Topical Steroid Use in Psoriasis Patient Leads to Severe Adrenal Insufficiency

This article is written live from the American Association of Clinical Endocrinologists (AACE) 2017 Annual Meeting in Austin, TX. MPR will be reporting news on the latest findings from leading experts in endocrinology. Check back for more news from AACE 2017.

At the AACE 2017 Annual Meeting, lead study author Kaitlyn Steffensmeier, MS III, of the Dayton Veterans Affairs (VA) Medical Center, Dayton, OH, presented a case study describing a patient “who developed secondary adrenal insufficiency secondary to long-term topical steroid use and who with decreased topical steroid use recovered.”

The patient was a 63-year-old white male with a 23-year history of psoriasis. For 18 years, the patient had been applying Clobetasol Propionate 0.05% topically on several areas of his body every day. Upon presentation to the endocrine clinic for evaluation of his low serum cortisol, the patient complained of a 24-pound weight gain over a 2-year period, feeling fatigued, as well as facial puffiness.

Laboratory analysis found that the patient's random serum cortisol and ACTH levels were low (0.2µg/dL and <1 .1pg="" 2mm="" a="" according="" additionally="" adrenal="" authors="" cleft="" consistent="" cyst="" gland="" hypoenhancing="" indicative="" insufficiency.="" labs="" lesion="" microadenoma.="" midline="" ml="" mri="" nbsp="" of="" p="" pituitary="" rathke="" respectively="" s="" secondary="" showed="" study="" the="" to="" versus="" were="" with="" within="">

The patient was initiated on 10mg of hydrocortisone in the morning and 5mg in the evening and was instructed to decrease the use of his topical steroid to one time per month. For the treatment of his psoriasis, the patient was started on apremilast, a phosphodiesterase-4 enzyme (PDE4) inhibitor, and phototherapy.

After 2.5 years, the patient had a subnormal response to the cosyntropin stimulation test. However, after 3 years, a normal response with an increase in serum cortisol to 18.7µg/dL at 60 minutes was obtained; the patient was then discontinued on hydrocortisone. Additionally, a stable pituitary tumor was shown via a repeat pituitary MRI.

The study authors explained that, although secondary adrenal insufficiency is not commonly reported, “one study showed 40% of patients with abnormal cortisol response to exogenous ACTH after two weeks of topical glucocorticoids usage.” Another meta-analysis of 15 studies (n=320) revealed 4.7% of patients developing adrenal insufficiency after using topical steroids. Because of this, “clinicians need to be aware of potential side effects of prolong topical steroid use,” added the study authors.

For continuous endocrine news coverage from the AACE 2017 Annual Meeting, check back to MPR's AACE page for the latest updates.

From http://www.empr.com/aace-2017/topical-steroid-psoriasis-clobestasol-propionate/article/654335/

Health Care Expenditure Burden High in Adrenal Insufficiency

Patients with adrenal insufficiency may accrue substantial health care costs and have more hospital stays and outpatient visits compared with healthy controls, according to findings published in the Journal of the Endocrine Society.

Candace Gunnarsson, PhD, vice president of health economics and outcomes research at CTI Clinical Trial and Consulting in Cincinnati, and colleagues evaluated data from a U.S.-based payer database on 10,383 patients with adrenal insufficiency to determine the estimated annual health care burden among them.

Participants were divided into groups based on their type of adrenal insufficiency: primary adrenal insufficiency (n = 1,014), adrenal insufficiency secondary to pituitary disease (n = 8,818) or congenital adrenal hyperplasia (n = 551). A group of matched controls was also evaluated for comparison.

Total annual health care expenditures were significantly higher in the primary adrenal insufficiency group ($18,624 vs. $4,320), adrenal insufficiency secondary to pituitary disease group ($32,218 vs. $6,956) and the congenital adrenal hyperplasia group ($7,677 vs. $4,203) compared with controls. The adrenal insufficiency secondary to pituitary disease group had the highest health care expenditure estimated with an incremental health care burden of $25,262, followed by the primary adrenal insufficiency group ($14,304) and the congenital adrenal hyperplasia group ($3,474).

Compared with controls, participants with adrenal insufficiency spent eight to 10 times more days in the hospital and had up to twice as many outpatient visits per year.

“When comparing [adrenal insufficiency] patients within each cohort based on their drug regimen, patients receiving prednisone therapy vs. hydrocortisone therapy had significantly higher total annual expenditures in the [primary adrenal insufficiency] and [congenital adrenal hyperplasia] and significantly lower total expenditures in the [pituitary disease] cohort,” the researchers wrote. “Patients taking only hydrocortisone and meeting the threshold of 50% adherence were found to have lower expenditures when medication adherence was 75% or higher.” – by Amber Cox

Disclosure: Gunnarsson reports being an employee of CTI Clinical Trial and Consulting. Please see the full study for a list of all other authors’ relevant financial disclosures.

From http://www.healio.com/endocrinology/adrenal/news/in-the-journals/%7B8f92bd0c-0c72-4902-beb5-663c356a61cb%7D/health-care-expenditure-burden-high-in-adrenal-insufficiency

Cushing’s Syndrome is Hazardous to Your Health

People with Cushing’s syndrome, even when treated, have higher morbidity and mortality rates that comparable controls. That is the conclusion of a new study published in the June issue of the Journal of Clinical Endocrinology Metabolism. The study by Olaf Dekkers et al, examined data records from the Danish National Registry of Patients and the Danish Civil Registration System of 343 patients with benign Cushing’s syndrome of adrenal or pituitary origin (i.e., Cushing’s disease) and a matched population comparison cohort (n=34,300).  Due to the lengthy delay of many patients being diagnosed with Cushing’s syndrome, morbidity was investigated in the 3 years before diagnosis while  morbidity and mortality were assessed during complete follow-up after diagnosis and treatment.

The study found that mortality was twice as high in Cushing’s syndrome patients (HR 2.3, 95% CI 1.8-2.9) compared with controls over a mean follow-up period of 12.1 years. Furthermore, patients with Cushing’s syndrome were at increased risk for:

• venous thromboembolism (HR 2.6, 95% CI 1.5-4.7)
• myocardial infarction (HR 3.7, 95% CI 2.4-5.5)
• stroke (HR 2.0, 95% CI 1.3-3.2)
• peptic ulcers (HR 2.0, 95% CI 1.1-3.6)
• fractures (HR 1.4, 95% CI 1.0-1.9)
• infections (HR 4.9, 95% CI 3.7-6.4).

The study also found that this increased multimorbidity risk was present before diagnosis indicating that it was due to cortisol overproduction rather than treatment.

Many of the Cushing’s syndrome patients underwent surgery to remove the benign tumor. For this group, the investigators performed a sensitivity analysis of the  long-term mortality and cardiovascular risk in this  subgroup (n=186)  considered to be cured after operation (adrenal surgery and patients with pituitary surgery in combination with a diagnosis of hypopituitarism in the first 6 months after operation).  The risk estimates for mortality (HR 2.31, 95% CI 1.62-3.28), venous thromboembolism (HR 2.03, 95% CI 0.75-5.48), stroke (HR 1.91, 95% CI 0.90-4.05), and acute myocardial infarction (HR 4.38, 95% CI 2.31-8.28) were also increased in this subgroup one year after the operation.

The standard treatment for endogenous Cushing’s syndrome is surgery. This past year, Signifor (pasireotide) was approved for treatment of adults patients with Cushing’s disease for whom pituitary surgery is not an option or has not been curative.  Cushing’s disease, which accounts for the majority of Cushing’s syndrome patients, is defined as the presence of an ACTH producing tumor on the pituitary grand. In the study by Dekker’s et al, the percentage of patients with Cushing’s disease is not known. We look forward to reexamination of this dataset in a few years following the introduction of more treatment options for Cushing’s disease as well as an analysis that explores the differences in mortality/morbidity rates in the different subsets of patients that make of Cushing’s syndrome (Cushing’s disease, ectopic Cushing’s syndrome, Exogenous Cyshing’s syndrome).

References

Dekkers OM, Horvath-Pujo, Jorgensen JOL, et al, Multisystem morbidity and mortality in Cushing’s syndrome: a cohort study. J Clin Endocrinol Metab 2013 98(6): 2277–2284. doi: 10.1210/jc.2012-3582

- See more at: http://www.raredr.com/medicine/articles/cushing%E2%80%99s-syndrome-hazardous-your-health-0

Adrenal Glands

Anatomy of the adrenal glands:

Adrenal glands, which are also called suprarenal glands, are small, triangular glands located on top of both kidneys. An adrenal gland is made of two parts: the outer region is called the adrenal cortex and the inner region is called the adrenal medulla.

Function of the adrenal glands:

The adrenal glands work interactively with the hypothalamus and pituitary gland in the following process:

• the hypothalamus produces corticotropin-releasing hormones, which stimulate the pituitary gland.
• the pituitary gland, in turn, produces corticotropin hormones, which stimulate the adrenal glands to produce corticosteroid hormones.

Both parts of the adrenal glands -- the adrenal cortex and the adrenal medulla -- perform very separate functions.

What is the adrenal cortex?

The adrenal cortex, the outer portion of the adrenal gland, secretes hormones that have an effect on the body's metabolism, on chemicals in the blood, and on certain body characteristics. The adrenal cortex secretes corticosteroids and other hormones directly into the bloodstream. The hormones produced by the adrenal cortex include:

• corticosteroid hormones
  • hydrocortisone hormone - this hormone, also known as cortisol, controls the body's use of fats, proteins, and carbohydrates.
  • corticosterone - this hormone, together with hydrocortisone hormones, suppresses inflammatory reactions in the body and also affects the immune system.
• aldosterone hormone - this hormone inhibits the level of sodium excreted into the urine, maintaining blood volume and blood pressure.
• androgenic steroids (androgen hormones) - these hormones have minimal effect on the development of male characteristics.

What is the adrenal medulla?

The adrenal medulla, the inner part of the adrenal gland, is not essential to life, but helps a person in coping with physical and emotional stress. The adrenal medulla secretes the following hormones:

• epinephrine (also called adrenaline) - this hormone increases the heart rate and force of heart contractions, facilitates blood flow to the muscles and brain, causes relaxation of smooth muscles, helps with conversion of glycogen to glucose in the liver, and other activities.
• norepinephrine (also called noradrenaline) - this hormone has little effect on smooth muscle, metabolic processes, and cardiac output, but has strong vasoconstrictive effects, thus increasing blood pressure.

From: University of Maryland Center for Diabetes and Endocrinology

Multisystem Morbidity and Mortality in Cushings Syndrome: a Cohort Study

Journal of Clinical Endocrinology and Metabolism, 03/28/2013  Clinical Article

Dekkers O.M. et al.– To examine the risks for mortality, cardiovascular disease, fractures, peptic ulcers, and infections in CS patients before and after treatment.Cushing’s syndrome (CS) is associated with hypercoagulability, insulin resistance, hypertension, bone loss, and immunosuppression. To date, no adequately large cohort study has been performed to assess the multisystem effects of CS. It was concluded that despite the apparently benign character of the disease, CS is associated with clearly increased mortality and multisystem morbidity, even before diagnosis and treatment.

Methods

• The study used Cox–regression, and computed hazard ratios (HR) with 95% confidence intervals (95% CI).
• Morbidity was investigated in the three years before diagnosis; morbidity and mortality was assessed during complete follow–up after diagnosis and treatment.

Results

• 343 CS patients and 34,300 controls were included. Mortality was twice as high in CS patients (HR 2.3, 95%CI 1.8–2.9) compared with controls.
• Patients with CS were at increased risk for venous thromboembolism (HR 2.6, 95%CI 1.5–4.7), myocardial infarction (HR 3.7, 95%CI 2.4–5.5), stroke (HR 2.0, 95%CI 1.3–3.2), peptic ulcers (HR 2.0, 95%CI 1.1–3.6), fractures (HR 1.4, 95%CI 1.0–1.9), and infections (HR 4.9, 95%CI 3.7–6.4).
• This increased multi–morbidity risk was present before diagnosis. Mortality and risk of myocardial infarction remained elevated during long–term follow–up.
• Mortality and risks for AMI, VTE, stroke and infections were similarly increased in adrenal and pituitary CS.

From MDLinx

Cushing's Awareness Blogging Challenge 2013

Do you blog? Want to get started?

Since April 8 is Cushing's Awareness Day, several people got their heads together to create the Second Annual Cushing's Awareness Blogging Challenge.

All you have to do is blog about something Cushing's related for the 30 days of April.

Robin designed this year's version of our "official logo" to put on your blogs.

 

 If your blog wants you to upload an image from your desktop, right-click on the image above and choose "save-as". Remember where you saved it to! 

 To link to the image with the yellow border, use this URL: http://www.cushings-help.com/images/challenge-2013b.jpg 

 To link to the image without a border, use this URL: http://www.cushings-help.com/images/challenge-2013nb.jpg 

 In all cases, the URL for the site is http://www.cushings-help.com 

Please let me know the URL to your blog in the comments area of this post or and I will list it on CushieBloggers ( http://cushie-blogger.blogspot.com/ ) 

The more people who participate, the more the word will get out about Cushing's. 

  Suggested topics - or add your own!

In what ways have Cushing's made you a better person?
What have you learned about the medical community since you have become sick?
If you had one chance to speak to an endocrinologist association meeting, what would you tell them about Cushing's patients?
What would you tell the friends and family of another Cushing's patient in order to garner more emotional support for your friend?
Challenges with Cushing's? How have you overcome challenges? Stuff like that.
I have Cushing's Disease....(personal synopsis)
How I found out I have Cushing's
What is Cushing's Disease/Syndrome? (Personal variation, i.e. adrenal or pituitary or ectopic, etc.)
My challenges with Cushing's
Overcoming challenges with Cushing's (could include any challenges)
If I could speak to an endocrinologist organization, I would tell them...
. What would I tell others trying to be diagnosed? What would I tell families of those who are sick with Cushing's?
Treatments I've gone through to try to be cured/treatments I may have to go through to be cured.
What will happen if I'm not cured?
I write about my health because...
10 Things I Couldn’t Live Without.
My Dream Day.
What I learned the hard way
Miracle Cure. (Write a news-style article on a miracle cure. What’s the cure? How do you get the cure? Be sure to include a disclaimer)
Health Madlib Poem. Go to http://languageisavirus.com/cgi-bin/madlibs.pl and fill in the parts of speech and the site will generate a poem for you.
The Things We Forget. Visit http://thingsweforget.blogspot.com/ and make your own version of a short memo reminder. Where would you post it?
Give yourself, your condition, or your health focus a mascot. Is it a real person? Fictional? Mythical being? Describe them. Bonus points if you provide a visual!
5 Challenges and 5 Small Victories.
The First Time I...
Make a word cloud or tree with a list of words that come to mind when you think about your blog, health, or interests. Use a thesaurus to make it branch more.
How much money have you spent on Cushing's, or, How did Cushing's impact your life financially?
Why do you think Cushing's may not be as rare as doctors believe?
What is your theory about what causes Cushing's?
How has Cushing's altered the trajectory of your life? What would you have done? Who would you have been?
What three things has Cushing's stolen from you? What do you miss the most? What can you do in your Cushing's life to still achieve any of those goals? What new goals did Cushing's bring to you?
How do you cope?
What do you do to improve your quality of life as you fight Cushing's?
Your thoughts...?

Evaluation of depression, quality of life and body image in patients with Cushing’s disease

Nilufer Alcalar, Sedat Ozkan, Pinar Kadioglu, Ozlem Celik, Penbe Cagatay, Baris Kucukyuruk and Nurperi Gazioglu

 

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Abstract

The aim of this study was to evaluate patients with Cushing’s disease (CD) who had undergone transsphenoidal surgery in terms of depression, quality of life (QoL), and perception of body image in comparison to healthy controls.

Forty patients with CD and 40 healthy controls matched for demographic characteristics were included in the study. The subjects were evaluated with the Beck depression inventory (BDI), the health survey-short form (SF-36) and the multidimensional body-self relations questionnaire (MBSRQ). Subgroups of the patients with CD were formed on the basis of remission status and BDI scores. In this study, QoL in the general health category and body image were lower in the patients with CD than in the healthy subjects. However, no differences in depression scores were found between the two groups.

When the CD group was evaluated according to remission rate, the mean BDI score was significantly higher in the CD patients without remission than in both the CD patients with remission and the healthy subjects (p = 0.04). However, the physical functioning, bodily pain and general health scores of the CD patients without remission on the SF-36 questionnaire were lower than in the CD patients in remission and the healthy subjects (p = 0.002, p = 0.04, p = 0.002, respectively). Fitness evaluation, health evaluation and body areas satisfaction scores of the MBSRQ were significantly different in the three groups (p = 0.003, p = 0.009 and p = 0.001, respectively). In this study, patients with CD were found to have lower QoL, lower body image perception and higher levels of depression compared to healthy controls, particularly if the disease is persistant despite surgery.

Keywords  Cushing’s disease – Pituitary surgery – Depression – Quality of life – Body image

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Use of ketoconazole in the treatment of Cushing's syndrome

An older, but still useful, abstract:

J Clin Endocrinol Metab. 1986 Dec;63(6):1365-71.

 

Loli P, Berselli ME, Tagliaferri M.

Abstract

The therapeutic value of ketoconazole for long term treatment of patients with Cushing's syndrome was studied. Seven patients with Cushing's disease and one with an adrenal adenoma received 600-800 mg/day ketoconazole for 3-13 months. Plasma ACTH, cortisol, and dehydroepiandrosterone sulfate levels and urinary cortisol, 17-ketosteroid, and tetrahydro-11-deoxycortisol excretion were determined periodically during the treatment period.

Plasma ACTH and cortisol responses to CRH stimulation were determined before and during treatment. Rapid and subsequently persistent clinical improvement occurred in each patient; plasma dehydroepiandrosterone sulfate and urinary 17-ketosteroid and cortisol excretion decreased soon after the initiation of treatment, subsequently remaining normal or nearly so throughout the treatment period. Urinary tetrahydro-11-deoxycortisol excretion increased significantly. Plasma cortisol levels decreased. Plasma ACTH levels did not change, and individual plasma ACTH and cortisol increments in response to CRH were comparable before and during treatment. The cortisol response to insulin-induced hypoglycemia improved in one patient and was restored to normal in another.

The seven patients tested recovered normal adrenal suppressibility in response to a low dose of dexamethasone during ketoconazole treatment. Ketoconazole is effective for long term control of hypercortisolism of either pituitary or adrenal origin. Its effect appears to be mediated by inhibition of adrenal 11 beta-hydroxylase and 17,20-lyase, and it, in some unknown way, prevents the expected rise in ACTH secretion in patients with Cushing's disease.

From http://www.ncbi.nlm.nih.gov/pubmed/3023421

 

Surgical Versus Medical Treatment for Cushing Disease, the New and the Old

Surgical Versus Medical Treatment for Cushing Disease the New and the Old

Interview with Dr. Amir H. Hamrahian

Amir H. Hamrahian, MD, is a Staff member in the Department of Endocrinology, Diabetes and Metabolism at Cleveland Clinic's main campus, having accepted that appointment in 2005. Prior to that appointment, he was also a clinical associate there for nearly five years. 

His clinical interests include pituitary and adrenal disorders.

Dr. Hamrahian received his medical degree from Hacettepe University in Ankara, Turkey, and upon graduation was a general practitioner in the provinces of Hamadan and Tehran, Iran. He completed an internal medicine residency at the University of North Dakota, Fargo, and an endocrinology fellowship at Case Western Reserve University and University Hospitals, Cleveland.

In 2003, he received the Teacher of the Year award from Cleveland Clinic's Department of Endocrinology, Diabetes and Metabolism. Dr. Hamrahian speaks three languages -- English, Turkish and Farsi -- and is board-certified in internal medicine as well as endocrinology, diabetes and metabolism. He is a member of the Endocrine Society, Pituitary Society and the American Association of Clinical Endocrinologists.

Some of the questions answered in this interview October 1, 2012 include (not in this order):

 

• Can you tell me a little about you endocrine practice and your experience with Cushing’s as part of your practice?
• What are some of biggest challenges you have in treating Cushing’s?
• How do you test cyclical/episodic Cushing's?
• Can someone with cyclical/episodic Cushing's take Korlym?
• I know that Cushing's patients (those that currently have it and/or are cured/in remission can have healthy pregnancies with the right care. How do doctors support this process? Through an endocrinologist and a high-risk ob/gyn? And what sort of treatment is given throughout the pregnancy to prevent hypercortisolism.
• While many patients have a successful long term result from surgery, there are just as many that don’t. Do you find that there are any particular challenges treating patients with Cushing’s disease when pituitary surgery has already failed?
• As I understand, you were an investigator in the clinical trial for Korlym, and I think you treated 4 patients. Did these patients all have a previous surgery that had failed?
• Many Cushing’s patients are trying to understand if they might be candidates for Korlym treatment, can you tell me a little history about the types of patients you treated with Korlym?  I hear that not all patients can take Korlym. Which type of patient should not take it?
• Every past treatment for Cushing’s has always had the goal of lowering cortisol levels, but Korlym doesn’t lower cortisol levels, can you explain how it works?
• So, how do you judge success for a Cushing’s patient on Korlym?
• I lost copious amounts of hair while on Korlym, is this a known side effect?
• Are there any long term reproductive implications due to use of Korlym?

Listen to this interview at http://www.blogtalkradio.com/cushingshelp/2012/10/01/dr-amir-hamrahian-answers-our-questions or to the podcast by searching for Cushings in the iTunes podcast area or click here: http://itunes.apple.com/podcast/cushingshelp-cushie-chats/id350591438

 

 

Dr. Amir Hamrahian Answers Our Questions About Cushing's and Korlym

October 1, 2012 at 6:30 PM eastern, Dr. Amir Hamrahian will answer our questions about Cushing's, pituitary or adrenal issues and Korlym (mifepristone) in BlogTalkRadio at http://www.blogtalkradio.com/cushingshelp/2012/10/01/dr-amir-hamrahian-answers-our-questions

 

You may listen live at the link above.  The episode will be added to the Cushing's Help podcast after the show is over.  Listen to the podcasts by searching for Cushings in the iTunes podcast area or click here: http://itunes.apple.com/podcast/cushingshelp-cushie-chats/id350591438

 

Dr. Hamrahian has had patients on Korlym for about 4 years.

 

Please submit your questions below or email them to CushingsHelp@gmail.com before Sunday, September 30.

 

From Dr. Hamrahian's bio at http://my.clevelandclinic.org/staff_directory/staff_display.aspx?doctorid=3676

 

 

Amir Hamrahian, M.D. 

(216) 444-6568

Appointed: 2000

Request an Appointment

Department:Endocrinology, Diabetes and Metabolism

Location:Cleveland Clinic Main Campus
Mail Code F20 
9500 Euclid Avenue
Cleveland, OH 44195

Appointment:(216) 444-6568

Desk:(216) 445-8538

Fax:(216) 445-1656

Department:Brain Tumor and Neuro-Oncology Center

Location:Cleveland Clinic Main Campus
Mail Code R20 
9500 Euclid Avenue
Cleveland, OH 44195

Appointment:(216) 444-6568

Desk:(216) 445-8538

Fax:(216) 445-1656

Surgeon:

No

Treats:

Adults Only

Research & Publications †

( † Disclaimer: This search is powered by PubMed, a service of the U.S. National Library of Medicine. PubMed is a third-party website with no affiliation with Cleveland Clinic.)

Biographical Sketch

Amir H. Hamrahian, MD, is a Staff member in the Department of Endocrinology, Diabetes and Metabolism at Cleveland Clinic's main campus, having accepted that appointment in 2005. Prior to that appointment, he was also a clinical associate there for nearly five years. 

His clinical interests include pituitary and adrenal disorders.

Dr. Hamrahian received his medical degree from Hacettepe University in Ankara, Turkey, and upon graduation was a general practitioner in the provinces of Hamadan and Tehran, Iran. He completed an internal medicine residency at the University of North Dakota, Fargo, and an endocrinology fellowship at Case Western Reserve University and University Hospitals, Cleveland.

In 2003, he received the Teacher of the Year award from Cleveland Clinic's Department of Endocrinology, Diabetes and Metabolism. Dr. Hamrahian speaks three languages -- English, Turkish and Farsi -- and is board-certified in internal medicine as well as endocrinology, diabetes and metabolism. He is a member of the Endocrine Society, Pituitary Society and the American Association of Clinical Endocrinologists.

Education & Fellowships

Fellowship - University Hospitals of Cleveland

Endocrinology
Cleveland, OH USA
2000

Residency - University of North Dakota Hospital

Internal Medicine
Fargo, ND USA
1997

Medical School - Hacettepe University School of Medicine

Ankara Turkey
1991

Certifications

• Internal Medicine
• Internal Medicine- Endocrinology, Diabetes & Metabolism

Specialty Interests

Cushing syndrome, acromegaly, pheochromocytoma, prolactinoma, primary aldosteronism, pituitary disorders, adrenal tumor, adrenocortical carcinoma, MEN syndromes, adrenal disorders

Awards & Honors

• Best Doctors in America, 2007-2008 

Memberships

• Pituitary Society
• Endocrine Society
• American Association of Clinical Endocrinologists
• American Medical Association

Treatment & Services

• Radioactive Iodine Treatment
• Thyroid Aspiration
• Thyroid Ultrasound

Specialty in Diseases and Conditions

• Acromegaly
• Addison’s Disease
• Adrenal disorders
• Adrenal insufficiency
• Adrenal Insufficiency and Addison’s Disease
• Adrenal Tumors
• Adrenocortical Carcinoma
• Adrenoleukodystrophy (ALD)
• Amenorrhea
• Androgen Deficiency (Low Testosterone)
• Androgen Excess
• Calcium Disorders
• Carcinoid Syndrome
• Conn's Syndrome
• Cushing's Syndrome
• Empty sella
• Erectile Dysfunction
• Familial Multiple Endocrine Neoplasia
• Fasting hypoglycemia
• Flushing Syndromes
• Galactorrhea
• Goiter
• Growth hormone deficiency
• Growth hormone excess
• Gynecomastia
• Hirsutism
• Hyperaldosteronism
• Hyperandrogenism
• Hyperprolactinemia
• Hypertension - High Blood Pressure
• Hyperthyroidism
• Hypocalcemia
• Hypoglycemia
• Hypogonadism
• Hypoparathyroidism
• Hypophysitis
• Hypopituitarism
• Hypothyroidism
• Mastocytosis
• Menopause, Male
• Menstrual Disorders
• Paget's Disease
• Panhypopituitarism
• Parathyroid Cancer
• Parathyroid Disease and Calcium Disorders
• Pheochromocytoma
• Pituitary Cysts
• Pituitary Disorders
• Pituitary stalk lesions
• Pituitary Tumors
• Premenstrual Syndrome (PMS)
• Primary Hyperaldosteronism
• Primary Hyperparathyroidism
• Prolactin Excess States
• Prolactinoma
• Thyroid and pregnancy
• Thyroid Cancer
• Thyroid Disease
• Thyroid Nodule

Cushing's syndrome

Betul A. Hatipoglu MD*

Article first published online: 27 JUN 2012

DOI: 10.1002/jso.23197

Keywords:

Cushing's syndrome; adrenal carcinoma; virilization; hypercortisolism

Abstract

Cushing's syndrome (CS) results from prolonged exposure to elevated endogenous cortisol. Majority of cases are caused by ACTH, pituitary, or ectopic origin. Primary adrenal hypersecretion is 15–20% caused by adenomas, carcinomas (ACC), and rarely by nodular adrenocortical disease. CS presents with all typical features.

Commonly recommended initial testing are urinary free cortisol, late-night salivary cortisol, and 1-mg overnight dexamethasone suppression test (DST). Imaging is the key to diagnosis. CS continues to pose diagnostic and therapeutic challenges; life-long follow-up is mandatory.

J. Surg. Oncol © 2012 Wiley Periodicals, Inc.

Read this article at Wiley Online Publications

Cushing’s Disease and Idiopathic Intracranial Hypertension

Gabriel Zada, Amir Tirosh, Ursula B. Kaiser, Edward R. Laws and Whitney W. Woodmansee

Department of Neurosurgery (G.Z., E.R.L.) and Division of Endocrinology, Diabetes, and Hypertension (A.T., U.B.K., W.W.W.), Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Gabriel Zada, M.D., 15 Francis Street, PBB3, Boston, Massachusetts 02115. E-mail: gzada@usc.edu.

Abstract

Case Illustration: A 33-yr-old woman with Cushing’s disease underwent successful surgical resection of a pituitary adenoma and developed IIH 11 months later after inadvertent withdrawal of oral glucocorticoids.

Methods: A review of the literature was conducted to identify previous studies pertaining to IIH in association with neuroendocrine disease, focusing on reports related to HPA axis dysfunction.

Results: A number of patients developing IIH due to a relative deficiency in glucocorticoids, after surgical or medical management for Cushing’s disease, withdrawal from glucocorticoid replacement, or as an initial presentation of Addison’s disease, have been reported. Hypotheses regarding the underlying pathophysiology of IIH in this context and, in particular, the role of cortisol and its relationship to other neuroendocrine and inflammatory mediators that may regulate the homeostasis of cerebrospinal fluid production and absorption are reviewed.

Conclusion: In a subset of patients, dysfunction of the HPA axis appears to play a role in the development of IIH. Hormonal control of cerebrospinal fluid production and absorption may be regulated by inflammatory mediators and the enzyme 11ß-hydroxysteroid dehydrogenase type 1. Further study of neuroendocrine markers in the serum and cerebrospinal fluid may be an avenue for further research in IIH.

Read the entire article at http://jcem.endojournals.org/content/95/11/4850.full