due primarily to additional expenditures on commercialization activities for the potential launch of Korlym for Cushing's Syndrome.

Our cash balance as of September 30, 2011 was $45.9 million, up from $24.6 million at December 31, 2010. "We anticipate that our current cash balance is sufficient to fund the company through the end of 2012," said Charles Robb, the company's Chief Financial Officer.

Anticipated Activities for the Remainder of 2011

We continue to concentrate our efforts on advancing Korlym toward approval and commercialization for the treatment of Cushing's Syndrome. We also continue our efforts to be prepared to respond in a timely fashion to any questions posed by the FDA during the course of their review of our NDA.

"We are focused intently on developing the commercial and logistical capabilities we will need to make Korlym available to patients suffering from Cushing's Syndrome, should the FDA approve our drug for this indication," added Dr. Belanoff. "Korlym is the first step in unlocking the value of our scientific platform. The regulation of cortisol is a critical biological function; its dysregulation is equally critical in many important disease states. Our own research and research from increasing numbers of academic investigators point to the potential importance of cortisol antagonism in a wide variety of diseases. We believe our expanding library of selective cortisol antagonists may help address these unmet medical needs."

About Cushing's Syndrome

Endogenous Cushing's Syndrome is caused by prolonged exposure of the body's tissues to high levels of the hormone cortisol and is generated by tumors that produce cortisol or ACTH. Cushing's Syndrome is an orphan indication which most commonly affects adults aged 20 to 50. An estimated 10 to 15 of every one million people are newly diagnosed with this syndrome each year, resulting in over 3,000 new patients in the United States. An estimated 20,000 patients in the United States have Cushing's Syndrome. Symptoms vary, but most people have one or more of the following manifestations: high blood sugar, diabetes, high blood pressure, upper body obesity, rounded face, increased fat around the neck, thinning arms and legs, severe fatigue and weak muscles. Irritability, anxiety, cognitive disturbances and depression are also common. Cushing's Syndrome can affect every organ system in the body and can be lethal if not treated effectively.

About Psychotic Depression

Psychotic depression is a serious psychiatric disorder that affects approximately three million people annually in the United States. It is more prevalent than either schizophrenia or bipolar I disorder. The disorder is characterized by severe depression accompanied by delusions, hallucinations or both. People with psychotic depression are approximately 70 times more likely to commit suicide than the general population and often require lengthy and expensive hospital stays. There is no FDA-approved treatment for psychotic depression.

About Weight Gain Caused by Antipsychotic Medications

The group of medications known as second-generation antipsychotics, including olanzapine (Zyprexa), risperidone (Risperdal), quetiapine (Seroquel) and clozapine (Clozaril), are widely used to treat schizophrenia and bipolar disorder. All medications in this group are associated with treatment emergent weight gain of varying degrees and also carry warning labels relating to treatment emergent hyperglycemia and diabetes mellitus. There is no FDA-approved treatment for the weight gain associated with the use of antipsychotic medications.

About Korlym

Corcept's first-generation compound, Korlym, also known as mifepristone, directly blocks the cortisol (GR-II) receptor and the progesterone (PR) receptor. Intellectual property protection is in place to protect important methods of use for Korlym. Corcept retains worldwide rights to its intellectual property related to Korlym.

About CORT 108297

CORT 108297 is a potent, selective antagonist of the cortisol (GR-II) receptor that we have discovered and for which Corcept owns worldwide intellectual property rights. In in vitro binding affinity and functional assays this compound has no affinity for the progesterone (PR), estrogen (ER), androgen (AR) or mineralocorticoid (GR-I) receptors.

About Corcept Therapeutics Incorporated

Corcept is a pharmaceutical company engaged in the discovery, development and commercialization of drugs for the treatment of severe metabolic and psychiatric disorders. The company has completed its Phase 3 study of Korlym for the treatment of Cushing's Syndrome, and has an ongoing Phase 3 study of Korlym for the treatment of the psychotic features of psychotic depression. Corcept also has a Phase 2 program for CORT 108297, a selective GR-II antagonist that blocks the effects of cortisol but not progesterone. Corcept has developed an extensive intellectual property portfolio that covers the use of GR-II antagonists in the treatment of a wide variety of psychiatric and metabolic disorders, including the prevention of weight gain caused by the use of antipsychotic medication, as well as composition of matter patents for our selective GR-II antagonists.

Statements made in this news release, other than statements of historical fact, are forward-looking statements, including, for example, statements relating to the potential benefit of Korlym for patients diagnosed with Cushing's Syndrome, Corcept's clinical development and research programs, the outcome of the FDA's review of our NDA filing, our estimates for our capital requirements and needs for additional financing, the introduction of Korlym and future product candidates, including CORT 108297, the ability to create value from Korlym or other future product candidates or our scientific platform and our commercialization plans. Forward-looking statements are subject to a number of known and unknown risks and uncertainties that might cause actual results to differ materially from those expressed or implied by such statements. For example, there can be no assurances with respect to the cost, rate of spending, completion or success of clinical trials; financial projections may not be accurate; there can be no assurances that Corcept will pursue further activities with respect to the development of Korlym, CORT 108297, or any of its other selective GR-II antagonists. These and other risk factors are set forth in the Company's SEC filings, all of which are available from our website ( www.corcept.com ) or from the SEC's website ( www.sec.gov ). We disclaim any intention or duty to update any forward-looking statement made in this news release.

CORCEPT THERAPEUTICS INCORPORATED CONDENSED BALANCE SHEETS (in thousands)  September 30,  December 31, 2011           2010 -------------- -------------- (Unaudited)      (Note) ASSETS: Current assets: Cash and cash equivalents                    $       45,909 $       24,578 Other current assets                                    427            418 -------------- -------------- Total current assets                               46,336         24,996  Other assets                                               43            108 -------------- -------------- Total assets                               $       46,379 $       25,104 ============== ==============  LIABILITIES AND STOCKHOLDERS' EQUITY: Current liabilities: Accounts payable                             $        1,066 $          817 Other current liabilities                             1,647          3,043 -------------- -------------- Total current liabilities                           2,713          3,860  Total stockholders' equity                             43,666         21,244 -------------- --------------  Total liabilities and stockholders' equity $       46,379 $       25,104 ============== ==============  Note: Derived from audited financial statements at that date.  CORCEPT THERAPEUTICS INCORPORATED CONDENSED STATEMENTS OF OPERATIONS (in thousands, except per share amounts)  (Unaudited)  For the Three Months Ended   For the Nine Months Ended September 30,               September 30, --------------------------  -------------------------- 2011          2010          2011          2010 ------------  ------------  ------------  ------------  Operating expenses: Research and development*      $      3,228  $      5,224  $     14,355  $     14,286 General and administrative*          3,209         1,881         8,049         5,327 ------------  ------------  ------------  ------------ Total operating expenses               6,437         7,105        22,404        19,613 ------------  ------------  ------------  ------------  Loss from operations       (6,437)       (7,105)      (22,404)      (19,613)  Interest and other income, net                    3             4             3           758 Other expense                  (1)           (3)          (17)          (18) ------------  ------------  ------------  ------------ Net loss         $     (6,435) $     (7,104) $    (22,418) $    (18,873) ============  ============  ============  ============   Basic and diluted net loss per share  $      (0.08) $      (0.10) $      (0.27) $      (0.28) ============  ============  ============  ============ Shares used in computing basic and diluted net loss per share                 84,188        72,045        83,000        66,982 ============  ============  ============  ============  *Includes non-cash stock-based compensation of the following: Research and development     $        110  $         45  $        432  $        170 General and administrative           844           500         1,971         1,361 ------------  ------------  ------------  ------------ Total non-cash stock-based compensation  $        954  $        545  $      2,403  $      1,531 ============  ============  ============  ============

CONTACT: Charles Robb Chief Financial Officer Corcept Therapeutics 650-688-8783 Email Contact  www.corcept.com

SOURCE: Corcept Therapeutics

http://www2.marketwire.com/mw/emailprcntct?id=150008C85C40D638      http://www.corcept.com/

Today in Medical History

2011-11-08T01:04:00.001-05:00

Among the important early researchers in X-rays were Professor Ivan Pulyui, Sir William Crookes, Johann Wilhelm Hittorf, Eugen Goldstein, Heinrich Hertz, Philipp Lenard, Hermann von Helmholtz, Nikola Tesla, Thomas Edison, Charles Glover Barkla, Max von Laue, and Wilhelm Conrad Röntgen.

Wilhelm Röntgen
On November 8, 1895, Wilhelm Conrad Röntgen, a German physics professor, began observing and further documenting X-rays while experimenting with Lenard and Crookes tubes. Röntgen, on December 28, 1895, wrote a preliminary report "On a new kind of ray: A preliminary communication". He submitted it to the Würzburg's Physical-Medical Society journal.^[13] This was the first formal and public recognition of the categorization of X-rays. Röntgen referred to the radiation as "X", to indicate that it was an unknown type of radiation. The name stuck, although (over Röntgen's great objections), many of his colleagues suggested calling them Röntgen rays. They are still referred to as such in many languages, including German. Röntgen received the first Nobel Prize in Physics for his discovery.

There are conflicting accounts of his discovery because Röntgen had his lab notes burned after his death, but this is a likely reconstruction by his biographers.^[14] Röntgen was investigating cathode rays with a fluorescent screen painted with barium platinocyanide and a Crookes tube which he had wrapped in black cardboard so the visible light from the tube wouldn't interfere. He noticed a faint green glow from the screen, about 1 meter away. The invisible rays coming from the tube to make the screen glow were passing through the cardboard. He found they could also pass through books and papers on his desk. Röntgen threw himself into investigating these unknown rays systematically. Two months after his initial discovery, he published his paper.

Röntgen discovered its medical use when he saw a picture of his wife's hand on a photographic plate formed due to X-rays. His wife's hand's photograph was the first ever photograph of a human body part using X-rays.

Johann Hittorf
Physicist Johann Hittorf (1824 – 1914) observed tubes with energy rays extending from a negative electrode. These rays produced a fluorescence when they hit the glass walls of the tubes. In 1876 the effect was named "cathode rays" by Eugen Goldstein, and today are known to be streams of electrons. Later, English physicist William Crookes investigated the effects of electric currents in gases at low pressure, and constructed what is called the Crookes tube. It is a glass cylinder mostly (but not completely) evacuated, containing electrodes for discharges of a high voltage electric current. He found, when he placed unexposed photographic plates near the tube, that some of them were flawed by shadows, though he did not investigate this effect. Crookes also noted that his cathode rays caused the glass walls of his tube to glow a dull blue colour. Crookes failed to realise that it wasn't actually the cathode rays that caused the blue glow, but the low-level X-rays produced when the cathode rays struck the glass.

Ivan Pulyui
In 1877 Ukranian-born Pulyui, a lecturer in experimental physics at the University of Vienna, constructed various designs of vacuum discharge tube to investigate their properties.^[15] He continued his investigations when appointed professor at the Prague Polytechnic and in 1886 he found that that sealed photographic plates became dark when exposed to the emanations from the tubes. Early in 1896, just a few weeks after Röntgen published his first X-ray photograph, Pulyui published high-quality x-ray images in journals in Paris and London.^[15] Although Pulyui had studied with Röntgen at the University of Strasbourg in the years 1873-75, his biographer Gaida (1997) asserts that his subsequent research was conducted independently.^[15]

The first medical X-ray made in the United States was obtained using a discharge tube of Pulyui's design. In January 1896, on reading of Röntgen's discovery, Frank Austin of Dartmouth College tested all of the discharge tubes in the physics laboratory and found that only the Pulyui tube produced X-rays. This was a result of Pulyui's inclusion of an oblique "target" of mica, used for holding samples of fluorescent material, within the tube. On 3 February 1896 Gilman Frost, professor of medicine at the college, and his brother Edwin Frost, professor of physics, exposed the wrist of Eddie McCarthy, whom Edwin had treated some weeks earlier for a fracture, to the x-rays and collected the resulting image of the broken bone on gelatin photographic plates obtained from Howard Langill, a local photographer also interested in Röntgen's work.^[16]

Nikola Tesla
In April 1887, Nikola Tesla began to investigate X-rays using high voltages and tubes of his own design, as well as Crookes tubes. From his technical publications, it is indicated that he invented and developed a special single-electrode X-ray tube ^[17] ^[18], which differed from other X-ray tubes in having no target electrode. The principle behind Tesla's device is called the Bremsstrahlung process, in which a high-energy secondary X-ray emission is produced when charged particles (such as electrons) pass through matter. By 1892, Tesla performed several such experiments, but he did not categorize the emissions as what were later called X-rays. Tesla generalized the phenomenon as radiant energy of "invisible" kinds.^[19] ^[20] Tesla stated the facts of his methods concerning various experiments in his 1897 X-ray lecture ^[21] before the New York Academy of Sciences. Also in this lecture, Tesla stated the method of construction and safe operation of X-ray equipment. His X-ray experimentation by vacuum high field emissions also led him to alert the scientific community to the biological hazards associated with X-ray exposure.^[22]

Fernando Sanford
X-rays were first generated and detected by Fernando Sanford (1854-1948), the foundation Professor of Physics at Stanford University, in 1891. From 1886 to 1888 he had studied in the Hermann Helmholtz laboratory in Berlin, where he became familiar with the cathode rays generated in vacuum tubes when a voltage was applied across separate electrodes, as previously studied by Heinrich Hertz and Philipp Lenard. His letter of January 6, 1893 (describing his discovery as "electric photography") to The Physical Review was duly published and an article entitled Without Lens or Light, Photographs Taken With Plate and Object in Darkness appeared in the San Francisco Examiner.^[23]

Heinrich Hertz
In 1892, Heinrich Hertz began experimenting and demonstrated that cathode rays could penetrate very thin metal foil (such as aluminium). Philipp Lenard, a student of Heinrich Hertz, further researched this effect. He developed a version of the Crookes tube and studied the penetration by X-rays of various materials. Philipp Lenard, though, did not realize that he was producing X-rays. Hermann von Helmholtz formulated mathematical equations for X-rays. He postulated a dispersion theory before Röntgen made his discovery and announcement. It was formed on the basis of the electromagnetic theory of light (Wiedmann's Annalen, Vol. XLVIII). However, he did not work with actual X-rays.

Thomas Edison
Diagram of a water cooled X-ray tube. (simplified/outdated) In 1895, Thomas Edison investigated materials' ability to fluoresce when exposed to X-rays, and found that calcium tungstate was the most effective substance. Around March 1896, the fluoroscope he developed became the standard for medical X-ray examinations. Nevertheless, Edison dropped X-ray research around 1903 after the death of Clarence Madison Dally, one of his glassblowers. Dally had a habit of testing X-ray tubes on his hands, and acquired a cancer in them so tenacious that both arms were amputated in a futile attempt to save his life. "At the 1901 Pan-American Exposition in Buffalo, New York, an assassin shot President William McKinley twice at close range with a .32 caliber revolver." The first bullet was removed but the second remained lodged somewhere in his stomach. McKinley survived for some time and requested that Thomas Edison "rush an X-ray machine to Buffalo to find the stray bullet. It arrived but wasn't used . . . McKinley died of septic shock due to bacterial infection."^[24]

The 20th century and beyond
Before the 20th century until the 1920s, X-rays were generated in cold cathode tubes, called Crookes tubes. These tubes had to contain a small quantity of gas (invariably air) as a current will not flow in such a tube if they are fully evacuated. One of the problems with early X-ray tubes is that the generated X-rays caused the glass to absorb the gas and consequently the efficiency quickly falls off. Larger and more frequently used tubes were provided with devices for restoring the air, known as 'softeners'. This often took the form of small side tube which contained a small piece of mica – a substance that traps comparatively large quantities of air within its structure. A small electrical heater heats the mica and causes it to release a small amount of air restoring the tube's efficiency. However the mica itself has a limited life and the restore process was consequently difficult to control.

In 1904, John Ambrose Fleming invented the thermionic diode valve (vacuum tube). This used a heated cathode which permitted current to flow in a vacuum. This idea was quickly applied x-ray tubes, and heated cathode x-ray tubes, called Coolidge tubes, replaced the troublesome cold cathode tubes by about 1920.

Two years later, physicist Charles Barkla discovered that X-rays could be scattered by gases, and that each element had a characteristic X-ray. He won the 1917 Nobel Prize in Physics for this discovery. Max von Laue, Paul Knipping and Walter Friedrich observed for the first time the diffraction of X-rays by crystals in 1912. This discovery, along with the early works of Paul Peter Ewald, William Henry Bragg and William Lawrence Bragg gave birth to the field of X-ray crystallography. The Coolidge tube was invented the following year by William D. Coolidge which permitted continuous production of X-rays; this type of tube is still in use today.

ROSAT image of X-ray fluorescence of, and occultation of the X-ray background by, the Moon. The use of X-rays for medical purposes (to develop into the field of radiation therapy) was pioneered by Major John Hall-Edwards in Birmingham, England. In 1908, he had to have his left arm amputated owing to the spread of X-ray dermatitis [1].

The X-ray microscope was invented in the 1950s.

The Chandra X-ray Observatory, launched on July 23, 1999, has been allowing the exploration of the very violent processes in the universe which produce X-rays. Unlike visible light, which is a relatively stable view of the universe, the X-ray universe is unstable, it features stars being torn apart by black holes, galactic collisions, and novas, neutron stars that build up layers of plasma that then explode into space.

An X-ray laser device was proposed as part of the Reagan Administration's Strategic Defense Initiative in the 1980s, but the first and only test of the device (a sort of laser "blaster", or death ray, powered by a thermonuclear explosion) gave inconclusive results. For technical and political reasons, the overall project (including the X-ray laser) was de-funded (though was later revived by the second Bush Administration as National Missile Defense using different technologies).

What Is the Best Approach for the Evaluation and Management of Endocrine Incidentalomas?

2011-11-05T07:54:00.001-04:00

Key points include: Advances and more frequent use of diagnostic radiology have led to the increased prevalence of endocrine incidentalomas; Pituitary, thyroid, and adrenal incidentalomas must be assessed for dysfunctional hormone secretion and malignant potential; Inpatient management of endocrine incidentalomas should include consultation of endocrine or surgical teams in cases of dysfunctional or malignant lesions; Post-discharge instructions shouldclearly delineate timelines for repeat imaging, laboratory testing, and subspecialist follow-up.

by Darlene Tad-y, MD, Section of Hospital Medicine, University of Colorado Denver

Benign adrenal gland tumors.

Case

A 54-year-old man with a history of hypertension treated with hydrocholorothiazide and Type 2 diabetes mellitus is admitted with abdominal pain and found to have an incidental 2.1-cm left adrenal mass on CT scan of the abdomen. He denies symptoms of headache, palpitations, weight gain, or muscle weakness. His exam is significant for mildly elevated blood pressure. What is the best approach for evaluation and management of this incidental finding?

Overview

Incidentalomas are mass lesions that are inadvertently discovered during radiolographic diagnostic testing or treatment for other clinical conditions that are unrelated to the incidental mass. In recent decades, improvements in radiographic diagnostic techniques and sensitivity have led to increasing discovery of incidental lesions that are often in the absence of clinical signs or symptoms.¹ Three commonly discovered lesions by hospitalists are pituitary, thyroid, and adrenal incidentalomas.² The concerns associated with these findings relate to the potential for dysfunctional hormone secretion or malignancy.

Patients found with pituitary incidentalomas can be susceptible to several types of adverse outcomes: hormonal hypersecretion, hypopituitarism, neurologic morbidity due to tumor size, and malignancy in rare cases. Thyroid incidentalomas are impalpable nodules discovered in the setting of ultrasound or cross-sectional neck scans, such as positron emission tomography (PET) scans. Discovery of a thyroid incidentaloma raises concern for thyroid malignancy.³ The increased use of abdominal ultrasound, CT scans, and MRI has fueled the growing incidence of adrenal incidentalomas (AIs).

The discovery of an endocrine incidentaloma in the inpatient setting warrants a systematic approach that includes both diagnostic and potentially therapeutic management. A hospitalist should consider an approach that includes (see Table 1):

click for large version

Table 1. General inpatient approach to endocrine incidentalomas

Characterization of the incidentaloma, including clinical signs and symptoms, size, hormonal function, and malignant potential;
Immediate management, including medical versus surgical treatment; and
Post-discharge management, including monitoring.

Review of the Data

Pituitary incidentalomas. The prevalence of pituitary incidentalomas found by CT ranges from 3.7% to 20%, while the prevalence found by MRI approximates 10%. Autopsy studies have revealed a prevalence ranging from 1.5% to 26.7% for adenomas less than 10 mm, considered to be microadenomas. Broad categories of etiologies should be considered: pituitary adenoma, nonpituitary tumors, vascular lesions, infiltrative disorders, and others (see Table 2). The majority of pituitary adenomas secrete prolactin (30% to 40%) or are nonsecreting (30% to 40%). Adenomas secreting adrenocorticotropin hormone (ACTH, 2% to 10%), growth hormone (GH, 2% to 10%), thyroid-stimulating hormone (TSH, <1%), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) are much less common.2 Significant morbidity and premature mortality are associated with hyperprolactinemia, acromegaly (growth hormone excess), Cushing’s syndrome, and hyperthyroidism. Additionally, up to 41% of patients with macroadenomas were found to have varying degrees of hypopituitarism due to compression of the hypothalamus, the hypothalamic-pituitary stalk, or the pituitary itself.⁴

TABLE 2. DIFFERENTIAL DIAGNOSIS FOR PITUITARY INCIDENTALOMAS^2,4,14

Pituitary adenoma:

Secreting: prolactin, growth hormone, ACTH, glycopeptides (LH, FSH, TSH, a-subunit)
Nonsecreting

Non-pituitary tumors:

Germ cell tumors
Craniopharyngioma
Meningioma
Metastatic disease

Vascular lesions:

Aneurysms
Hamartomas
Infarctions

Infiltrative:

Sarcoidosis
Histiocytosis
Lymphocytic hypophysitis
Eosinophilic granulomas

Other:

Rathke’s cleft cyst
Anatomic abnormalities

ACTH=adrenocorticotropin hormone, GH=growth hormone, TSH=thyroid-stimulating hormone (thyrotropin), LH=luteinizing hormone, FSH=follicle-stimulating hormone

Recently, the Endocrine Society released consensus recommendations to guide the evaluation and treatment of pituitary incidentalomas, which are included in the approach outlined below.⁵ A detailed history and physical examination should be obtained with specific inquiry as to signs and symptoms of hormonal excess and mass effect from the tumor. Examples of symptoms of hormone excess can include:

Prolactin: menstrual irregularity, anovulation, infertility, decreased libido, impotence, osteoporosis;
Growth hormone: high frequency of colonic polyps and colon cancer (chronic excess);
TSH: thyrotoxicosis, atrial fibrillation; and
ACTH: hypertension, osteoporosis, accelerated vascular disease.

Symptoms related to the mass effect of the tumor include visual field defects and hypopituitarism related to the deficient hormone, including:

FSH/LH: oligomenorrhea, decreased libido, infertility;
TSH: hypothyroidism (weight gain, constipation, cold intolerance);
ACTH: adrenal insufficiency (hypotension, hypoglycemia, weight loss); and
ADH: polyuria, polydypsia.

The size and location of the pituitary lesion must be assessed. Lesions greater than 10 mm are considered macroademonas, and their size will affect their management. If the lesion was initially identified by CT scan, an MRI is recommended to better evaluate it.⁵ If the MRI locates the incidentaloma abutting the optic nerve or chiasm, then the patient should undergo a formal visual field examination.

Indications for an inpatient surgical referral for treatment include: a lesion larger than 2 cm, evidence of mass effect such as visual field defects, neurologic compromise, opthalmoplegia, hypopituitarism, a tumor abutting the optic nerve or chiasm, pituitary apoplexy, and hypersecretion of hormones other than prolactin. Patients with prolactinomas warrant an inpatient endo-crinology consult and may need medical management with a dopamine agonist. Hormone replacement therapy can also be provided for patients with hypopituitarism.^2,5

For patients who do not meet the criteria for inpatient surgical therapy, follow-up management must be arranged at the time of discharge. Clinical, laboratory assessment, and an MRI should be scheduled six months after the initial finding of the incidentaloma with the patient’s PCP or with an endocrinologist.⁵

Thyroid incidentalomas. The prevalence of thyroid nodules based on ultrasound studies ranges from 19% to 46%, with autopsy studies estimating an incidence of approximately 50%.^2,6 Incidence of thyroid nodules also increases with age, as almost 60% of people over the age of 60 harbor a thyroid incidentaloma. The rate of malignancy in the general population has ranged between 8% and 24%; however, in the last decade, the rates have increased by 2.4 times as more sophisticated ultrasound techniques and liberal use of fine-needle aspiration (FNA) biopsies have detected subclinical disease.^7,8

Etiologies for incidental thyroid nodules can be divided into benign and malignant causes. Benign etiologies include thyroid cyst (simple or complex), multinodular goiter, and Hashimoto’s thryoiditis, while malignant causes include papillary, medullary, follicular, Hurthle cell, and anaplastic carcinomas, thyroid lymphomas, and rare instances of metastatic cancers.^2,3

Targeted history and physical examination helps to characterize the thyroid incidentaloma. Historical features, such as palpitations, weight loss, anxiety, new onset atrial fibrillation, or menstrual irregularities, coupled with tachycardia, tremors, proximal muscle weakness, and a palpable nodule aid in the diagnosis of hyperthyroidism. Findings such as a family history of thyroid cancer, symptoms of hoarseness or dysphagia, rapid growth of the nodule, environmental or history of head or neck irradiation along with physical findings of a hard, fixed nodule, or cervical lymphadenopathy increase the suspicion for malignancy.^2,7

The functionality of the nodule can be assessed by checking TSH, free T3, and free T4 levels. Suppression of TSH (< 0.1 mU/L) with elevated levels of free T3 and T4 indicates nodule production of excess thyroid hormone and warrants thyroid scintography. Thyroid scintography will identify the nodule as “hot” (hyperfunctioning) or “cold” (nonfunctioning).²

Regardless of the radiographic modality that initially identified the thyroid incidentaloma, a dedicated thyroid high-resolution ultrasound should be ordered to assess the size, multiplicity (single or multinodular), location, and character (solid, cystic, or mixed).⁷

Recommendations for proceeding to FNA to evaluate for malignancy differ among subspecialty societies. Generally, nodules larger than 1 cm or nodules smaller than 1 cm with risk factors for malignancy should be referred for FNA.^2,7

If diagnostic workup identifies a patient with hyperthyroidism due to an autonomously functional nodule or a nodule that may be at high risk for malignancy, it is appropriate to involve an endocrinologist and possibly a surgical subspecialist prior to discharge. Management of hyperthyroidism can include starting antithyroid agents (methimazole or propylthiouracil), radioactive iodine ablation, or referral for surgery.

Preparation for discharge of the patient whose incidentaloma is nonfunctional or does not appear to be malignant should include appointments to recheck thyroid hormone levels, including TSH as well as a thyroid ultrasound within one year of the initial discovery.

Adrenal incidentaloma. The prevalence of AIs found by CT of the abdomen ranges from 0.4% to 4%, while autopsy studies have found a prevalence of 1.4% to 9% with increasing prevalence with age.^2,9,10 The majority of AIs are benign and nonfunctioning adenomas, in the absence of known malignancy. Other differential diagnoses include Cushing’s syndrome, pheochromocytoma, adrenocortical adenoma, aldosteronoma, and metastatic lesions.

Because functioning adrenal incidentalomas may be clinically silent, any patient found with an AI must undergo biochemical workup as part of their evaluation to assess for pheochromocytoma, Cushing’s syndrome, and if he or she has a history of hypertension or hyperaldosteronism (Conn’s syndrome). Table 3 outlines the approach for characterizing adrenal incidentalomas.^2,11,12 An important point is that imaging studies are not useful in distinguishing a functioning versus nonfunctioning tumor but rather can help to discriminate malignant lesions.¹¹

click for large version

Table 3. Characterization of the adrenal incidentaloma^2,11

Inpatient surgical consult for resection is indicated if the patient is found to have pheochromocytoma, clinically apparent functioning adrenocortical adenoma, or a tumor size greater than 4 cm. Consultation with an endocrinologist is also recommended if biochemical tests are positive. If the diagnostic workup leads to suspicion for infection or metastatic disease, the patient should be referred for FNA.^2,12

For patients whose lesions do not require surgical resection, repeat CT scan of the abdomen is recommended six months from the initial finding. Hospitalists should also arrange for the patient to repeat biochemical testing, including an overnight dexamethasone test.^12,13

Back to the Case

The patient underwent biochemical testing and was found to have normal levels of plasma-free metanephrines, a plasma aldosterone, plasma renin activity ratio less than 20, and a serum cortisol level of 7 mg/dL after his overnight dexamethasone suppression test. The 24-hour urine collection for free cortisol revealed elevated levels of cortisol in the urine, and the ACTH level was low.

Endocrinology and endocrine surgery teams were consulted, and recommended surgical resection. After surgical resection of his tumor, the patient was started on glucocorticoid replacement and was discharged with a follow-up appointment with endocrinology.

Bottom Line

An inpatient approach to endocrine incidentalomas should include characterization of the clinical signs and symptoms, size, function, and malignant potential of the lesion. Based on this, inpatient surgical or medical management can be determined. Post-discharge management should include arrangements for surveillance testing and follow-up with appropriate subspecialists.

Dr. Tad-y is assistant professor of medicine and a hospitalist at the University of Colorado Denver.

KEY POINTS

Advances and more frequent use of diagnostic radiology have led to the increased prevalence of endocrine incidentalomas.
Pituitary, thyroid, and adrenal incidentalomas must be assessed for dysfunctional hormone secretion and malignant potential.
Inpatient management of endocrine incidentalomas should include consultation of endocrine or surgical teams in cases of dysfunctional or malignant lesions.
Post-discharge instructions should clearly delineate timelines for repeat imaging, laboratory testing, and subspecialist follow-up.

ADDITIONAL READING

Shirodkar M, Jabbour SA. Endocrine incidentalomas. Int J Clin Pract. 2008; 62:1423-1431.
Freda PU, Beckers AM, Katznelson L, et al. Pituitary incidentaloma: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2011;96:894-904.
Iyer NG, Shaha AR, Silver CE, et al. Thyroid incidentalomas: to treat or not to treat. Eur Arch Otorhinolaryngol. 2010;267:1019-1026.
Zeiger MA, Siegelman SS, Hamrahian AH. Medical and surgical evaluation and treatment of adrenal incidentalomas. J Clin Endocrinol Metab. 2011;96:2004-2015.

References

From http://www.the-hospitalist.org/details/article/1380161/What_Is_the_Best_Approach_for_the_Evaluation_and_Management_of_Endocrine_Inciden.html

Cushing's News

2011-11-02T19:54:00.001-04:00

Something new of interest to Cushies most every day. Please note that there is a current backlog of about three weeks for submitted bios to be added to the website.

November 2, 2011:

New Comment has been added: Crystal's son, undiagnosed bio http://cushie.info
Doctors Use Google For Health Information, Too, Survey Finds http://cushie.info
Endoscopic endonasal compared with microscopic transsphenoidal and open transcranial resection of giant pituitary adenomas http://www.cushie.info
The CushieWiki updated 11/2/2011. http://www.CushieWiki.com
New Comment added: Gail M W, undiagnosed bio http://cushie.info
Clinical trial: Effects of Hormone Stimulation on Brain Scans for Cushing's Disease http://cushings.posterous.com
New FAQ Question added http://www.cushie.info
Tweeting about Cushing's? Use this hashtag: #cushings
Where Does My Donation Go? Spreadsheet https://docs.google.com/a/cushings-help.org
Help Cushing's Help at No Cost to You http://www.cushie.info
Comment has been added: Discussion/debate topics http://cushie.info
Updated Upcoming Meetings (Updated 11/2/11) http://www.cushie.info
Cushing's and Cancer Blog (Updated 10/27/11) http://www.cushingshelp.blogspot.com
Cushing's Help on Posterous Blog (Updated 10/27/11) http://cushings.posterous.com
The Cushing's Daily http://www.cushie.info
Cushing's Podcasts on Posterous Blog (Updated 10/20/11) http://cushingspodcasts.posterous.com
A New FAQ (Frequently Asked Questions) is being added. 109 questions answered so far. Last updated 10/28/11. http://cushie.info
Addison's and Cushing's Help and Support RSS Feed. Last updated 11/2/11. http://www.cushingsonline.com
New Male Only bio. http://cushie.info
Our Locations (Updated 11/2/11) http://cushie.info
Updated: Gail M W, pituitary bio http://www.cushie.info
Kim, pituitary bio http://www.cushie.info
Crystal's son, undiagnosed bio http://www.cushie.info
Maureen, adrenal bio http://www.cushie.info
Lou, undiagnosed bio http://www.cushie.info
Carmen, undiagnosed bio http://www.cushie.info
Maureen, adrenal bio http://www.cushie.info

Effects of Hormone Stimulation on Brain Scans for Cushing's Disease

2011-10-27T13:13:00.001-04:00

This study is currently recruiting participants.

Verified on August 2011 by National Institutes of Health Clinical Center (CC)

First Received on October 21, 2011. No Changes Posted

Sponsor:	National Institute of Neurological Disorders and Stroke (NINDS)
Information provided by:	National Institutes of Health Clinical Center (CC)
ClinicalTrials.gov Identifier:	NCT01459237

Purpose

Background:

Cushing's disease can be caused by a tumor of the pituitary gland, a small gland about the size of a pea located at the base of the brain. These tumors produce high levels of hormones, which cause obesity, diabetes, and growth problems. The cure for this type of Cushing's disease is to have surgery that removes the tumor but leaves the pituitary gland alone. Currently, magnetic resonance imaging scans are the best way to find these tumors. However, many of these tumors do not show up on the scan.
Positron emission tomography (PET) scans use radioactive chemicals to light up parts of the body that are more active, such as tumors. Researchers want to try to make the small Cushing's disease tumors more active to help them show up on the scans. A special hormone will be given before the scan to make the tumors more active.

Objectives:

- To test the use of hormone stimulation to improve brain scans for Cushing's disease tumors.

Eligibility:

- Individuals at least 8 years of age who will be having surgery to remove Cushing's disease tumors.

Design:

Participants will be screened with a medical history, physical exam, blood and urine tests, and imaging studies.
They will have three brain scans before surgery. The first scan is a magnetic resonance imaging scan to show a full picture of the brain. The second and third scans are PET scans.
The first PET scan will be given without the special hormone. The second PET scan will be done more than 24 hours but less than 14 days after the first PET scan. The second PET scan will be given with the special hormone.
Participants will have tumor removal surgery through another study protocol....

Condition
Pituitary Neoplasm

Study Type:	Observational
Official Title:	Prospective Evaluation of the Effect of Corticotropin-Releasing Hormone Stimulation on 18F-Fludeoxyglucose High-Resolution Positron-Emission Tomography in Cushing's Disease

Resource links provided by NLM:

Drug Information available for: Corticotropin Corticotropin-releasing hormone

U.S. FDA Resources

Further study details as provided by National Institutes of Health Clinical Center (CC):

Estimated Enrollment:	30
Study Start Date:	October 2011

Detailed Description:

Objective

Preoperative imaging identification and localization of adrenocorticotropin hormone (ACTH)-secreting pituitary adenomas is critical for the accurate diagnosis and the successful surgical treatment of Cushing's disease (CD). Unfortunately, over 40 percent of CD patients do not have a visible pituitary adenoma on magnetic resonance (MR)-imaging (the most sensitive imaging modality for ACTH-positive adenoma detection and localization). Lack of MR-imaging for diagnosis and to guide surgical resection results in significantly higher rates of surgical failure compared to cases associated with adenomas visible on MR-imaging. Because ACTH-adenomas are metabolically active compared to the surrounding pituitary gland, (18)F-fludeoxyglucose ((18)F-FDG) positron emission tomography (PET)-imaging in CD patients could be used to detect adenomas not detectable on MR-imaging. Moreover, corticotropin-releasing hormone (CRH) can be given to selectively increase the metabolic activity of ACTH-secreting pituitary adenomas to increase the likelihood of their detection and localization by (18)F -FDG PET-imaging. To determine the effect of CRH stimulation on (18)F-FDG uptake using PET-imaging in CD, we will perform (18)F-FDG high-resolution PET-imaging (with and without CRH stimulation) in CD patients.

Study Population

Thirty male and female CD patients 8 years and older will participate in this study.

Study Design

This is a single center trial to determine the effect of CRH stimulation on (18)F-FDG uptake in high-resolution PET-imaging of ACTH-adenomas in CD patients. CD patients will undergo (18)F-FDG high-resolution PET-imaging without CRH stimulation and (18)F-FDG high-resolution PET-imaging with intravenous CRH stimulation. The order of the PET scans will be randomized and the second PET scan will occur greater than 24 hours but less than 14 days after initial PET-imaging. For (18)F-FDG PET-imaging with CRH stimulation, intravenous (18)F-FDG will be given just before CRH administration. The PET images will be read by radiologists who are blinded to the administration of CRH. Within 12 weeks after completion of the last (18)F-FDG high-resolution PET-imaging scan, patients will undergo surgical resection of the pituitary adenoma. Surgical and histological confirmation of adenoma location will be used to assess the diagnostic and localization accuracy of PET-imaging and to compare to preoperative MR-imaging results in CD patients. Inferior petrosal sinus sampling (IPSS) results will be compared with imaging results and with surgical and histological findings.

Outcome Measures

The primary objective of this study is to determine the effect of CRH stimulation on (18)F-FDG uptake in high-resolution PET-imaging for CD. To assess and compare (18)F-FDG uptake without and with CRH stimulation, we will compare (18)F-FDG standardized uptake values (SUVs) in the region of interest (pituitary gland and pituitary adenoma). Secondary objectives include determining if CRH stimulation enhances detection of ACTH-adenomas as demonstrated on (18)F-FDG high-resolution PET-imaging and assessing the accuracy and sensitivity of (18)F-FDG high-resolution PET-imaging detection of ACTH-adenomas compared to MR-imaging. Measures to assess for these secondary objectives include comparing (18)F-FDG high-resolution PET-imaging (with and without CRH stimulation) detection to (1) MR-imaging detection of adenomas, (2) IPSS results, and (3) actual tumor location confirmed by histological findings to location predicted by PET- and MR-imaging within patients.

Eligibility

Ages Eligible for Study:	8 Years and older
Genders Eligible for Study:	Both
Accepts Healthy Volunteers:	No

Criteria

INCLUSION CRITERIA:

To be eligible for entry into the study, patients must meet all the following criteria:

Be 8 years of age or older and able to undergo PET-imaging without needing general anesthesia.
Able to provide informed consent (or guardian is able to provide consent in case of minor).
Clinical diagnosis of CD based on medical records.
Medically able to undergo resection of pituitary adenoma and planning to undergo surgical resection of adenoma within 12 weeks of PET-imaging.
Normal liver enzymes: tests should be completed within 14 days before injection of the radiopharmaceutical; SGOT, SGPT less than or equal to 5 times ULN; bilirubin less than or equal to 2 times ULN.

EXCLUSION CRITERIA:

Candidates will be excluded if they meet any of the following criteria:

Pregnant or nursing women.
Contraindication to MR-scanning, including pacemakers or other implanted electrical devices, brain stimulators, some types of dental implants, aneurysm clips (metal clips on the wall of a large artery), metallic prostheses (including metal pins and rods, heart valves, and cochlear implants), permanent eyeliner, implanted delivery pump, or shrapnel fragments
Severe chronic renal insufficiency (glomerular filtration rate < 30 mL/min/1.73 m(2)), hepatorenal syndrome or post-liver transplantation.
Elevated blood glucose level above 200 mg/dL on the day of the scan prior to (18)F-FDG administration.

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT01459237

Contacts

Contact: Patient Recruitment and Public Liaison Office	(800) 411-1222	prpl@mail.cc.nih.gov
Contact: TTY	1-866-411-1010

Locations

United States, Maryland
National Institutes of Health Clinical Center, 9000 Rockville Pike	Recruiting
Bethesda, Maryland, United States, 20892

Sponsors and Collaborators

National Institute of Neurological Disorders and Stroke (NINDS)

More Information

Additional Information:

NIH Clinical Center Detailed Web Page

Publications:

Alzahrani AS, Farhat R, Al-Arifi A, Al-Kahtani N, Kanaan I, Abouzied M. The diagnostic value of fused positron emission tomography/computed tomography in the localization of adrenocorticotropin-secreting pituitary adenoma in Cushing's disease. Pituitary. 2009;12(4):309-14. Epub 2009 Apr 22.

Arnaldi G, Angeli A, Atkinson AB, Bertagna X, Cavagnini F, Chrousos GP, Fava GA, Findling JW, Gaillard RC, Grossman AB, Kola B, Lacroix A, Mancini T, Mantero F, Newell-Price J, Nieman LK, Sonino N, Vance ML, Giustina A, Boscaro M. Diagnosis and complications of Cushing's syndrome: a consensus statement. J Clin Endocrinol Metab. 2003 Dec;88(12):5593-602. Review.

Batista D, Gennari M, Riar J, Chang R, Keil MF, Oldfield EH, Stratakis CA. An assessment of petrosal sinus sampling for localization of pituitary microadenomas in children with Cushing disease. J Clin Endocrinol Metab. 2006 Jan;91(1):221-4. Epub 2005 Oct 11.

Today in Medical History

2011-09-21T00:58:00.001-04:00

Synthesized Cortisone

In 1948, Edward Kendall and Philip Hench created the first of the many “miracle drugs," which were actually synthesized hormones, to treat rheumatoid arthritis and other diseases. Hench and Kendall, who each headed a medical department at the Mayo Clinic in Rochester, Minn., realized that the adrenal glands play an important role in rheumatoid arthritis. The two noticed that a woman with rheumatoid arthritis had a lessening of symptoms while she was pregnant, and they worked to discover what caused the change. They were able to isolate a hormone in the cortex, or outer part, of the adrenal glands, which they called cortisone.

On Sept. 21, 1948, Hench administered a synthesized version of cortisone developed by Kendall to a patient with arthritis. The two researchers were awarded the Nobel Prize in physiology or medicine in 1950 for their achievements.

The Cushie.info Blog got a Top Cushings Syndrome blog award!

2011-09-20T11:05:00.001-04:00

Read the blog here

RegisteredNurse.org

Just like Cushing's?

2011-09-09T11:46:00.001-04:00

Today in Medical History

2011-09-03T00:54:00.001-04:00

A Growing Knowledge

On this date in 1931, chemists discovered that the pituitary gland contains a hormone, hGH, that controls growth. Overactivity of the pituitary, which sits at the base of the brain, results in gigantism. Underactivity results in dwarfism.

The discovery in 1931 eventually led to physicians treating children suffering from a deficiency of the hormone by injections of hGH obtained from the pituitaries of cadavers. More recently, scientists have discovered a way to produce genetically engineered hGH in bacteria.

Selective inferior petrosal sinus sampling without venous outflow diversion in the detection of a pituitary adenoma in Cushing’s syndrome

2011-08-18T09:51:00.001-04:00

Lukas Andereggen, Gerhard Schroth, Jan Gralla, Rolf Seiler, Luigi Mariani, Jürgen Beck, Hans-Rudolf Widmer, Robert H. Andres, Emanuel Christ and Christoph Ozdoba

Neuroradiology

DOI: 10.1007/s00234-011-0915-6

Abstract

Introduction

Conventional MRI may still be an inaccurate method for the non-invasive detection of a microadenoma in adrenocorticotropin (ACTH)-dependent Cushing’s syndrome (CS). Bilateral inferior petrosal sinus sampling (BIPSS) with ovine corticotropin-releasing hormone (oCRH) stimulation is an invasive, but accurate, intervention in the diagnostic armamentarium surrounding CS. Until now, there is a continuous controversial debate regarding lateralization data in detecting a microadenoma. Using BIPSS, we evaluated whether a highly selective placement of microcatheters without diversion of venous outflow might improve detection of pituitary microadenoma.

Methods

We performed BIPSS in 23 patients that met clinical and biochemical criteria of CS and with equivocal MRI findings. For BIPSS, the femoral veins were catheterized bilaterally with a 6-F catheter and the inferior petrosal sinus bilaterally with a 2.7-F microcatheter. A third catheter was placed in the right femoral vein. Blood samples were collected from each catheter to determine ACTH blood concentration before and after oCRH stimulation.

Results

In 21 patients, a central-to-peripheral ACTH gradient was found and the affected side determined. In 18 of 20 patients where transsphenoidal partial hypophysectomy was performed based on BIPSS findings, microadenoma was histologically confirmed. BIPSS had a sensitivity of 94% and a specificity of 67% after oCRH stimulation in detecting a microadenoma. Correct localization of the adenoma was achieved in all Cushing’s disease patients.

Conclusion

BIPSS remains the gold standard in the detection of a microadenoma in CS. Our findings show that the selective placement of microcatheters without venous outflow diversion might further enhance better recognition to localize the pituitary tumor.

Keywords Angiography, Digital subtraction – Cushing disease – Petrosal sinus sampling – Pituitary gland – Magnetic resonance imaging

Fulltext Preview

From http://www.springerlink.com/content/l487284736173002/

Johns Hopkins Pituitary Patient Day

2011-08-16T01:15:00.001-04:00

Join us on September 24, 2011, for the 3rd Annual Patient Education Day at the Johns Hopkins Pituitary Center.

When: Saturday, September 24, 2011
Time: 9:00 a.m.
Location:
Johns Hopkins Mt. Washington Conference Center
5801 Smith Avenue,
Baltimore, MD 21209
map and directions

Patient Education Day Agenda:
9:00-9:30 AM	REGISTRATION AND BREAKFAST
9:30-10:00 AM	Introduction to Sellar Masses	Gary Wand, MD
10:00-10:30 AM	Neuro-ophthalmological issues in pituitary patients	Prem Subramanian, MD
10:30-11:00 AM	Medical therapy of pituitary disease	Roberto Salvatori, MD
11:00-11:30 AM	Surgical Therapy of Pituitary Tumors	Alfredo Quinones-Hinojosa, MD
11:30-12:00 PM	Approach to Large Invasive Tumors	Gary Gallia, MD
12:00-12:30 PM	Radiotherapy of pituitary masses	Kirsten Redmond, MD
12:30-01:25 PM	Lunch
1:30-03:00 PM	Breakout sessions: Medical therapy (Wand/Salvatori) Surgical therapy (Gallia/Quinones) Radiation therapy (Redmond/Lim) Vision issues (Subramanian)
To RSVP, please contact Colleen Hickson at 410-614-5887 by September 9, 2011.

For more information, contact the Johns Hopkins Pituitary Center at 410-955-GLAN (4526).

Help Cushing's Help at No Cost to You

2011-08-15T17:36:00.001-04:00

Help Cushing's Help at no charge to you!

From iGive.com:

We've just surpassed 21,000 "Likes" on Facebook, so we're celebrating.

We're inviting 21,000 new people to start using iGive by Aug. 31. They'll earn $10 or more free for Cushings Help. Actually, you get to do the inviting, we'll provide the money.

Just send invitees this link or post it on Facebook or other sites (you can even forward this e-mail):

http://www.iGive.com/welcome/warmwelcome6.cfm?c=17825&m=241976

Some Quick Celebration Details:

$5 is donated just for using iGive through 10/31/11. No purchase necessary.

Another $5 (or more) is donated if the new member also makes a purchase by 10/31/11.

Shopping more means helping more. Over 900 great stores participate.

No pop ups, ads, toolbars, special search engine, or unwanted emails.

Our Facebook Page has great testimonials: http://www.facebook.com/igive

New, never before having joined iGive people only qualify for this celebration.

It's a bit of a race so get those invites out soon. Once 21,000 new members are using the iGive Button (for Cushings Help or other causes) or August 31, 2011 happens, the celebration ends.

Yours,

Robert N. Grosshandler

Founde

Archived Interviews with MaryO, Cushing's Help Founder

2011-08-11T15:25:00.001-04:00

From August 10, 2011

Listen to internet radio with CushingsHelp on Blog Talk Radio

The Co-Hosts also provided a TweetChat Transcription

#TCK_-_Healthcare_Social_Media_Transcript.pdf Download this file

From January 3, 2008

Interview with Mary O'Connor (MaryO), founder of Cushings-Help.com and 20-year pituitary Cushing's Survivor. Robin (staticnrg) hosts.

Listen to internet radio with CushingsHelp on Blog Talk Radio

These episodes and many more are also available on iTunes podcasts

Read MaryO's bio

MaryO will be talking about Cushing's

2011-08-09T22:58:00.001-04:00

Tomorrow night at 9:00PM eastern

Read MaryO's bio

Archived Interview with Sue, Adrenal Patient, July 27, 2011

2011-07-28T15:09:00.001-04:00

Sue had Cushings for approximately fifteen years. She diagnosed herself with the help of a nurse friend and a book. Read Sue's bio.

Sue's interview was interesting, funny, informative. She has an adrenal tumor that she hopes will be removed soon. She'll be going to the NIH on the 31st.

Listen to internet radio with CushingsHelp on Blog Talk Radio

This interview is also available as a podcast on iTunes at http://itunes.apple.com/podcast/cushingshelp-cushie-chats/id350591438

Today in Medical History

2011-07-23T00:11:00.001-04:00

Master Of The Endocrines

The pituitary, which is located at the base of the brain, is considered the master gland because it controls the other endocrine glands and produces a number of hormones that stimulate growth, metabolic or sexual functions.

Much is now known about this tiny organ, but three doctors at Yale University School of Medicine broke new ground more than 60 years ago by being the first to isolate a pituitary hormone in pure form.

On this date in 1937, Drs. Abraham White, Hubert Catchpole and Cyril Long announced their findings in the journal Science. Researchers have since isolated nine hormones in three sections of the pituitary.

From http://www.intelihealth.com/IH/ihtIH/WSIHW000/333/7087/1339844.html

Cushing's Help is Turning 11!

2011-07-21T12:01:00.001-04:00

Cushings Help is 11 Years Old Today!

2011-07-21T10:15:00.001-04:00

It's unbelievable but the idea for Cushing's Help and Support arrived 11 years ago tonight. I was talking with my dear friend Alice, who runs a wonderful menopause site called Power Surge, wondering why there weren't many support groups online (OR off!) for Cushing's and I wondered if I could start one myself and we decided that I could.

The first website (http://www.cushings-help.com) first went "live" July 21, 2000 and the message boards September 30, 2000. Hopefully, with these sites, I'm going to make some helpful differences in someone else's life!

The message boards are very active and we have weekly online text chats, weekly live interviews, local meetings, email newsletters, a clothing exchange, a Cushing's Awareness Day Forum, podcasts, Wiki, phone support and much more.

Whenever one of the members of the boards gets into NIH, I try to go to visit them there. Other board members participate in the "Cushie Helper" program where they support others with one-on-one support, doctor/hospital visits, transportation issues and more.

Unusually overweight woman with Cushing's Syndrome to get treatment

2011-07-10T11:45:00.001-04:00

With the help of the GMA Kapuso Foundation, unusually overweight Evelyn Sambrano who is suffering from Cushing's Syndrome, has been brought from Bataan to Manila to receive hospital treatment.

GMA's Cesar Apolinario reported that Sambrano, who was too large for a stretcher, had to be carried by her neighbors using a thick blanket.

Cuhsing's Syndrome is caused by exposure to high levels of cortisol, a hormone produced by the adrenal gland.

Cortisol is known as the "stress hormone" because it is released in response to stress. One of its primary functions is to aid in fat, protein and carbohydrate metabolism.

In Sambrano's case, a tumor in her pituitary gland causes an imbalance in her hormone levels, which results in her continuous growth even though she does not overeat.

"Nagpapasalamat po ako nang marami at sa lahat ng taong tumutulong po sa akin, at sa mga tutulong po sa akin nagpapasalamat na rin po ako sa inyong lahat," she said through tears.

For the latest Philippine news stories and videos, visit GMANews.TV

Multi-step treatment

Kapuso Foundation executive vice president Mel Tiangco told Sambrano that the treatment would involve various steps.

"Kasi kahit pumayat ka, halimbawa na gamot na yung ano mo, syempre yung skin mo babagsak. Excess skin lahat yan pag natanggal yan. Cosmetic surgeon naman ang susunod diyan," said Tiangco.

"Kailangan matuon natin yung cost, so if she needs an MRI, at siguro mga blood tests natin for cortisol levels para ma-adress natin yung pagiging overweight. We need to do that step by step," said Manila Doctors Hospital Endocrinoligist Dr. Roberto Mirasol.

Grateful

Sambrano's mother Iluminada also expressed her gratitude, saying they could not afford the treatment on their own.

"Ako ay talagang awang awa po diyan...maraming maraming salamat naman sa tulong sa aking anak. Talagang wala ho kaming pera," she said.

Hermosa Vice-Mayor Cris Vitug said,"Natutuwa din ako sa GMA Foundation...sa pamamagitan ninyo yung problema ni Belen (Evelyn's nickname) masosolusyonan na kahit papano."— VVP, GMA News

From http://www.gmanews.tv/story/225686/nation/unusually-overweight-woman-with-cushings-syndrome-to-get-treatment

Treatments for Pituitary Tumors

2011-07-07T09:41:00.001-04:00

Pituitary Adenoma

Located at the base of the skull, the pituitary gland serves as the body’s control center for hormones. Pituitary adenomas are slow growing, benign tumors within the gland.

Patients are diagnosed with an MRI scan and an endocrinological evaluation that determines whether hormone levels have been affected by the tumor. If the tumor is large, a visual evaluation may be needed as well.

Small tumors less than 1 centimeter are called microadenomas, while tumors larger than 1 centimeter are macroadenomas. Pituitary tumors are also divided into functioning and nonfunctioning varieties. As the terms imply, functioning tumors produce hormones, though often in large, unregulated amounts. Nonfunctioning tumors don’t produce significant amounts of hormones.

What are the symptoms?

Symptoms of pituitary adenomas depend on the type of hormone production affected by the tumor.

A tumor that produces large amounts of ACTH causes a condition known as Cushing Disease, which leads to obesity, high blood pressure, and muscle weakness, among other symptoms. A prolactinoma produces large amounts of prolactin. Symptoms include irregular menstruation, sexual dysfunction and breast discharge. A growth-hormone producing tumor leads to acromegaly, a condition that causes progressive enlargement of hands and feet as well as altered facial features.

A nonfunctioning adenoma leads to problems by compressing the pituitary gland and decreases or even cuts off normal hormone production.

Large tumors also can affect the optic nerves leading to a form of tunnel vision called bitemporal hemianopsia. In some cases, a pituitary adenoma causes headaches or a sensation of pressure or fullness behind the eyes. Rarely, bleeding into a tumor can lead to severe headaches, along with double and blurred vision.

What are the treatment options?

Surgery

Medication can help correct hormone production with pituitary adenomas, though the gold-standard treatment is surgical removal. Doctors remove, or resect, as much of the tumor as safely as possible to eliminate pressure on the optic structures and remove parts of the tumor affecting hormone production.

Most pituitary surgeries don’t involve cutting into the skull. Surgeons access the gland through the sphenoid sinus, an air-filled space behind the nose, in a procedure known as transsphenoidal surgery. An incision is made either under the patient’s lip or inside the nose. A variation of the surgery using endoscopic assistance is even less invasive.

The major risk of transsphenoidal surgery is injury to the carotid arteries, to nearby tissues that affect vision or to healthy pituitary tissues that are often indistinguishable from the tumor. If the pituitary gland doesn’t function properly after surgery, the patient may require life-long hormone replacement.

Not all pituitary tumors require treatment. Sometimes a microadenoma is found on an MRI scan performed for other reasons. In such cases, a period of observation may be recommended. Treatment may be needed only when the microadenoma enlarges over time.

Radiation therapy

If the entire tumor can’t be removed surgically, radiation treatment may be needed to prevent its growth. Radiation may be an option for patients who are medically unable to undergo surgery or who oppose surgery.

Conventional radiation therapy uses a comparatively small number of radiation beams on the entire region around the pituitary gland, which usually results in a significant amount of normal, healthy tissue being irradiated as well. To compensate, conventional radiation treatment is given in daily doses over several weeks. The technique is generally effective in preventing tumor growth and in correcting hormone-producing tumors for many years.

Radiation therapy usually results in lower hormone production. Therefore, even if a pituitary adenoma doesn’t affect the patient’s hormone production, treatment with conventional radiation therapy can cause abnormally low hormone levels. In treating adenomas, conventional radiation therapy also irradiates nearby parts of optic tissues, though the risks of impaired vision are usually low.

Stereotactic radiosurgery

A newer option for treating pituitary adenomas, radiosurgery focuses radiation on the tumor only, minimizing exposure to other tissues. Emerging data indicates radiosurgery may be more effective than conventional radiation in lowering abnormal hormone production and does so over a shorter time period.

Most radiosurgery techniques are one-time treatments, which increases the risk of some side effects, including vision loss. The risk of radiation injury is greater for patients when the tumor is close to or involves nearby optic tissues or part of the brain known as the hypothalamus. For higher-risk patients, staged, or fractionated, treatments may reduce the risk of injuring other tissues.

How effective is CyberKnife treatment?

Treating pituitary adenomas with the CyberKnife combines the advantages of conventional radiation and radiosurgery. Since CyberKnife performs radiosurgery, radiation exposure is limited to the adenoma. CyberKnife treatment can be fractionated, however, like conventional radiation therapy.

This approach lessens the radiation risk to sensitive structures around the tumor, like optic tissues and part of the brain known as the hypothalamus. CyberKnife fractionated stereotactic radiosurgery is also well suited for treating adenomas that invade the cavernous sinus, which contains nerves that control eye movement and facial sensation.

CyberKnife works best with:

Patients with small tumors that overproduce a pituitary hormone
Patients who have a residual tumor after transsphenoidal surgery
Patients with hormone-producing tumors and who continue to have higher than normal hormone levels after surgery
Patients with an adenoma that has invaded the cavernous sinus
Patients who are unable to have or opposed to transsphenoidal surgery

From http://www.chicagock.com/conditions-treated/brain-tumors/pituitary-adenoma/

Changes to the CushieWiki

2011-07-07T06:31:00.001-04:00

We have been getting spammers lately, so changes have had to be made. Anonymous editing is no longer possible. Even signing up for an account on the CushieWiki isn't enough to keep the spam folks at bay, so... if you want to post/edit/create, you'll need to get permission first.

To do so, send a PM to MaryO through the message boards, send a note through the Contact Us page or send a message through FaceBook.

I am sorry for all the annoyances that these spam folks make us go through.

FDA Accepts Submission of New Drug Application for CORLUX for Cushing's Syndrome

2011-06-30T18:03:00.001-04:00

MENLO PARK, CA, Jun 30, 2011 (MARKETWIRE via COMTEX) -- Corcept Therapeutics Incorporated (NASDAQ: CORT), a pharmaceutical company engaged in the discovery, development and commercialization of drugs for the treatment of severe metabolic and psychiatric disorders, today announced that the U.S. Food and Drug Administration (FDA) has accepted for filing the New Drug Application (NDA), which was submitted on April 15, 2011, for CORLUX, a glucocorticoid receptor type II (GR-II) antagonist, for the treatment of the manifestations of Cushing's Syndrome.

The FDA has indicated that this application will receive a standard review and that the Prescription Drug User Fee Act (PDUFA) goal date for completion of its review is February 17, 2012.

We are executing our commercial plans related to CORLUX for the treatment of Cushing's Syndrome based on the projected timeline for the FDA review of our NDA. This includes conducting market research and engaging third-party vendors to support distribution and other logistical needs for product launch, if CORLUX is approved by the FDA.

"Many patients with Cushing's Syndrome suffer debilitating manifestations of their disease, despite receiving the best available treatment," said Joseph K. Belanoff, M.D., Chief Executive Officer at Corcept. "In our Phase 3 study, CORLUX demonstrated its potential to significantly improve the clinical condition of these patients in a wide variety of important ways. We believe that CORLUX has the potential to provide a meaningful advance over the current standard of care for patients with Cushing's Syndrome and are gratified to receive the formal notice of the FDA's acceptance of the NDA for filing."

About Cushing's Syndrome

Endogenous Cushing's Syndrome results from prolonged exposure of the body's tissues to high levels of the hormone cortisol generated by tumors. Cushing's Syndrome is an orphan indication which most commonly affects adults aged 20 to 50. An estimated 20,000 people in the United States have Cushing's Syndrome, with more than 3,000 newly diagnosed patients each year. Symptoms vary, but most patients have one or more of the following: diabetes mellitus, high blood pressure, weight gain, a rounded face, increased fat around the neck, severe fatigue, weak muscles, osteoporosis, skin changes, infections, poor quality of life irritability, anxiety and depression.

About CORLUX

Corcept's first-generation compound, CORLUX, also known as mifepristone, directly blocks the cortisol (GR-II) receptor and the progesterone (PR) receptor. Intellectual property protection is in place to protect important methods of use for CORLUX. Corcept retains worldwide rights to its intellectual property related to CORLUX.

About Corcept Therapeutics Incorporated

Corcept is a pharmaceutical company engaged in the discovery, development and commercialization of drugs for the treatment of severe metabolic and psychiatric disorders. The company has completed its Phase 3 study of CORLUX for the treatment of Cushing's Syndrome, and has an ongoing Phase 3 study of CORLUX for the treatment of the psychotic features of psychotic depression. Corcept also has a Phase 2 program for CORT 108297 and an IND-enabling program for CORT 113083. Both of these novel compounds are selective GR-II antagonists -- compounds which block the effects of cortisol but not progesterone. Corcept has developed an extensive intellectual property portfolio that covers the use of GR-II antagonists in the treatment of a wide variety of psychiatric and metabolic disorders, including the prevention of weight gain caused by the use of antipsychotic medication, as well as composition of matter patents for our selective GR-II antagonists.

Statements made in this news release, other than statements of historical fact, are forward-looking statements, including, for example, statements relating to the potential benefit of CORLUX for patients diagnosed with Cushing's Syndrome, commercialization plans for CORLUX for the treatment of Cushing's Syndrome, the timing of completion and outcome of FDA review of the NDA, Corcept's clinical development and research programs, the timing of introduction of CORLUX and future product candidates, including CORT 108297 and CORT 113083 and the ability to create value from CORLUX or other future product candidates. Forward-looking statements are subject to a number of known and unknown risks and uncertainties that might cause actual results to differ materially from those expressed or implied by such statements. For example, there can be no assurances with respect to the cost, rate of spending, completion or success of clinical trials, of the timing of completion of the FDA's review of the NDA for CORLUX in Cushing's Syndrome, that the results of FDA's review will be favorable or that Corcept will pursue further activities with respect to the development of CORLUX, CORT 108297, CORT 113083 or any of its other selective GR-II antagonists. These and other risk factors are set forth in the Company's annual report on Form 10-K for the fiscal year ended December 31, 2010 and subsequent SEC filings, all of which are available from our website (www.corcept.com) or from the SEC's website (www.sec.gov). We disclaim any intention or duty to update any forward-looking statement made in this news release.

INVESTOR CONTACT:Joseph K. Belanoff, M.D.Chief Executive OfficerCorcept Therapeutics650-327-3270Email ContactMEDIA CONTACT:Edie DeVine415-365-8543Email ContactFrom http://news.tradingcharts.com/futures/4/7/160929774.html

Glucocorticoid- and Androgen-Secreting Black Adrenocortical Adenomas: Unique Cause of Corticotropin-Independent Cushing Sydrome

2011-06-29T14:53:00.001-04:00

Glucocorticoid- and Androgen-Secreting Black Adrenocortical Adenomas: Unique Cause of Corticotropin-Independent Cushing Sydrome

Journal	Endocrine Practice
Publisher	American Association of Clinical Endocrinologists
ISSN	1530-891X (Print) 1934-2403 (Online)
Subject	Health Services, Medical Sciences and Endocrinology
Issue	Volume 17, Number 3 / May-June 2011
Pages	e73-e78
Online Date	Thursday, June 23, 2011

PDF (1.8 MB)

Authors

Satoshi Tanaka, MD, PhD¹, Akiyo Tanabe, MD, PhD¹, Motohiko Aiba, MD, PhD², Naomi Hizuka, MD, PhD¹, Kazue Takano, MD, PhD¹, Jun Zhang, MD³, William F. Young, MD, MSc, Jr.⁴

¹Department of Medicine, Tokyo Women's Medical University, Tokyto, Japan
²Department of Clinical Pathology, Tokyo Women's Medical University Medical Center East, Tokyo, Japan
³Department of Anatomic and Clinical Pathology, Mayo Clinic, Rochester, Minnesota
⁴Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic, Rochester, Minnesota

Abstract

Objective: To describe the unique association of corticotropin-independent Cushing syndrome caused by cortisol- and androgen-secreting black adrenal cortical adenomas with myelolipomatous change.

Methods: We report the clinical, laboratory, radiologic, and pathologic findings from 2 patients who presented with androgen excess and typical signs and symptoms of Cushing syndrome.

Results: Endocrine investigations showed high serum cortisol concentrations that lacked diurnal rhythm, undetectable plasma corticotropin concentrations, and absence of serum cortisol suppression after overnight dexamethasone suppression tests. Serum levels of adrenal androgens were elevated. Computed tomography of the abdomen revealed unilateral adrenal masses (largest lesional diameters 4.0 and 3.1 cm). On the basis of the plurihormonal hypersecretion and the imaging characteristics, adrenocortical carcinoma was considered as a possible diagnosis. However, histopathologic analysis in both patients revealed black adrenal cortical adenomas with myelolipomatous change. After surgery, adrenal androgens normalized, and the signs and symptoms of Cushing syndrome and androgen excess resolved. There was no evidence of recurrent disease at last follow-up.

Conclusions: A unique form of corticotropin-independent Cushing syndrome is described: cortisol- and androgen-secreting black adrenal cortical adenomas with myelolipomatous change. Although most patients with corticotropin-independent Cushing syndrome associated with androgen excess prove to have adrenocortical carcinoma, the clinician should be aware of the possibility of benign, black adrenal adenomas in this clinical setting.

Show References

From http://aace.metapress.com/content/yg61xw4671161wg6/

Paternal deprivation prior to adolescence and vulnerability to pituitary adenomas

2011-06-28T13:01:00.001-04:00

L. G. Sobrinho, J. S. Duarte, I. Paiva, L. Gomes, V. Vicente and P. Aguiar

Pituitary

DOI: 10.1007/s11102-011-0324-1

It has been reported that women with prolactinoma were exposed, early in life, to an environment characterized by an absent or violent father.

The present study was designed to evaluate whether paternal absence or violent paternal behavior were more prevalent in patients with pituitary adenomas (prolactinoma, acromegaly, non-secreting adenoma and Cushing’s disease) compared to a control population.

We conducted an observational case–control multicenter study. We interviewed 395 patients with prolactinoma (296 females and 99 males), 130 with acromegaly (87 females and 43 males), 237 with non-secreting adenoma (144 females and 93 males) and 68 with Cushing’s disease (61 females and 7 males) and 365 patients from the same clinics with nodular thyroid disease or lymphocytic thyroiditis with euthyroidism as controls.

Violent or absent fathers were significantly more prevalent in patients with prolactinoma or acromegaly than in controls (P = 0.001 and P = 0.002, respectively) but not in patients with non-secreting adenoma or corticotrophinoma.

Absent fathers in prolactinoma and acromegaly versus controls: P = 0.001 and P = 0.119. Violent fathers in prolactinoma and acromegaly versus controls: P = 0.069 and P = 0.001. The prevalence of absent or violent fathers was also significantly higher in prolactinoma and acromegaly when compared to non-secreting adenoma (P = 0.039 and P = 0.033, respectively).

Paternal deprivation before adolescence may be a risk factor for prolactinoma and acromegaly but not for non-secreting pituitary adenomas or Cushing’s disease.

Keywords Acromegaly – Paternal deprivation – Pituitary adenomas – Prolactinoma

This study is conducted for the Grupo de Estudos de Tumores da Hipófise (GETH).

Fulltext Preview

From http://www.springerlink.com/content/38j3u73175427473/

Addison's Help

Brochures for Primary Care Physicians, to increase awareness of Cushing’s syndrome. In English and Spanish

Making sense of your child's health numbers

Clinical relevance of cardiac structure and function abnormalities in patients with Cushing's syndrome before and after cure

New Endocrinology App

Pregnancy-induced Cushing’s Syndrome: A Case Report

Treatment Options in Cushing’s Disease

Healthy New Year Video Challenge

(Adrenal Cushing's) Tumour behind 7-yr-old's weight gain, moustache

What is the best long-term management strategy for patients with primary adrenal insufficiency?

Synchronous bilateral adrenalectomy by midline incision: A reliable method for treatment of hypercortisolism

Abstract

A New Link in the Stress Response Could Mean Better Treatment Soon

Disturbances of the hypothalamic-pituitary-adrenal axis and plasma electrolytes during experimental sepsis.

We have been Nominated for a Health Activist Hero 2011!

Red alert: Hypertension on the prowl

FDA Rare Disease Patient Advocacy Day

Registration:

Location and Directions:

Date:

Agenda:

Webcast:

Rare Disease Day at NIH

Subclinical Cushings syndrome: definition and management

Investigational drugs may expand medical treatment of Cushing’s syndrome

A Pill That Stops Stress In Your Brain Before You Feel It

P36 - Severe Osteoporosis in Cushing’s Syndrome

Cushing’s Syndrome Clinical Analysis of 77 Cases

Adrenal glands: The reserve tank for stress?

A Few Other Site Links

The Message Boards will be Down

Endocrine disorders & female infertility

Not the Usual Suspects: Animal Study Finds Surprising Clues to Obesity-Induced Infertility

(Addison's Disease) Coma man defies odds to write book

Diabetes in Cushing syndrome: basic and clinical aspects

November Cushing's News

DuoCort Pharma's Orphan Drug Plenadren® Granted European Marketing Authorization for Adrenal Insufficiency

Endoscopic bilateral adrenalectomy (BLA) in patients with ectopic Cushing's syndrome

Alberda WJ, van Eijck CH, Feelders RA, Kazemier G, de Herder WW, Burger JW; Surgical Endoscopy (Nov 2011)

Corlux: Corcept Therapeutics Announces Third Quarter Results and Corporate and Development Update

Today in Medical History

What Is the Best Approach for the Evaluation and Management of Endocrine Incidentalomas?

Case

Overview

Review of the Data

TABLE 2. DIFFERENTIAL DIAGNOSIS FOR PITUITARY INCIDENTALOMAS2,4,14

Back to the Case

Bottom Line

KEY POINTS

ADDITIONAL READING

References

Cushing's News

Effects of Hormone Stimulation on Brain Scans for Cushing's Disease

Today in Medical History

The Cushie.info Blog got a Top Cushings Syndrome blog award!

Just like Cushing's?

Today in Medical History

Selective inferior petrosal sinus sampling without venous outflow diversion in the detection of a pituitary adenoma in Cushing’s syndrome

Abstract

Introduction

Methods

Results

Conclusion

Fulltext Preview

Johns Hopkins Pituitary Patient Day

Join us on September 24, 2011, for the 3rd Annual Patient Education Day at the Johns Hopkins Pituitary Center.

For more information, contact the Johns Hopkins Pituitary Center at 410-955-GLAN (4526).

Help Cushing's Help at No Cost to You

Archived Interviews with MaryO, Cushing's Help Founder

MaryO will be talking about Cushing's

Archived Interview with Sue, Adrenal Patient, July 27, 2011

Today in Medical History

Cushing's Help is Turning 11!

Cushings Help is 11 Years Old Today!

Unusually overweight woman with Cushing's Syndrome to get treatment

Treatments for Pituitary Tumors

Changes to the CushieWiki

FDA Accepts Submission of New Drug Application for CORLUX for Cushing's Syndrome

Glucocorticoid- and Androgen-Secreting Black Adrenocortical Adenomas: Unique Cause of Corticotropin-Independent Cushing Sydrome

Glucocorticoid- and Androgen-Secreting Black Adrenocortical Adenomas: Unique Cause of Corticotropin-Independent Cushing Sydrome

TABLE 2. DIFFERENTIAL DIAGNOSIS FOR PITUITARY INCIDENTALOMAS^2,4,14