Lower health-related quality of life observed in patients with Addison’s disease, Cushing’s syndrome

Patients with hypothalamic-pituitary-adrenal axis dysregulations report health-related quality of life that is far lower than that of the general population, according to findings of a prospective study.

“In most centers, both patients with adrenal deficiency and patients with Cushing’s syndrome are managed by the same team,” Charlotte De Bucy, of the Center for Rare Adrenal Diseases at Cochin Hospital in Paris, and colleagues wrote. “Despite the usual perception that both types of diseases alter quality of life, few studies have similarly investigated the impact of cortisol dysregulations on [health-related quality of life]. Such studies are important, however, to identify meaningful differences that would be important to consider to improve management and outcome.”

De Bucy and colleagues analyzed data from 343 patients with Addison’s disease or Cushing’s syndrome followed in routine practice at a single center in France between September 2007 and April 2014 (78% women; mean age, 48 years; mean length of time since diagnosis, 7.8 years; 61% married). All participants completed the short-form health survey (SF-36), a survey of health-related quality-of-life measures and the 12-item general health questionnaire (GHQ-12), a measure of psychological well-being or distress. Questionnaires were completed at baseline and at 6, 12, 24 and 36 months. Patients with Cushing’s syndrome were also assessed for cortisol status at baseline and at follow-up evaluations.

Within the cohort, 206 had Cushing’s syndrome of pituitary origin, 91 had Cushing’s syndrome of adrenal origin and 46 patients had Addison’s disease; 16% were included in the study before any treatment was initiated.

Researchers found that mean standard deviation scores for psychological and physical dimensions of the SF-36 were “well below” those of the general population, but diagnosis, cortisol status and time since treatment initiation all influenced individual scores. Cushing’s syndrome of pituitary origin was associated with worse health-related quality of life, especially for physical functioning, social functioning and mental health. In Cushing’s syndrome, health-related quality of life was generally worse during periods of hypercortisolism, but scores for these patients were lower than those of patients with Addison’s disease even during periods of hypocortisolism or eucortisolism, according to the researchers.

“The differences were particularly large for physical functioning and role-physical subscales,” the researchers wrote.

They also found that mental health scores for patients with Cushing’s syndrome decreased during periods of hypocortisolism, whereas other adrenal conditions were associated with higher mental health scores.

More than half of patients, regardless of diagnosis and cortisol status, had psychological distress requiring attention, according to the GHQ-12 survey.

“Our findings are important for clinical practice,” the researchers wrote. “The consequences of cortisol dysregulation on [health-related quality of life] should be considered in the management of adrenal insufficiency and even more (in) Cushing’s syndrome patients, and these consequences can be long term, affecting apparently cured patients. Early information on these consequences might be helpful for patients who often perceive a poor quality of life as the result of inadequate disease control or treatment. Even if this possibility exists, knowing that adrenal diseases have long-lasting effects on [health-related quality of life] may be helpful for patients to cope with them.” – by Regina Schaffer

Disclosure: L'association Surrénales supported this study. The researchers report no relevant financial disclosures.

From http://www.healio.com/endocrinology/adrenal/news/in-the-journals/%7B842655ce-e710-4476-a3c2-2909b06434ed%7D/lower-health-related-quality-of-life-observed-in-patients-with-addisons-disease-cushings-syndrome

Action For Adrenal Disease

 

Watch online Saturday April 16 at 1:00 PM eastern at https://plus.google.com/events/cpjbd8celcbfgngp8und662s198?hl=en

Secondary Adrenal Insufficiency and Addison's Disease can be deadly, mostly because of the lack of education and awareness. We have lost too many and need to be proactive in preventing unnecessary deaths! Join us as we educate on what these diseases are, how easily they can become deadly and preventive measures we can all take to help this community. Brought to you by the National Adrenal Disease Foundation, with speakers who have personal experience with these diseases.

Our program will include:

Senior Administrator Nichole Klute Rushton••• of the Addison’s Disease Support Group (https://www.facebook.com/groups/addisons.support/) on Facebook, will speak in detail about the unfortunate adrenal insufficient patients who have tragically passed, reminding us that the danger of loss of life is a reality for every person with adrenal insufficiency who doesn’t receive the vital hormones they need

Administrator Debby Hunter ••• of the Living With Addison's Disease Support on Facebook (https://www.facebook.com/groups/LivingWithAddisonsDisease/) who will give us tips on how we can approach our local emergency facilities and hospitals with information about adrenal insufficiency and its care in a crisis situation. She will also share her own personal experience with going through an adrenal crisis.

Deputy Sheriff Chris Spires••• who will speak on life as the husband of an Addison’s disease patient, and share with us how the law enforcement community views adrenal insufficient patients

Melanie Wong ••• National Adrenal Disease Foundation (http://www.NADF.us) Executive Director, who will speak about the recent tragic losses, and the vital importance of reminding the medical community about adrenal insufficiency, as well as NADF’s latest project to get NADF Adrenal Crisis Care posters displayed in every emergency room facility in the United States.

Addison's disease may cause psychosis, say researchers

Research suggests that chronic adrenal insufficiency, more commonly known as Addison's disease, may be responsible for psychiatric symptoms in those who suffer with it. Unfortunately, these symptoms are poorly understood and inadequately studied. In one case, a 41-year-old construction worker was admitted to a psychiatric clinic complaining of depression. He had trouble sleeping and concentrating and had lost 6 pounds due to a loss of appetite. He was placed on 20mg of fluoxetine but returned 2 weeks later complaining that the therapy did not work, and even reported hallucinating his ex-wife, who had recently died in a car accident. He returned again later 4 months later and was found to have a weak pulse, major hypotension, and hyponatremia and hyperkalemia. It was at this point that he was diagnosed with Addison's disease.

The disease was first described by Thomas Addison in the mddle of the 19th century. It involves inadequate secretion from the adrenal glands, leading to lower secretion of glucocorticoids. Its usual symptom pigmentation involves fatigue, weight loss, nausea, vomiting, weakness and abdominal pain. Among its psychiatric symptoms are psychosis and delirium.

"An array of neuropsychiatric symptoms is associated with AD. Addison is quoted as saying in 1855 that AD patients might present with “attacks of giddiness, anxiety in the face, and delirium.”1 Anglin et al1 also noted four case series published in the 1940s and 1950s that found the prevalence of neuropsychiatric symptoms in AD to be between 64 and 84 percent. Iwata et al6 reported that in some cases, the neuropsychiatric symptoms were the initial and sole presentation of AD, even though such symptoms are more common in the late course of the disease; this might lead to a patient initially being misdiagnosed, as it did in our case, and in turn, incorrectly treated. Neuropsychiatric symptoms of AD include, but are not limited to, depression, lack of energy, and sleep disturbances. During an Addisonian crisis, agitation, delirium, and, in some cases, visual and auditory hallucinations are reported.1 According to Smart,7 neuropsychiatric symptoms might also be the first presentation of an Addisonian crisis, especially in a patient who was previously symptom free while under therapy."

It is not clear exactly why these neuropsychiatric symptoms appear. It is possible that electrolytic and metabolic disturbances could produce these symptoms, and hyponatremia, which is its central expression, can result in brain damage. Other researchers believe that the neuropsychiatric symptoms are the effects of glucocorticoid abnormalities on the brain. Some researchers believe that unusually low amounts of the substance could produce hallucinations. In one report, Addison's disease presented as a psychotic break:

"A Caucasian 63-year-old man presented a five-month history of progressive depressive symptoms with sadness, anhedonia, asthenia, hyporexia, insomnia, limb weakness, and psychotic symptoms. He was a former heavy smoker and had been diagnosed with chronic occupational lung disease (silicosis). After a specialized psychiatric consultation, the patient started taking fluoxetine, risperidone, and nitrazepam. After a short period of time, the patient withdrew his medication by his own because of worsening of the limb weakness. The patient became severely paranoid with persecutory beliefs, delusions, an infantile speech, progressive social isolation, fear of leaving his home, periods of mental confusion and disorientation, and sporadic nausea and vomits. A few days before hospital admission, the patient almost stopped fluid intake and evolved with syncope."

From http://www.examiner.com/article/addison-s-disease-may-cause-psychosis-say-researchers

(Addison's Disease) Consider Celiac Disease in Autoimmune Disorder Patients

By: SHARON WORCESTER, Internal Medicine News Digital Network

DESTIN, FLA. – Consider screening for celiac disease in children with juvenile idiopathic arthritis, arthromyalgias, and myositis, advised Dr. Alexa B. Adams at the Congress of Clinical Rheumatology. 

Celiac disease has a strong association with numerous autoimmune disorders. Untreated celiac disease poses serious health consequences, such as short stature, failure to thrive, osteopenia/osteoporosis, and enteropathy-associated T-cell lymphoma. Early diagnosis and treatment could obviate or reduce the need for the more aggressive treatments that are typically prescribed for these associated autoimmune disorders, said Dr. Adams, a pediatric rheumatologist and pediatrician at Cornell University, New York. 

The identification and treatment of celiac disease in the setting of autoimmune disorders also appear to have the potential to alter the course of subsequent autoimmune disease, she said.

A link between celiac disease and juvenile idiopathic arthritis (JIA), for example, is well established. Several studies have demonstrated an increased prevalence of celiac disease among children with JIA, and cases of celiac disease in association with juvenile spondyloarthropathies and with pauciarticular, polyarticular, and psoriatic arthritis also have been reported. Furthermore, data show that a gluten-free diet can improve the musculoskeletal symptoms that are associated with celiac disease. 

The mechanisms for the association between JIA and celiac disease are unknown, but may be related to ongoing intestinal permeability in untreated celiac disease, Dr. Adams said, adding that she advocates screening for celiac disease in all JIA patients. 

She described a case involving a 6-year-old boy who presented with pain and swelling of the knee as well as morning stiffness. He had previously been treated for Lyme disease, and he had a 2-year history of headaches, behavioral problems, and poor growth, compared with his identical twin. 

Based on physical and laboratory examinations (serology was negative for celiac disease) and after the young patient was referred to pediatric infectious disease and neurology specialties where he underwent lumbar puncture and brain MRI, the treatment focused on possible central nervous system Lyme disease. Although his joint complaints were resolved, he had persistent headaches, poor growth, and worsening transaminitis. 

The boy tested negative for infectious and autoimmune hepatitis. An abdominal ultrasound showed fatty infiltration of the liver. Ultimately, the child was referred to a pediatric gastroenterologist. Work-up, including duodenal biopsy, showed findings that were consistent with celiac disease, and a gluten-free diet was initiated. 

"On a gluten-free diet, the child’s headaches resolved, he had no recurrence of joint pain, he was growing and gaining weight, and he had no further behavioral issues," Dr. Adams said.

An early diagnosis of celiac disease in a JIA patient and early initiation of a gluten-free diet can prevent unnecessary treatment with NSAIDs, disease-modifying antirheumatic drugs, and anti–tumor necrosis factor agents. The patent can also avoid unnecessary imaging and joint injections. 

Associations between celiac disease and adult rheumatoid arthritis/seronegative arthritides also exist, but are not as robust as that seen between celiac disease and JIA. 

The coexistence of adult RA and positive celiac antibodies – including EmA (endomysial antibodies) and gliadin IgA – has been well described, but an association with biopsy-proven celiac disease has not borne out, Dr. Adams said. 

The same is true in adult spondyloarthropathy. 

It is possible that there are age-related differences in gluten tolerance or in the pathogenesis of arthritis and/or gut permeability that can explain the age-related differences, but this remains unclear, she noted. 

As for celiac disease and myositis, the associations are well documented in both the pediatric rheumatology and pediatric gastroenterology literature, and also (although only more recently) in the adult literature. 

Interestingly, a high prevalence of the DQAI*0501 allele is found in both diseases, Dr. Adams noted. 

Because treatment of inflammatory myositis often requires significant use of glucocorticoids and sometimes additional immunosuppressive therapy, screening for celiac disease should be considered in myositis patients, she said, describing two cases involving young girls who were diagnosed with myositis and polymyositis, respectively. Both failed to respond adequately to prednisone/methotrexate, and both are doing well now on only a gluten-free diet after being diagnosed with celiac disease on biopsy. 

Screen for celiac disease in patients with vague musculoskeletal complaints who don’t respond to treatment, she said. These are the patients with whom "you just don’t know what to do," she said, adding that these are the patients who don’t clearly have arthritis, whose symptoms are out of proportion to findings on examination, whose symptoms impact their participation in sports or other activities, and who fail to respond well to a number of treatments. Often these patients will be diagnosed with fibromyalgia – a diagnosis that is unusual in young patients and should raise concern about possible other causes, she added.

In these cases, maintain a high index of suspicion for celiac disease, she said, describing the case of a 16-year-old girl who had given up sports because of a 2-year history of increasing pain in the calves, forearms, Achilles tendon, heels, and back. The skin on her thighs and calves was sensitive to touch, but she had no GI symptoms and had normal growth. 

Massage, chiropractic manipulation, acupuncture, electrical stimulation, and saline injection in her calf all failed to alleviate her symptoms. The child was diagnosed with fibromyalgia and treated with gabapentin, an over-the-counter NSAID, as well as intensive physical therapy.

After a gastroenterology referral, she was diagnosed with celiac disease based on biopsy findings, and was started on a gluten-free diet. At 5 months, she was symptom free and was once again active in sports activities. 

Given the consistent findings associating celiac disease with certain autoimmune disorders, and the safety and effectiveness of the gluten-free diet that is used to treat celiac disease, screening deserves consideration in these patients, she concluded. 

An association between celiac disease and systemic autoimmune disease has been reported, but is less established than the association between celiac disease and nonsystemic autoimmune disorders, Dr. Adams said. 

Reports of a link between celiac disease and systemic lupus erythematosus (SLE), for example, are limited to case reports, and at this point should be "taken with a grain of salt," she said. 

However, it does appear that in children the celiac disease diagnosis typically precedes the SLE diagnosis, whereas the converse is true in adults. 

Also, reports of SLE following celiac disease despite histologic normalization of the celiac disease on biopsy suggest that the treatment of celiac disease via a gluten-free diet does not modify the disease course in SLE, as it appears to do in cases of arthritis and myositis (J. Clin. Gastroenterol. 2008;42:252-5), Dr. Adams said. 

There does, however, appear to be a fairly strong association between celiac disease and Sjögren’s syndrome. 

A 2003 report said Sjögren’s syndrome is present in up to 15% of patients with biopsy-proven celiac disease, and demonstrated that anti-tTG (tissue transglutaminase, a marker for celiac disease) is more prevalent in Sjögren’s syndrome than in other systemic rheumatic diseases (J. Rheumatol. 2003;30:2613-9). 

Systemic sclerosis and morphia have also been reported in association with celiac disease, Dr. Adams said. 

The strongest associations between celiac disease and systemic autoimmune disease are with adult idiopathic diabetes mellitus, autoimmune thyroid disease, Addison’s disease, and polyendocrinopathies, she added. 

More data are needed to define the prevalence of celiac disease in various subtypes of systemic autoimmune disease, she concluded. 

Dr. Adams serves as a speaker for Abbott Pharmaceuticals. She had no other relevant disclosures.

From http://www.internalmedicinenews.com/news/gastroenterology/single-article/consider-celiac-disease-in-autoimmune-disorder-patients/9e1f371327.html

NIH Adrenal Clinical Trials Updated 5/5/2011

Rank	Status	Study
1	Completed	Cardiovascular Risk in Patients With Non-Functional Adrenal Incidentaloma Condition: Adrenal Cortex Neoplasms Intervention:
2	Completed Has Results	Changes in Adrenal Hormones During Adrenal Radiofrequency Ablation Condition: Adrenal Gland Neoplasms Intervention: Procedure: Radiofrequency ablation
3	Completed	Adrenal Scans With Radioiodine-Labeled Norcholesterol (NP-59) Conditions: Adrenal Gland Neoplasms;   Adrenal Malignancies;   Abnormal Hormonal Secretions;   Electrolytes Abnormalities Intervention: Other: Imaging, Adrenal acans
4	Recruiting	Trial of Vasopressin and Epinephrine to Epinephrine Only for In-Hospital Pediatric Cardiopulmonary Resuscitation Conditions: Cardiopulmonary Arrest;   Cardiac Arrest Interventions: Drug: Vasopressin;   Drug: Epinephrine
5	Completed	Adrenal Suppression and Adrenal Recovery Induced by Megestrol Acetate Condition: Adrenal Function Intervention: Drug: megestrol acetate
6	Recruiting	Test Predicting Adrenal Insufficiency in Volunteers Under Prednisone Treatment Condition: Adrenal Gland Hypofunction Interventions: Procedure: adrenal insufficiency testing;   Drug: prednisone
7	Recruiting	The Bupivacaine Dose Sparing Effect of Intrathecal Epinephrine Condition: Spinal Anesthesia Interventions: Drug: Placebo;   Drug: epinephrine 25;   Drug: Epinephrine 50;   Drug: epinephrine 100;   Drug: Epi 200
8	Recruiting	SPARTACUS: Subtyping Primary Aldosteronism: a Randomized Trial Comparing Adrenal Vein Sampling and Computed Tomography Scan. Condition: Hyperaldosteronism Intervention: Other: Ct-scan or adrenal vein sampling
9	Completed	Make up for the Epinephrine Autoinjector Condition: Anaphylaxis Intervention: Device: Epinephrine autoinjector
10	Completed	Epinephrine Inhalation Aerosol USP, a HFA-MDI Study for Assessment of Pharmacokinetics Conditions: Asthma;   Bronchospasm;   Wheezing;   Shortness of Breath Interventions: Drug: Epinephrine Inhalation Aerosol, HFA;   Drug: Epinephrine Inhalation Aerosol
11	Completed	Once-Daily Oral Modified-Release Hydrocortisone in Patients With Adrenal Insufficiency Condition: Adrenal Insufficiency Interventions: Drug: hydrocortisone (modified release), oral tablet 20 and 5 mg;   Drug: Hydrocortisone, oral tablet, 10 mg
12	Completed	Pharmacokinetics (PK) Study of Epinephrine Inhalation Aerosol in Healthy Volunteers Condition: Asthma Intervention: Drug: epinephrine inhalation aerosol
13	Completed	ED50 and ED95 of Intrathecal Bupivacaine With or Without Epinephrine for Total Knee Replacement Arthroplasty Conditions: Spinal Anesthesia;   Total Knee Replacement Arthroplasty Interventions: Drug: intrathecal bupivacaine 6 mg with 100 mcg of epinephrine;   Drug: intrathecal bupivacaine 7 mg with 100 mcg of epinephrine;   Drug: intrathecal bupivacaine 8 mg with 100 mcg of epinephrine;   Drug: intrathecal bupivacaine 9 mg with 100 mcg of epinephrine;   Drug: intrathecal bupivacaine 10 mg with 100 mcg of epinephrine;   Drug: intrathecal bupivacaine 11 mg with epinephrine 100 mcg;   Drug: intrathecal bupivacaine 6 mg with 200 mcg of epinephrine;   Drug: intrathecal bupivacaine 7 mg with 200 mcg of epinephrine;   Drug: intrathecal bupivacaine 8 mg with 200 mcg of epinephrine;   Drug: intrathecal bupivacaine 9 mg with 200 mcg of epinephrine;   Drug: intrathecal bupivacaine 10 mg with 200 mcg of epinephrine;   Drug: intrathecal bupivacaine 11 mg with 200 mcg of epinephrine
14	Active, not recruiting	Study of UK Adults With Congenital Adrenal Hyperplasia. Condition: Congenital Adrenal Hyperplasia Intervention:
15	Not yet recruiting	Intranasal Injection Versus Topical Administration of Epinephrin During Endoscopic Sinus Surgery Conditions: Hypertension;   Hypotension;   Tachycardia;   Bradycardia;   Arrhythmia Interventions: Drug: Epinephrin (Intranasal injection);   Drug: Epinephrin (Topical administration)
16	Recruiting	Adrenal Insufficiency in Septic Shock Conditions: Septic Shock;   Acute Adrenal Insufficiency Intervention: Drug: Corticosteroid
17	Recruiting	Performance of 18F-Fluorodeoxyglucose Positron Emission Tomography (FDG-PET) in the Diagnosis of Indeterminate Adrenal Tumors on Conventional Imaging: A French Prospective Multicentric Study Condition: Adrenal Gland Neoplasms Intervention: Other: FDG-PET scan
18	Unknown †	Prospective Study on the Incidence of Adrenal Crisis in Patients With Chronic Adrenal Insufficiency Condition: Adrenal Insufficiency Intervention:
19	Completed	Dose Response Relationship for Single Doses of Corticotropin Releasing Hormone (CRH) in Normal Volunteers and in Patients With Adrenal Insufficiency Conditions: Adrenal Gland Hyperfunction;   Adrenal Gland Hypofunction;   Cushing's Syndrome;   Healthy Intervention: Drug: Ovine Corticotropin-Releasing Hormone (oCRH)
20	Recruiting	Adrenal Function in Critical Illness Condition: Adrenal Insufficiency Intervention:

Rank	Status	Study
21	Recruiting	Study of Adrenal Gland Tumors Condition: Adrenal Gland Neoplasm Intervention:
22	Recruiting	The Effects of Epinephrine in Endotoxemia in Normal Volunteers Condition: Immune System Interventions: Biological: Endotoxin, Lipopolysaccharide, LPS;   Biological: Endotoxin, Lipopolysaccharide, LPS /Epinephrine
23	Unknown †	Does Topical Steroid Treatment Impair the Adrenal Function? Conditions: Hypothalamus-Pituitary-Adrenal Axis Assessement;   Topical Steroid Therapy in Chronic Skin Diseases Intervention:
24	Recruiting	Combination Local Anesthetics Condition: Perioperative Pain Interventions: Drug: 1% Lidocaine with Epinephrine;   Drug: 0.25% Bupivacaine with epinephrine;   Drug: 1% Lidocaine + 0.25% Bupivacaine with Epinephrine;   Drug: 2% Lidocaine + 0.5% Bupivacaine with epinephrine
25	Recruiting	Study Comparing Peri-articular Injection of Bupivacaine With and Without Epinephrine Condition: Osteoarthritis Interventions: Procedure: Peri-articular injection of marcaine/epinephrine;   Procedure: Peri-articular injection of marcaine alone
26	Not yet recruiting	Gluing Lacerations Utilizing Epinephrine Condition: Lacerations Intervention: Drug: LET - Lidocaine Epinephrine Tetracaine
27	Recruiting	Use of Local Analgesia With Epinephrine During Total Hip Arthroplasty (THA) Condition: Arthroplasty, Replacement, Hip Intervention: Drug: ropivacaine, physical serum and adrenalin
28	Recruiting	Relative Adrenal Insufficiency in Preterm Very Low Birth Weight Infants With Shock Condition: Adrenal Insufficiency Intervention:
29	Unknown †	Adrenal Insufficiency in Cirrhotics With Ascites. Effects of Hydrocortisone on Renal and Haemodynamic Function Condition: Cirrhosis With Ascites Interventions: Drug: hydrocortisone;   Drug: dextrose solution 5%
30	Recruiting	Bronchiolitis, Optimal Treatment in Infants and Prognosis Condition: Bronchiolitis Interventions: Drug: Racemic adrenaline;   Drug: Isotonic saline
31	Recruiting	RAD001 in Pheochromocytoma or Nonfunctioning Carcinoid Conditions: Pheochromocytoma;   Extra-Adrenal Paraganglioma;   Non-functioning Carcinoid Intervention: Drug: RAD001
32	Not yet recruiting	Hypoglycemia Associated Autonomic Failure in Type 1 DM, Q4 Condition: Type 1 Diabetes Intervention: Drug: epinephrine
33	Recruiting	Effect of Epinephrine/ Phenylephrine for Preventing the Postreperfusion Syndrome During Reperfusion in Liver Transplantation Condition: Hypotension After Reperfusion in Liver Transplantation Interventions: Drug: phenylephrine;   Drug: epinephrine;   Drug: placebo control
34	Recruiting	Safety Study Evaluating the Adrenal Suppression Potential of Product 0405 in Pediatric Subjects With Atopic Dermatitis Condition: Atopic Dermatitis Intervention: Drug: Product 0405
35	Recruiting	Merits of Continuous Paravertebral Block in the Management of Renal/Adrenal Surgery by Laparotomy Condition: Patient Scheduled for Renal and/or Adrenal Surgery Intervention: Procedure: Continuous Paravertebral block
36	Not yet recruiting	Adrenalectomy Versus Follow-up in Patients With Subclinical Cushings Syndrome Condition: Adrenal Tumour With Mild Hypercortisolism Intervention: Procedure: Adrenalectomy
37	Recruiting	Role of the Protein Osteoprotegerin in the Bone Health of Women With Congenital Adrenal Hyperplasia Condition: Adrenal Hyperplasia, Congenital Intervention:
38	Recruiting	Gene Polymorphisms Influencing Steroid Synthesis and Action Conditions: Disorders of Sex Development;   Congenital Adrenal Hyperplasia;   Congenital Adrenal Hypoplasia;   Adrenal Insufficiency;   Mineralocorticoid Deficiency;   Intersex Intervention:
39	Recruiting	Adrenal Function and Use of Intralesional Triamcinolone Acetonide 10 mg/mL (Kenalog-10) in Patients With Alopecia Areata Condition: Alopecia Areata Intervention: Drug: Triamcinolone Acetonide 10 mg/mL (Kenalog-10)
40	Recruiting	Assessment of the Efficacy of Nebulised 3% Hypertonic Saline Among Infants Aged 6 Weeks- 24 Months With Bronchiolitis Condition: Bronchiolitis Interventions: Drug: L-Epinephrine and 0.9% Normal Saline;   Drug: L-Epinephrine and 3% Hypertonic Saline

More on last article: Additional autoimmune disease found in one-third of patients with type 1 diabetes

At diagnosis of type 1 diabetes, approximately 33% of patients are positive for at least one additional organ-specific autoantibody, according to new data.

Researchers at the Barbara Davis Center for Childhood Diabetes assessed 491 children diagnosed with type 1 diabetes from 2004 to 2009 for other autoimmune conditions. They measured thyroid peroxidase autoantibodies (TPOAb) to screen for autoimmune thyroid disease, tissue transglutaminase autoantibodies (TTGAb) for celiac disease and 21-hydroxylase autoantibodies (21OHAb) for Addison’s disease.

“We sought to define the prevalence of nonislet, organ-specific autoantibodies at the diagnosis of type 1 diabetes and to determine the prevalence of comorbid autoimmune diseases,” the researchers wrote.

Of the 491 children, 82.7% were white and 53.4% were boys. At the time of diagnosis with type 1 diabetes, mean age was 9.6 years and the average HbA1c level was 11.6%.

Measurements of TPOAb, TTGAb and 21OHAb were collected within 16 days, on average, and patients were diagnosed with autoimmune thyroid disease, celiac disease or Addison’s disease within 45 days.

Overall, 32.6% of the children had at least one nonislet, organ-specific autoantibody. Of these, 18.6% were diagnosed with additional autoimmune disease. Results revealed that 24.8% were positive for TPOAb, of whom 12.3% had autoimmune thyroid disease. Of the 11.6% with TTGAb, 24.6% had celiac disease. Just 1% of children had 21OHAb, and the researchers found only one case of Addison’s disease.

“Ongoing follow-up of this cohort will be important to determine the natural history of organ-specific autoimmunity in patients with type 1 diabetes,” the researchers wrote. “Key questions remain, including the incidence of autoantibodies over time, the evolution from positive antibodies to disease, the genetic influences on autoimmunity and disease, and patient characteristics that may influence antibody or disease development.”

For more information:

• Triolo TM. Diabetes Care. 2011;doi:10.2337/dc10-1756.

Disclosure: The researchers report no relevant financial disclosures.
From http://www.endocrinetoday.com/view.aspx?rid=83019

Type 1 Diabetes, Celiac or Addison’s?

After noticing a growing trend in children diagnosed with Type 1 Diabetes, doctors and medical researchers have announced a new study measuring the correlation between this autoimmune disorder as well as three others. Addison’s disease, celiac disease, and autoimmune thyroid disease often have antibodies present in children at the same time that they are diagnosed with Type 1 Diabetes.


It has recently been reported that fifteen to thirty percent of people with Type 1 diabetes have also been diagnosed, and about 4 to 9 percent have been diagnosed with celiac disease. Addison’s disease is at the bottom of the list with less than one percent being diagnosed. Children who have been confirmed to have diabetes should be tested yearly for an autoimmune thyroid disease, and for celiac disease if other symptoms become apparent. There is no real screening schedule for Addison’s disease.

From http://www.adi-news.com/type-1-diabetes-celiac-or-addisons/211165/

Book explains adrenal dysfunction

Adrenal Glands

Another dysfunction

“Are You Tired and Wired?” (Hay House, $24.95, Amazon price, $16.47)

Simultaneous feelings of exhaustion and being “keyed up” characterize early adrenal dysfunction, the subject of nurse practitioner Marcelle Pick’s self-help book. The adrenal glands are responsible for providing the fight-or-flight hormones in response to stress. If they’re under-producing, that’s Addison’s disease, and if they’re overproducing, that’s Cushing’s syndrome. “But if your adrenal imbalance is less extreme — as is true for hundreds of thousands of U.S. women — your practitioner is unlikely to recognize your condition,” Pick writes. She suggests a 30-day plan to solve adrenal dysfunction, including dietary supplements, exercise, stress-reduction techniques and, the biggie, an adrenal-friendly diet with regular meal times and no processed foods.

From http://www.washingtonpost.com/national/book-explains-adrenal-dysfunction-vegan-magazine-applauds-herbivore-heroes/2011/02/24/ABKaGxV_story.html

Addison's Blog Alerts ~ February 2, 2011

Addison's Disease (Primary Adrenal Insufficiency) | NurseXchange
By isl30fvi3w
Addison's Disease is the hyposecretion of adrenocortical hormones. Addisonian Crisis - can be precipitated by stress, fatal if not treated. SIGNS AND.
NurseXchange - http://nursexchange.com/


Anyone else have Addison's Disease? – 4HealthAnswers.com
By michele
Anyone else have Addison's Disease? Asked By: michele; Category: Addison's Disease. Answer this Question : You must be logged in to post an answer. Signup Here, it takes 5 seconds :). Other Questions ...
4HealthAnswers.com - http://4healthanswers.com/

Adrenal Crisis Tips

From Ellen, on the Cushing's Help Message Boards

I have a very good friend who has had more adrenal crises than anyone care to count (more than 20). She has tried hard to teach me some important things for the day I should ever have a crisis. Among them is the reality that (as before surgery) success of your care depends on YOU getting everything prepared for the worst as best you can. We can no more depend on the ER staff than any other doc out there who isn't a specialist in pituitary medicine. You all have already done much of preparing by having your medic alert bracelets on, your injectable Cortef (bring it with you in case they don't have it there) and your letter from Dr. F. But that isn't enough much of the time as you have painfully discovered.

1) Prevention is the key. You, Mary, are SO overdoing it, I don't know what to say. You shouldn't even be leaving your house right now, let alone taking on the care of small children. You need a good talking to, missy. Perhaps you can choose to do ONE easy task a day but overall-you should be bored out of your gourd sitting on your tuckus. The more you do, the more you risk events like this. The hardest part is understanding that recovery is not a linear improvement every day. You are going to have weeks or maybe months where you can do no more than you did the first week after surgery. This recovery takes a long time when surgery works. Each tiny task you accomplish depletes you in an additive way. It might not have seemed much at the time to unload the dishwasher but you better believe it counts when you add in each additional task you want to accomplish.

2) Everything is additive. It isn't just what you did today but also what you did the last three, four or five days. You may have felt good the first day but each successive day my guess is you could feel your body pushing a bit. I find I say things like, "If I could just get this ONE more job done, then I will rest" before I am off to the next job. Before I know it, it is too late. Think hard about the twinges you feel the days before this happened this time around, when you were tired. How do you feel in the evenings after a day of activity? Those are the signs to look for and treat early the next time. You are having to listen to your body in a whole new way. Learn your earliest signs.

3) Take more Cortef when you first get those twinges above--the days before a crisis might strike.

4) Everyone in your household needs to be trained to give you Cortef. Teach them that confusion on your part indicates a crisis coming on-if you aren't making sense they need to understand that YOU are not able to help yourself. In most cases the oral cortef will keep you out of the ER if someone else makes sure you take it. Don't hesitate, don't let yourself talk them out of helping you-just take it-it is better to err high than low with your history of crises right now.

5) Knowing that in spite of all of this you need ER care potentially, consider calling the liason in person and talking real-time about your needs for future visits-explaining how quickly things become life threatening. They need to have something about your history in the computer already-a copy of that letter from Dr. F plus their own notes that it is on the up and up along with the note to please page your doctor. Give them a recipe to follow that they have pre-approved and it will help greatly. Most ER doctors will never see an adrenal crisis patient in their ER. Doctors have limits on their abilities just as everyone else does. I can read English really well but if you handed me a book written by someone in 1610, I would likely take longer to get through it because I am not as familiar with the format...the 'wherefore art thous' are English but they sure slow you down. That is what happens in the ER to Addisonians...doctors eventually get there but it takes longer because it is unfamiliar. Help them out by giving them the Cliff-Notes before you ever get there.

5A) Also insist that for now they order and keep Solu-Cortef on the shelves for you. Many (most?) hospitals do NOT have it stocked, as my friend discovered over and over again when she went to the ER. It took hours for them to track some down and give it to her. In the meantime, she was getting sicker and sicker. She finally asked the liason to help be certain they had it for her, ready to go. Now, they have it ready for her, they know her and they know what to do. She is often out of there in about 3 hours.

6) If you are vomiting/collapsed clearly in serious trouble, by the time you head off to the ER, call 911/ambulance so you get taken in and cared for without waiting. Your life is at risk by that stage and you need immediate care. It is justified and potentially life-saving.

7) Always have a trained advocate with you, have several back ups in your life. My friend has her husband but she also has me ready to go-have the hospital list several people to call ahead of time in case you arrive on your own and they can't reach your primary person. Your advocates need to know what to do independently of you. They need to know what to say and how to push the ER staff to get things done on your behalf. We, as patients struggling with Cushing's, are used to having to push but most people are very intimidated by medical personnel and often hang back, figuring they must know what to do. Make sure they understand this just isn't the case sometimes and that your life may depend on what they say or get the staff to do. It is critical they contact your endocrinologist-have your advocate INSIST they do this. If they won't, have your advocate page the doctor for you. Be sure you go over a plan with your advocate periodically or answer their questions about what may happen. I went over much of my plan with my husband prior to my surgery but discovered that within days of surgery, he had forgotten most of what I said. He really wanted to help but just hadn't taken in the medical stuff because it was overwhelming and scary. Keep going over it until they are comfortable.

I really hope these are the last ER visits for you all. I have agonized each time my friend goes into another crisis. I know that in spite of everything you do (or don't do) to prevent a crisis, they still happen. Hopefully the next time around, everything will be in place for you all to have a smooth experience.

So, sit down, turn on that television and get comfy girls. TAKE IT EASY!!

About the Adrenal Glands

Adapted from cushings-help.com and The Merck Manual

Adrenal Gland Disorders

The body has two adrenal glands, one near the top of each kidney. The inner part (medulla) of the adrenal glands secretes hormones such as adrenaline (epinephrine) that affect blood pressure, heart rate, sweating, and other activities also regulated by the sympathetic nervous system. The outer part (cortex) secretes many different hormones, including corticosteroids (cortisone-like hormones), androgens (male hormones), and mineralocorticoids, which control blood pressure and the levels of salt and potassium in the body.

The adrenal glands are part of a complex system that produces interacting hormones. The hypothalamus produces corticotropin-releasing hormone, triggering the pituitary gland to secrete corticotropin, which regulates the production of corticosteroids by the adrenal glands. Adrenal glands may stop functioning when either the pituitary or hypothalamus fails to produce sufficient amounts of the appropriate hormones. Underproduction or overproduction of any adrenal hormones can lead to serious illness.

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Underactive Adrenal Glands

Addison's disease (adrenocortical insufficiency) results when underactive adrenal glands produce insufficient amounts of corticosteroids.

 

Addison's disease affects about 4 out of every 100,000 people. The disease can strike at any age and affects males and females about equally. In 30 percent of people with Addison's disease, the adrenal glands are destroyed by a cancer, amyloidosis, an infection such as tuberculosis, or another identifiable disease. In the other 70 percent, the cause isn't known for certain, but scientists strongly suspect the adrenal glands are destroyed by an autoimmune reaction.

 

The adrenal glands are also suppressed in people who take corticosteroids such as prednisone. Ordinarily, the dose of corticosteroids is tapered slowly before the drug is stopped completely. When corticosteroids are stopped suddenly after being taken for a month or more, the adrenal glands may be unable to produce corticosteroids in sufficient amounts for several weeks or even months, depending on the dose of corticosteroids and the duration of treatment. Certain other drugs, such as ketoconazole taken to treat fungal infections, can also block the natural production of corticosteroids, resulting in a deficiency.

Corticosteroid deficiency can lead to many problems. For example, when corticosteroids are lacking, the body excretes large amounts of sodium and retains potassium, leading to low levels of sodium and high levels of potassium in the blood. The kidneys aren't able to concentrate urine, so when a person with a corticosteroid deficiency drinks too much water or loses too much sodium, the blood level of sodium falls. Inability to concentrate urine ultimately causes the person to urinate excessively and become dehydrated. Severe dehydration and a low sodium level reduce blood volume and can culminate in shock.

corticosteroid deficiency also leads to an extreme sensitivity to insulin, a hormone normally present in the blood, so that the blood sugar levels may fall dangerously low. The deficiency prevents the body from manufacturing carbohydrates from protein, fighting infections, or healing wounds very well. Muscles weaken, and even the heart can become weak and unable to pump blood adequately.

 

To compensate for a deficiency of corticosteroids, the pituitary gland produces more corticotropin, the hormone that normally stimulates the adrenal glands. Since corticotropin also affects melanin production, people with Addison's disease often develop a dark pigmentation of the skin and the lining of the mouth. The excessive pigmentation usually occurs in patches. Even people with dark skin can develop excessive pigmentation, although the change may be hard to recognize. Excessive pigmentation doesn't occur when adrenal insufficiency is caused by pituitary or hypothalamus insufficiency, conditions in which the basic problem is a deficiency of corticotropin.

Symptoms

Soon after developing Addison's disease, a person feels weak, tired, and dizzy when standing up after sitting or lying down. The skin becomes dark; this darkness may seem like tanning, but it appears on both sun-exposed and nonexposed areas. Black freckles may develop over the forehead, face, and shoulders; a bluish-black discoloration may develop around the nipples, lips, mouth, rectum, scrotum, or vagina. Most people lose weight, become dehydrated, have no appetite, and develop muscle aches, nausea, vomiting, and diarrhea. Many become unable to tolerate cold. Unless the disease is severe, symptoms tend to become apparent only during times of stress.

 

If the disease isn't treated, severe abdominal pains, profound weakness, extremely low blood pressure, kidney failure, and shock may occur, especially if the body is subjected to stress such as an injury, surgery, or severe infection. Death may quickly follow.

Diagnosis

Because the symptoms may start slowly and be subtle, and because no single laboratory test is definitive, doctors often don't suspect Addison's disease at the outset. Sometimes a major stress, such as an accident, operation, or serious illness, makes the symptoms more obvious and precipitates a crisis.

 

Blood tests may show a lack of corticosteroids, especially cortisol, as well as low sodium and high potassium levels. Measures of kidney function, such as tests for blood urea nitrogen and creatinine, usually indicate that the kidneys aren't working well. Corticosteroid levels, usually tested after an injection of corticotropin (a challenge test), can help the doctor distinguish adrenal gland insufficiency from pituitary gland insufficiency. When it is the latter, an injection of corticotropin-releasing hormone reveals whether the cause of the problem is hypothalamus insufficiency.

Treatment

Regardless of the cause, Addison's disease can be life-threatening and must be treated first with corticosteroids. Usually treatment can be started with prednisone taken orally. However, people who are severely ill may be given cortisol intravenously at first and then prednisone tablets. Most people with Addison's disease also need to take 1 or 2 tablets of fludrocortisone every day to help restore the body's normal excretion of sodium and potassium. Fludrocortisone can eventually be reduced or discontinued in some people; however, they will need to take prednisone every day for the rest of their lives. Larger doses of prednisone may be needed when the body is stressed, especially from an illness. Although treatment must be continued for life, the outlook for a normal life span is excellent.

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Overactive Adrenal Glands

The adrenal glands can produce too much of one or more hormones. Changes in the adrenal glands themselves or overstimulation by the pituitary gland may be the cause. The symptoms and treatment depend on which hormones--androgenic steroids, corticosteroids, or aldosterone--are being overproduced.

Overproduction of Androgenic Steroids

Overproduction of androgenic steroids (testosterone and similar hormones) is a condition that leads to virilization, the development of exaggerated masculine characteristics in either men or women.

 

Mild overproduction of androgens is common but may lead only to increased hair growth (hirsutism). True virilizing disease is rare, affecting only about 1 or 2 of every 100,000 women. The incidence of virilizing disease in men is almost impossible to guess.

Symptoms

Signs of virilization include hairiness of the face and body, baldness, acne, deepening of the voice, and increased muscularity. In women, the uterus shrinks, the clitoris enlarges, the breasts become smaller, and normal menstruation stops. Both men and women may experience an increased sex drive.

Diagnosis

The combination of body changes makes virilization relatively easy for a doctor to recognize. A test can determine the level of androgenic steroids in the urine. If the level is high, the dexamethasone suppression test can help determine whether the problem is a cancer, a noncancerous tumor (adenoma), or an enlargement of the hormone-producing portions of the adrenal cortex (adrenal hyperplasia). With this test, the corticosteroid dexamethasone is given orally. If the problem is adrenal hyperplasia, dexamethasone prevents the adrenal glands from producing androgenic steroids. If the problem is an adenoma or cancer of the adrenal glands, dexamethasone reduces androgenic steroid production only partially or not at all. The doctor may also order a computed tomography (CT) or magnetic resonance imaging (MRI) scan to obtain a view of the adrenal glands.

Treatment

Androgen-producing adenomas and adrenal cancers are usually treated by surgically removing the adrenal gland. For adrenal hyperplasia, small amounts of corticosteroids such as dexamethasone generally reduce the production of androgenic steroids, but these drugs may also cause symptoms of Cushing's syndrome if too large a dose is given.

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Overproduction of Corticosteroids

Overexposure to corticosteroids, whether from overproduction by the adrenal glands or from administration of excessive amounts by a doctor, results in Cushing's syndrome.

An abnormality in the pituitary gland, such as a tumor, can cause the pituitary to produce large amounts of corticotropin, the hormone that controls the adrenal glands. Pituitary tumors that overproduce corticotropin occur in about 6 in every 1 million people. Small-cell carcinoma in the lung and some other tumors outside the pituitary gland can produce corticotropin as well (a condition called ectopic corticotropin syndrome). This is the most common cause of excessive adrenal cortical function, found in at least 10 percent of people with small-cell carcinoma in the lung, a common type of tumor.

Sometimes the adrenal gland produces excessive corticosteroids even when corticotropin levels are low, usually when a benign tumor (adenoma) has developed in the adrenal gland. Benign tumors of the adrenal cortex are extremely common; half of all people have them by the age of 70. Only a small fraction of these benign tumors are active; the incidence of adenomas causing disease is about 2 in every 1 million people. Cancerous tumors of the adrenal cortex are equally common, but cancers causing endocrine disease are quite rare.

Symptoms

Because corticosteroids alter the amount and distribution of body fat, a person with Cushing's syndrome usually has a large, round face (moon face). Excessive fat develops throughout the torso and may be particularly noticeable at the top of the back (buffalo hump). Fingers, hands, and feet are usually slender in proportion to the thickened trunk. Muscles lose their bulk, leading to weakness. The skin becomes thin, bruises easily, and heals poorly when bruised or cut. Purple streaks that look like stretch marks may develop over the abdomen.

 

High corticosteroid levels over time raise the blood pressure, weaken bones (osteoporosis), and diminish resistance to infections. The risk of developing kidney stones and diabetes is increased, and mental disturbances, including depression and hallucinations, may occur. Women with Cushing's syndrome usually have an irregular menstrual cycle. Children who have the condition grow slowly and remain short. In some people, the adrenal glands also produce large amounts of androgenic steroids, leading to increased facial and body hair, balding, and an increased sex drive.

Diagnosis

Doctors who suspect Cushing's syndrome after observing the symptoms measure the blood level of cortisol, the main corticosteroid hormone. Normally, cortisol levels are high in the morning and decrease during the day. In people who have Cushing's syndrome, cortisol levels are very high in the morning and don't decrease late in the day as would be expected. Measuring cortisol in the urine can be useful because tests performed a few hours apart can indicate how much cortisol has been produced in that time.

 

If the cortisol levels are high, the doctor may recommend a dexamethasone suppression test. The test is based on the ability of dexamethasone to suppress the pituitary gland, thereby reducing adrenal gland stimulation. First a urine sample is tested for cortisol. Then dexamethasone is given, and cortisol levels are measured in another sample of urine. If the Cushing's syndrome is caused by pituitary stimulation, the level of cortisol will fall; if the Cushing's syndrome is caused by stimulation from a nonpituitary source of corticotropin or an adrenal tumor, the urinary cortisol level will remain high.

 

Results of a dexamethasone suppression test may not be clear-cut. Other laboratory tests may be needed to help determine the precise cause of the syndrome. These tests may be followed by a computed tomography (CT) or magnetic resonance imaging (MRI) scan of the pituitary or adrenal glands and by a chest x-ray or CT scan of the lungs.

Treatment

Treatment is directed at the pituitary or adrenal gland depending on the source of the problem. Surgery or radiation therapy may be needed to remove or destroy a pituitary tumor. Adenomas of the adrenal gland can often be removed surgically. Both adrenal glands may have to be removed if these treatments aren't effective or if no tumor is present. Any person who has had both adrenal glands removed, and many people who have had part of their adrenal glands removed, must take corticosteroids for life.

 

Some 5 to 10 percent of the people who have both adrenal adrenal glands removed develop Nelson's syndrome. In this condition, the pituitary gland enlarges, producing large amounts of corticotropin and other hormones such as beta-melanocyte-stimulating hormone, which darkens the skin. If necessary, Nelson's syndrome can be treated with radiation or surgical removal of the pituitary gland.

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Overproduction of Aldosterone

Overproduction of aldosterone (hyperaldosteronism) by the adrenal glands is a condition that affects the blood levels of sodium, potassium, bicarbonate, and chloride, leading to high blood pressure, weakness, and, rarely, periods of paralysis.

 

Aldosterone, a hormone produced and secreted by the adrenal glands, signals the kidney to excrete less sodium and more potassium. Aldosterone production is regulated partly by corticotropin in the pituitary and partly by a control mechanism in the kidneys (the renin-angiotensin-aldosterone system).  Renin, an enzyme produced in the kidneys, controls the activation of the hormone angiotensin, which stimulates the adrenal glands to produce aldosterone.

 

Hyperaldosteronism can be caused by a tumor (usually noncancerous) in the adrenal gland (a condition called Conn's syndrome). Sometimes hyperaldosteronism is a response to certain diseases. For example, the adrenal glands secrete large amounts of aldosterone if the blood pressure is very high or if the artery that carries blood to the kidneys is narrowed.

Symptoms

High levels of aldosterone can lead to low levels of potassium, causing weakness, tingling, muscle spasms, and paralysis. The nervous system may not function properly. Some people become extremely thirsty and urinate frequently, and some experience personality changes.

Symptoms of hyperaldosteronism are also associated with eating licorice, which contains a chemical very similar to aldosterone. In rare cases, people who eat a great deal of candy with real licorice flavoring may develop all the symptoms of hyperaldosteronism.

Diagnosis and Treatment

A doctor who suspects that high blood pressure or related symptoms are caused by hyperaldosteronism may measure the sodium and potassium levels in the blood. The doctor may also measure aldosterone levels and, if they're high, may prescribe spironolactone, a drug that blocks the action of aldosterone, to see if the levels return to normal. Other tests generally aren't needed.

 

When too much aldosterone is being produced, doctors examine the adrenal glands for an adenoma or cancer. While a computed tomography (CT) or magnetic resonance imaging (MRI) scan can be helpful, exploratory surgery is often necessary. If a growth is found, it can usually be removed. When a simple adenoma is removed, blood pressure returns to normal and other symptoms disappear about 70 percent of the time. If no tumor is found and the entire gland is overactive, partial removal of the adrenal glands may not control high blood pressure and complete removal will produce adrenal insufficiency, requiring treatment for the rest of the person's life. However, spironolactone can usually control the symptoms, and drugs for high blood pressure are readily available. Rarely do both adrenal glands have to be removed.

 

More:

Addison’s Disease Knol at http://knol.google.com/k/addison-s-disease#

Addison's Disease (Adrenal insufficiency): Caused by low levels of cortisonelike hormones produced by the adrenal glands. The cause is usually unknown, but may be a complications of tuberculosis, cancer, pituitary disease of cortisone drugs.

Addison's Disease
This Topic on the Message Boards.

 

Adrenal: Pertaining to one or both of these endocrine glands located on top of the kidneys. These glands secrete many hormones, including epinephrine (adrenaline), norepinephrine, and the corticosteroid, and play an important part in the body's endocrine system.

The adrenal is made up of an outer wall (the cortex) and an inner portion (the medulla).

A closer look at the adrenal glands, including an illustration.

Adrenal cortex: Outer layer of the adrenal gland, it secretes various hormones including cortisone, estrogen, testosterone, cortisol, androgen, aldosterone and progesterone.

 

Adrenalectomy: Surgical removal of the adrenal glands is a final measure for halting excess cortisol production This is used only when all other measures fail in individuals with pituitary tumors.

 

Adrenal gland tumor: A benign tumor, or adenoma, that usually results in the excess production of adrenal gland hormones.

 

Sometimes, an abnormality of the adrenal glands, most often an adrenal tumor, causes Cushing's syndrome. The average age of onset is about 40 years. Most of these cases involve non-cancerous tumors of adrenal tissue, called adrenal adenomas, which release excess cortisol into the blood. adrenal glands. In Primary Pigmented Micronodular Adrenal Disease and the familial Carney's complex, surgical removal of the adrenal glands is required.

 

Adrenal insufficiency: See Addison's Disease. Adrenal insufficiency is a life threatening chronic illness. An active and vigorous lifestyle with normal life expectancy is possible as long as the prescribed medications are taken regularly and adjusted when indicated. As with most chronic diseases, adrenal insufficiency demands that the patients take responsibility and develop self-management skills and techniques.

Read an article on Adrenal insufficiency

Adrenal medulla: Middle part of the adrenal gland, it secretes epinephrine (adrenalin) and norepinephrine.

 

Adrenocortical carcinomas, or adrenal cancers: These are the least common cause of Cushing's syndrome. Cancer cells secrete excess levels of several adrenal cortical hormones, including cortisol and adrenal androgens. Adrenocortical carcinomas usually cause very high hormone levels and rapid development of symptoms.

 

Adrenocortical hyperplasia: Increase in the number of cells of the adrenal cortex. It secretes cortisol, androgens and aldosterone. Increased production of any or all of these hormones may result in a variety of disorders, such as Cushing's syndrome and hypertension.

 

Adrenocorticotropic-hormone deficiency: Not enough ACTH is produced by the pituitary gland.

 

Adrenoleukodystrophy: Disturbance in brain substance caused by abnormal function of the adrenal gland.

 

Aldosterone: Adrenal hormone that affects the body's handling of sodium, chloride, and potassium.

Read an article on Aldosterone testing