Monday, May 30, 2011

Cushing’s Syndrome Can Cause Stretch Marks

The majority of people think that stretch marks are caused by pregnancy. Pregnancy is indeed one of the chief reasons why people develop stretch marks. Stretch marks, however, are not exclusive to pregnant women. The most common causes include pregnancy, weight gain, use of medication, and even disease or medical conditions.

Pregnancy is the most common cause of stretch marks. Our skin is elastic, and as such, it can stretch. A woman’s abdomen will undergo a tremendous amount of stretching during pregnancy so that the fetus can have room to develop and grow. Stretch marks are actually scars that are the result of the skin stretching too much. Typically, this is seen in the last three months before a baby is born, when the woman’s belly increases by several times its normal size. The skin will begin to show markings once it is at a point of full stretching potential. Obviously Now, our skin’s elasticity means that if you just bloat your stomach up, you won’t have stretch marks. Women tend to have stretch marks around their stomach area due to pregnancy. Although it’s not uncommon to see stretch marks appear on hips, thighs, and other areas that are supposedly unaffected by pregnancy.

Another culprit of stretch marks is weight gain. Gaining a substantial amount of weight is another factor in stretch marks. The worst part is the fact that those stretch marks are often times much worse than the ones found during pregnancy. Ironically, the more fit you are, the more likely you are to get stretch marks since your muscle groups may experience rapid growth in a short amount of time. When somebody’s body increases size quickly, the skin can’t stretch far enough and markings develop due to the stress placed on the skin. But if you chose to develop your muscles in a slowed down fashion, you will see that stretch marks are less likely to appear.

Medication use or diseases can cause Stretch marks they can also appear in the event of medicine usage and illnesses. Cushing’s Syndrome is a disease that causes stretch marks to appear. Two other diseases that act in the same way as Cushing’s Sydrome are Marfan syndrome and Ehlers-Danlos Syndrome. The disorders and diseases causing stretch marks can be caused by the adrenal gland and generally are hereditary. Conversely, teenagers tend to develop stretch marks as well simply because they are undergoing tremendous amount of physiological change in which their bodies can grow as much as six inches in a year.

After giving birth, the first thing many women do is look for ways to get rid of their stretch marks. You can find lots of different treatment for stretch marks, be it natural treatments, over-the-counter treatments, or even prescription drugs. Over time, the markings caused by quick growth or stretching of the skin eventually fade after time and you will no longer be able to see them. In most cases, they will last for several years before the marks begin to fade away. If you want your stretch marks to disappear, then good skin care is an absolute must. Stretch marks on the skin are a natural part of life, but they can certainly make someone uncomfortable with a low self-esteem.


Thursday, May 26, 2011

The Endocrine System - in poster form

A new way of looking at the endocrine system! Note that several areas have scroll bars for more info.

Wednesday, May 25, 2011

Author of NIA talks about Cushing's

twinkie from the message board writes:

Hello all! As some of you know I have written and published a book. I'll be interviewed tomorrow (May 25, 2011) and I asked the interviewer if, along with questions about my book, she would ask one or two questions about Cushing's. TRYING to get the word out! I'm also doing a blog tour and most of the hosts have been kind enough to put my bio up on their sites which includes information about cushing's and this site.

Here is the link if you want to listen in: 

The podcast is at 3:30 Pacific time.

You can also find info regarding my tour at You don't have to buy a book but you could always ask a question about cushings in the comment section of the hosting blog.

Thanks Mary O for this fabulous tool you've created here! You saved my life.

Growth Hormone improves stroke recovery

A hormone naturally produced by the body has been found to greatly improve long-term recovery rates following a stroke, writes Siski Green

Researchers at the Sahlgrenska Academy in Gothenburg assessed the progress of 407 patients aged between 18 and 70; all had all had a stroke and were then followed for two years afterwards. Measuring levels of a specific hormone – insulin-like growth factor 1 (IGF-1) -  the researchers found that patients who recovered most successfully also had higher levels of the hormone. This remained true for up to two years after the stroke.

The IGF-1 hormone is naturally higher in people who exercise often but levels are also affected by other growth hormones, heredity and nutrition, say the researchers. Body mass index also affects a person’s IGF-1 levels. It’s a hormone that plays in an important role in growth during childhood and it naturally declines with age, but although it appears linked to longevity (some animal studies have indicated it has a positive effect), no studies have been able to show whether it has a negative or positive impact on longevity in humans.

The researchers say that their results may help explain why patients who do more regular exercise, including physiotherapy, are more likely to make better progress than those who don’t. Now they plan to assess whether drug treatments that artificially raise the levels of IGF-1 could also help with recovery after a stroke.


Monday, May 23, 2011

Prevalence and Incidence of Diabetes Mellitus in Adult Patients on Growth Hormone Replacement for Growth Hormone Deficiency

  1. Andrea F. Attanasio,
  2. Heike Jung,
  3. Daojun Mo,
  4. Philippe Chanson,
  5. Roger Bouillon,
  6. Ken K. Y. Ho,
  7. Steven W. J. Lamberts,
  8. David R. Clemmons and
  9. for the HypoCCS International Advisory Board

- Author Affiliations

  1. Cascina del Rosone (A.F.A.), 14041 Agliano Terme, Italy; Lilly Deutschland GmbH (H.J.), 61352 Bad Homburg, Germany; Lilly Research Center (D.M.), Eli Lilly and Co., Indianapolis, Indiana 46285; University Paris-Sud 11 and Institut National de la Santé et de la Recherche Médicale Unité 693 (P.C.), 94270 Le Kremlin-Bicêtre, France; Katholieke Universiteit Leuven (R.B.), Laboratory for Experimental Medicine and Endocrinology, 3000 Leuven, Belgium; Garvan Institute of Medical Research (K.K.Y.H.), St. Vincent's Hospital, Sydney, New South Wales 2010, Australia; Department of Internal Medicine (S.W.J.L.), Erasmus Medical Center, 3015 CE Rotterdam, The Netherlands; Department of Medicine (D.R.C.), University of North Carolina, Chapel Hill, North Carolina 27599
  1. Address all correspondence and requests for reprints to: Prof. David R. Clemmons, Division of Endocrinology, Department of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599-7170. E-mail:


Context: GH replacement in adult GH-deficient patients may cause insulin resistance, raising concerns of potential increased risk of developing diabetes mellitus (DM).

Objective: Our objective was to assess DM prevalence and incidence in the international Hypopituitary Control and Complications Study (HypoCCS) surveillance database.

Design and Participants: GH-treated patients enrolled into HypoCCS (2922 U.S. and 3709 European patients) were assessed for DM, defined as recorded on the clinical report form, reported as adverse events, fasting glucose at least 7 mmol/liter recorded at least twice, or insulin treatment reported.

Results: DM prevalence was 8.2% [95% confidence interval (CI) = 7.6–8.9] overall, 11.3% in the United States and 5.7% in Europe. Incidence (n/1000 patient-years) was 9.7 (95% CI = 8.4–10.9) overall, 14.1 (11.5–16.7) in the United States, and 7.0 (5.6–8.3) in Europe. Overall incidence was 2.1 (0.9–3.3) for patients with body mass index (BMI) below 25 kg/m2 increasing to 16.4 (13.7–19.1) for BMI over 30 kg/m2. Obesity (BMI > 30 kg/m2) prevalence was higher in the United States than Europe and higher in U.S. patients than a U.S. reference population. After age, gender, and BMI adjustment, U.S. HypoCCS DM incidence was 10.6 (8.1–13.0), compared with 7.1 (6.0–8.1) in the National Health Interview Survey. In Europe, incidence for French and German patients was comparable to reference populations; for Sweden, the point estimate was higher than the reference population, but 95% CI overlapped. GH dose was not correlated with DM incidence.

Conclusions: The present analysis showed no evidence for increased DM incidence in GH-treated adult hypopituitary patients. However, those more prone to develop DM exhibited a higher than normal prevalence of obesity.


Cushing's Awareness Day passes but disease lingers for reader

Dear Dr. Gott: Would you please mention that April 8 was Cushing's Awareness Day

I was a healthy woman until the age of 55. After more a year, I was diagnosed with Cushing's disease. I have had two brain surgeries, Graves' disease, recurring Cushing's and 25 radiation treatments to the pituitary. Eight years later, I still live with the effects of this monster. Thank you, Dr. Gott.

Dear Reader: Unfortunately, I was not able to print your letter on April 8, having only received it on April 6. It takes about three weeks before any letter appears in the newspaper.

Cushing's syndrome is a rare endocrine disorder. It occurs when the body produces or receives too much cortisol over an extended period of time.

Cortisol is a vital component in the body. It helps the body respond to stress, maintain blood pressure and cardiovascular function, regulates carbohydrate, fat and protein metabolism, reduces the inflammatory response of the immune system, and balances the effects of insulin.

The most common symptoms include a rounded face and upper body (abdomen, upper back, neck and between the shoulders ("buffalo hump"), obesity and relatively slender arms and legs.

Other symptoms can include acne, slow-healing cuts, bites or infection, bone loss, muscle weakness, fatigue, cognitive difficulties, high blood pressure, high blood glucose levels, headaches, thin skin with easy bruising, purple/red stretch marks, depression and/or anxiety, abnormal menstruation and excess body and facial hair in women, and erectile dysfunction and a decrease in libido and fertility in men. Children typically present with obesity and slowed growth.

Write to Dr. Gott, c/o NEA-United Media, 200 Madison Ave., Fourth Floor, New York, NY 10016.


The Cushing's Help Family of Sites

Sunday, May 22, 2011

Overactive adrenal glands (Cushing's syndrome)


If your child’s adrenal glands produce excessive amounts of certain hormones, they are said to be overactive. The symptoms (and treatment) of overactive adrenal glands depends on which hormone is being overproduced.

Some of the most commonly overproduced hormones are:

  • Androgenic steroids (also known as androgen hormones)
    • Testosterone is one of the most well-known androgen hormones. Excessive production of this or other androgen hormones can lead to exaggerated male characteristics in both men and women (like excess hair on the face and body, baldness, acne, a deeper voice and increased muscle mass).
    • If a female fetus is exposed to high levels of androgens early during a mother’s pregnancy, her genitals may develop abnormally. Young boys who experience high levels of androgen levels may grow faster, but their bones may also mature faster and stop growing too soon.
  • Aldosterone hormone
    • Overproduction of aldosterone hormone can lead to high blood pressure and to symptoms associated with low levels of potassium (like weakness, muscle aches, spasms and sometimes paralysis).
  • Corticosteroids
    • An overproduction of corticosteroids leads to the condition known as Cushing’s syndrome. Rare in children, it’s more commonly seen in adults.

What causes Cushing’s syndrome?

Cushing’s syndrome—the overproduction of corticosteroids—may be caused by an overproduction of cortisol (the hormone that controls the adrenal gland) by the pituitary gland. Other causes of Cushing’s syndrome include:

  • certain lung cancers and other tumors outside the pituitary gland
  • benign (non-cancerous) or cancerous tumors on the adrenal gland(s)

What are the symptoms of Cushing’s syndrome?

Children and adolescents with Cushing's syndrome experience weight gain, growth retardation and hypertension (high blood pressure). Other symptoms may include:

How do doctors diagnose an overactive adrenal glands?

In addition to a complete medical history and physical examination, your child’s doctor will order specific blood and/or urine tests to measure hormone levels.

How can doctors tell if my child has Cushing’s syndrome?

In addition to a complete medical history and physical examination, your child’s doctor may request some or all of the following procedures:

  • x-ray - a diagnostic test which uses invisible electromagnetic energy beams to produce images of internal tissues, bones and organs onto film
  • 24-hour urinary test (urine is collected over a 24-hour period to measure corticosteroid hormones)
  • computerized tomography scan (Also called a CT or CAT scan) - a diagnostic imaging procedure that uses a combination of x-rays and computer technology to produce cross-sectional images (often called slices), both horizontally and vertically, of the body
  • magnetic resonance imaging (MRI) - a diagnostic procedure that uses a combination of large magnets, radiofrequencies and a computer to produce detailed images of organs and structures within the body
  • dexamethasone suppression test (to differentiate whether the excess production of corticotropins originates from the pituitary gland or tumors elsewhere)
  • corticotropin-releasing hormone (CRH) stimulation test (to differentiate whether the cause is a pituitary tumor or an adrenal tumor)

How are overactive adrenal glands/Cushing’s syndrome treated?

Treatment for overactive adrenal glands may include surgical removal of growths on the adrenal gland(s) or the adrenal gland(s) itself. Your doctor may also prescribe medications that block the excessive production of certain hormones.





Saturday, May 21, 2011

Growth Hormone and the Hypothalamic-Pituitary-Somatotrophic Axis

The American Psychiatric Publishing Textbook of Psychopharmacology, 4th Edition

Growth Hormone and the Hypothalamic-Pituitary-Somatotrophic Axis

Sections: Growth Hormone Studies in Psychiatric Disorders.

Topics Discussed: somatotropin.

Excerpt: "Growth hormone (GH) or somatotropin is another stress-sensitive neuroendocrine system. GH is synthesized by the anterior pituitary, and although it can be used as an endpoint in itself for neuroendocrine research in psychiatry, its predominant use is as a marker of the integrity of the noradrenergic system following challenge. The hypothalamic-pituitary-somatotrophic (HPS) axis is under complex regulatory control that is not yet fully understood since cross-species variations in GH regulation make it difficult to extrapolate to humans from animal studies. It is well established, however, that the final common pathways for control of GH release from the pituitary are hypothalamic growth hormone–releasing hormone (GHRH) (stimulation) and somatostatin (inhibition). The wide variety of metabolic, endocrine, and neural influences that alter GH secretion do so primarily through effects on GHRH and/or somatostatin. Neural influences may be mediated by noradrenergic, cholinergic, dopaminergic, aminobutyric acid (GABA)–ergic, and serotonergic..."

DOI: 10.1176/appi.books.9781585623860.417048


Friday, May 20, 2011

Cushings Syndrome Secondary to a Thymic Carcinoid Tumor Due to Multiple Endocrine Neoplasia Type 1

Journal Article

Cushing's Syndrome Secondary to a Thymic Carcinoid Tumor Due to Multiple Endocrine Neoplasia Type 1

Cushing's Syndrome Secondary to a Thymic Carcinoid Tumor Due to Multiple Endocrine Neoplasia Type 1

Journal Endocrine Practice
Publisher American Association of Clinical Endocrinologists
ISSN 1530-891X (Print)
1934-2403 (Online)
Subject Health Services, Medical Sciences and Endocrinology
Pages 1-16
DOI 10.4158/EP11038.CRR1
Online Date Friday, May 06, 2011

Ali A Ghazi, MD1, Azizollah Abbasi Dezfooli, MD2, Farzaneh Mohamadi, MD2, Seyed Vahid Yousefi, MD1, Alireza Amirbaigloo, MD1, Siavash Ghazi, MD1, Marina Pourafkari, MD3, Dan Berney, MD, FRCPath4, Sian Ellard, PhD5, Ashley B. Grossman, MD, FRCP, FMedSci6

1Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2Departments of Thoracic Surgery and Pathology, Masih Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
3Department of Radiology, Taleghani General Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
4Consultant Histopathologists, Barts and the London NHS Trust, London, United Kingdom
5Consultants Molecular Geneticist, Royal Devon & Exeter NHS Foundation Trust, Exeter, London, United Kingdom
6William Harvey Research Institute, Barts, London School of Medicine, London, United Kingdom


Objective: To present an Iranian patient who had a non-classic form of MEN1 and presented with ectopic Cushing's syndrome (CS) secondary to an ACTH-producing thymic neuroendocrine tumor (NET), recurrent renal stones and a giant cell granuloma of the jaw, due to primary hyperparathyroidism (PHPT), without involvement of the pituitary or pancreas.

Methods: Relevant imaging and hormonal evaluations were performed. The patient was operated on 2 occasions for a thymic NET and on 3 occasions for PHPT. DNA from a peripheral blood sample was extracted for sequencing of the MEN1 gene.

Result: Histopathologic evaluation of thymic tumor showed atypical carcinoid tumor at first surgery with a Ki-67 of 5% and an invasive carcinoid tumor, with a Ki-67 of 30% at second surgery. Parathyroid pathology was in favor of glandular hyperplasia. Menin gene sequencing revealed a novel frame shift mutation "c1642-1648" in exon 10.

Conclusion: This case of MEN1 is unusual because most thymic NETs in MEN1 have been claimed to be non-functional, and secretion of ACTH or other ectopic hormones to rarely occur. In patients presenting with thymic NETs, the possibility of a MEN1 should be considered, especially in the presence of hyperparathyroidism. The case also shows that the behavior of thymic NETs can change with the passage of time from a slow-growing tumor to a highly invasive neoplasia, and that ectopic ACTH can be produced by these tumors in the context of MEN1.

Cushings's syndrome, ectopic ACTH, thymic carcinoid, NET, MEN1

Show References


Thursday, May 19, 2011

Adrenal venous sampling is crucial before an adrenalectomy whatever the adrenal-nodule size on computed tomography

Journal of Hypertension:
June 2011 - Volume 29 - Issue 6 - p 1196–1202
doi: 10.1097/HJH.0b013e32834666af
Original papers: Aldosterone

Adrenal venous sampling is crucial before an adrenalectomy whatever the adrenal-nodule size on computed tomography

Sarlon-Bartoli, Gabriellea; Michel, Nicolasa; Taieb, Davidb; Mancini, Julienc; Gonthier, Camillea; Silhol, Françoisa; Muller, Cyrild; Bartoli, Jean-Micheld; Sebag, Frédérice; Henry, Jean-Françoise; Deharo, Jean-Claudea; Vaisse, Bernarda


Objective: To assess the additional value of adrenal venous sampling (AVS) to diagnose primary aldosteronism sub-types in patients who have a unilateral nodule detected by computed tomography (CT scan) and who should undergo an adrenalectomy.

Methods: A retrospective study to assess consecutive patients with primary aldosteronism undergoing an adrenal CT scan and AVS. Criterion for selective cannulation was an equal or higher cortisol level in the adrenal vein compared to the inferior vena cava. An adrenal-vein aldosterone-to-cortisol ratio of at least two times higher than the other side defined lateralization of aldosterone production.

Results: Sixty-seven patients (mean age 52 years, 39 men) underwent a CT scan accccand AVS. In nine patients (13%), cannulation of the right adrenal vein led to a technical failure. Both procedures led to diagnosis of 29 patients with adenoma-producing aldosterone (APA; 50%), 23 bilateral adrenal hyperplasias (40%), and six unilateral adrenal hyperplasias (10%). Of the 45 patients with a nodule detected by CT, subsequent AVS showed bilateral secretion in 16 patients (36%). Compared to the strategy of coupling CT scans with AVS to diagnosis APA, a CT scan alone had an accuracy of 72.4% (P < 0.001). Among patients with a macronodule detected by CT, 13 (37%) had bilateral secretion as assessed by AVS. The patients with a macronodule detected by CT alone had the same risk of a discrepancy as those with a small nodule (P = 0.99).

Conclusion: AVS is essential to diagnose the unilateral hypersecretion of aldosterone, even in patients in whom a unilateral macronodule is detected by CT, to avoid unnecessary surgery.


Wednesday, May 18, 2011

Hair cortisol content in patients with adrenal insufficiency on hydrocortisone replacement therapy

Authors: Gow, Rachel1; Koren, Gideon; Rieder, Michael; Van Uum, Stan

Source: Clinical Endocrinology, Volume 74, Number 6, June 2011 , pp. 687-693(7)

Publisher: Wiley-Blackwell


Summary Objective  Patients with adrenal insufficiency (AI) require life-long replacement therapy with exogenous glucocorticoids. Several studies have shown impaired subjective health status in these patients as well as increased morbidity and mortality risk, which may be caused by glucocorticoid over-replacement. As a measure of long-term cortisol exposure, the usefulness of hair cortisol analysis in patients receiving glucocorticoid replacement therapy was investigated.

Patients and design  Hair samples, demographics, medical history and perceived stress scale questionnaires were collected from 93 patients across North America diagnosed with primary or secondary AI. Sixty-two household partners served as a control group. Cortisol was measured in the proximal 2 cm of hair, representing the most recent 2 months of exposure. A modified enzyme immunoassay was used for the measurement of cortisol.

Results  The male patients had significantly higher hair cortisol levels than the male controls (P  < 0·05), while there was no significant difference among females. Hair cortisol content correlated significantly with glucocorticoid dose (r = 0·3, P < 0·01). Patients with AI had significantly higher subjective stress scores than control subjects.

Conclusions  Hair cortisol content correlates with hydrocortisone (HC) dose in patients with AI. Our results suggest that some AI patients may be over-treated and hence may be at risk for the adverse effects of cortisol. Measurement of HC in hair may become a useful monitoring tool for long-term cortisol exposure in patients treated with glucocorticoids.

Document Type: Research article

DOI: 10.1111/j.1365-2265.2011.04001.x

Affiliations: 1: Department of Physiology and Pharmacology

Publication date: 2011-06-01


Tuesday, May 17, 2011

Cushing's Syndrome: All Variants, Detection, and Treatment

Endocrinol Metab Clin North Am. 2011 Jun;40(2):379-91.


Program on Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Building 10, CRC, 1East, Room 3140, 10 Center Drive, Bethesda, MD 20892-1109, USA.


Diagnosis of Cushing's syndrome involves a step-wise approach and establishing the cause can be challenging. Several pathogenic mechanisms have been proposed for glucocorticoid-induced hypertension, including a functional mineralocorticoid excess state, upregulation of the renin angiotensin system, and deleterious effects of cortisol on the vasculature. Surgical excision of the cause of excess glucocorticoids remains the optimal treatment. Antiglucocorticoid and antihypertensive agents and steroidogenesis inhibitors can be used as adjunctive treatment modalities in preparation for surgery and in cases where surgery is contraindicated or has not led to cure.

Published by Elsevier Inc.

[PubMed - in process]


Specific Electrocardiographic Features Associated with Cushing's Disease

Krystallenia I. Alexandraki; Gregory A. Kaltsas; Apostolos-Ilias Vouliotis; Theodoros G. Papaioannou; Lauren Trisk; Athanasios Zilos; Márta Korbonits; G. Michael Besser; Aris Anastasakis; Ashley B. Grossman

Authors and Disclosures

Posted: 05/16/2011; Clin Endocrinol. 2011;74(5):558-564. © 2011 Blackwell Publishing

Abstract and Introduction


Objective Hypercortisolaemia is associated with an increased risk of cardiovascular disease (CVD), either through a direct action on the myocardium or by increased traditional cardiovascular risk factors. The aim of this study was to investigate whether the alterations in the ECG in Cushing's disease (CD) are predictable from risk factor analysis alone.

Design In 79 patients with a diagnosis of CD, retrospectively recruited, ECG features [corrected for heart rate QT (QTc), QTc dispersion (QTcd), left ventricular hypertrophy (ECG-LVH), right ventricular hypertrophy (ECG-RVH)], systolic (SBP) and diastolic (DBP) blood pressure were assessed. Biochemical, hormonal (cortisol at 09·00 h or cortisol day curve, CDC) and carbohydrate abnormalities (CHA), history of hypertension and cardiovascular disease were recorded. For comparison reasons, a group of 42 healthy subjects matched for gender, age and body mass index previously subjected to ECG assessment were selected.

Results In patients with CD, we noted the following prevalence: metabolic syndrome 39%, hypertension 81%, CVD 21·5%, hypercholesterolaemia 37%, hypertriglyceridaemia 29%, CHA 41%, but a history of cardiac dysrhythmia was only noted in a single patient. No difference in QTc or QTcd was shown between patients with normal or low potassium levels. QTcd >50 ms was associated with both increased ECG-LVH and ECG-RVH. When compared to the control group, patients had longer QTcd (P < 0·001), more prevalent LVH (P < 0·001) and RVH (P = 0·001), and higher SBP and DBP (P < 0·001), but similar QTc. Both CD and ECG evidence of LVH predicted prolonged QTcd, but the association of CD with a prolonged QTcd was independent of other risk factors, including hypertension.

Conclusions Prolonged QTcd in association with ECG evidence of LVH appears to be the specific feature of CD. This may be relevant in the choice of medical therapy for CD and for consideration of treatment of the comorbidities that are associated with hypercortisolaemia.


Untreated hypercortisolaemia, Cushing's syndrome (CS), is associated with the presence of a number of cardiovascular (CV) risk factors, increased CV morbidity, and a mortality rate that is fourfold higher than that expected in the normal population.[1–3] In terms of CV morbidity, this may result from the increased prevalence of traditional metabolic risk factors[2,3] or reflect a direct glucocorticoid effect on the myocardium,[4–7] particularly as glucocorticoid receptors have been demonstrated in the human heart.[4,6]

Analysis of the QT interval measured from electrocardiographs (ECGs) and ECG features of left (ECG-LVH) and right ventricular hypertrophy (ECG-RVH) represent established and readily assessable indicators of CV pathology. Despite the fact that the clinical value of QT abnormalities as indicators of repolarization abnormalities has been questioned,[8] their role as predictors of cardiovascular disease (CVD),[9–16] along with cardiac death and overall mortality,[17–20] appear to be generally accepted.

We speculated that the increased CV morbidity in Cushing's disease (CD) is associated with changes in the QT interval and have questioned whether any such changes were specific to CD or may be secondary to the known risk factors. This is particularly important as recent data have reported increased QTc in patients with CD treated with the recently introduced somatostatin analogue pasireotide (Novartis, Basel, Switzerland: data on file), as well as other established and frequently used medical treatments for CD (;[21]

Materials and Methods

Patients and Metabolic Variables

Seventy-nine patients [61 women, age: 40·76 ± 1·38 years, range: 18–72] from the CD patient database of the Department of Endocrinology, St Bartholomew's Hospital, diagnosed after the completion of a full diagnostic work-up, as previously described,[22] and with an adequate ECG performed on their first admission to the hospital, were retrospectively studied. The study protocol was approved by the Institutional Committee on Human Research as a case record review study [audit numbers 08–76/09–143].

In the patient group, biochemical [total cholesterol (TC), triglycerides, glucose] and hormonal [09·00 h serum cortisol and cortisol day curve (CDC, involving measuring serum cortisol levels at 5 fixed times through a day)][22] measurements were recorded. Hypertension was defined a blood pressure measurement of ≥130 mmHg systolic (SBP) and/or ≥85 mmHg diastolic (DBP) or history of antihypertensive treatment. Abnormalities of carbohydrate metabolism (CHA) were defined as diabetes mellitus (DM), impaired glucose tolerance (IGT) or impaired fasting glucose (IFG). Hypercholesterolaemia was defined as TC levels >5·2 mm or a history of treatment for hypercholesterolaemia. Hypertriglyceridaemia was defined as triglycerides levels ≥1·7 mm or a history of treatment for hypertriglyceridaemia. To characterize the population studied metabolically and since HDL-cholesterol was not assessed, the presence of the metabolic syndrome (MS) was estimated from any three of the following four parameters:[23] (1) hypertriglyceridaemia, (2) hypertension, (3) glucose ≥5·6 mm and (4) presence of abdominal obesity as registered in the case notes (because waist circumference was not routinely measured). Body mass index (BMI) was calculated [BMI = weight (kg)/height (m)2]. The ethnic group and drug history was also recorded.[24] In particular, the medications used at the time of ECG assessment were registered and compared to a contemporary published list of drugs generally accepted to be associated or weakly associated with prolonged QT interval (; The period between the time of occurrence of the first feature(s) of CS and diagnosis was defined as 'CD duration'.

The patient population was divided into subgroups according to the presence or absence of a history of overt CVD (angina, myocardial infarction, arrhythmias, stroke, thromboembolic disease, cardiac failure) and/or hypertension, according to low or normal range levels of potassium and according to their gender.

For comparison reasons, a gender, age and BMI-matched group of 42 healthy subjects (29 women; age: 41·76 ± 0·84 years) was selected from the database of the 1st Department of Cardiology, Hippokration Hospital, Athens. None of these subjects had ever received chronic treatment with glucocorticoids or drugs known to affect glucose, lipid metabolism or blood pressure. All these subjects fasted and abstained from smoking, caffeine and ethanol intake for at least 12 h before evaluation. All subjects in this database were Caucasian.

Analysis of the Electrocardiograms

In all subjects, a standard 12-lead ECG was performed under similar conditions (supine position and normal respiration) at a paper speed of 25 mm/s. Because of the documented problems in reproducibility using automated screening of the QT, all measurements were performed manually by two investigators and repeated twice; average values were computed for each of the ECG features.[8,25] The degree of concordance between the two investigators was 95%; the degree of concordance for each individual investigator was 97% and 98%.

ECGs were obtained at the first admission of the patient group and before any type of treatment for CS. ECGs were only accepted if all 12 leads could be analysed.[10] All patients were admitted for investigation of CS, and all of them were haemodynamically stable without symptoms of any acute CV event. Patients with known CVD as already reported were included in the study, because CVD is included in the previous medical history of patients with untreated CS; however, they were analysed as a separate subgroup.

For the QT interval measurements, the Tangent method was used: the end of the T-wave was defined as the intersection of a tangent to the steepest slope of the last limb of the T-wave and the baseline. The Tangent method was also useful for patients with co-existing hypokalaemia and U waves in resting ECGs (five patients had hypokalemia and prominent U-wave in the ECG). If a U wave appeared immediately after the T wave, the QT interval was measured at the nadir between T and U waves, and thus the 'second hump' (U wave) was excluded; QT intervals were measured in all 12 leads and corrected for heart rate (QTc) with Bazett's formula: QT interval/square root of the RR interval.[26] However, in the standard 12-lead ECG, only two of the six extremity leads are actually recorded, because the other four leads are derived mathematically from these two leads. Thus, if we find the shortest QT interval in one of the extremity leads, the other five extremity leads must have the same QT interval. Hence, we took the shortest QT value recorded from the extremity leads and the mean value of the other five QT intervals. Furthermore, we excluded QT interval measurements from lead V1 because very often the T wave has an isoelectric segment in that lead. Hence, two QT-interval values were recorded from the extremity leads, and another five were recorded from the precordial leads (V2–V6). Thus, we obtained a maximal value for QTc in a lead and a minimal QTc value in another lead: QTc dispersion (QTcd) was defined as the maximum QTc interval (QTc max) minus the minimum QTc interval (QTc min) in seven leads (i.e., the five precordial, the shortest extremity lead and the median of the other five extremity leads).[10,18,27–29] The prevalence of patients with QTcd >80 ms and >50 ms was calculated, as these thresholds have been associated with increased mortality.[16,19,30]

To increase sensitivity (because of the female preponderance in CD),[31] we preferred to use the Sokolow-Lyon product criterion for women and the Cornell criterion for men to diagnose ECG-LVH in both groups.[32] ECG-RVH was defined by the use of any two combinations of the following criteria: (1) R/S ratio in lead V5 or V6 less than or equal to 1; (2) S V5 or V6 greater than or equal to 7 mm; (3) right-axis deviation of more than +90 degrees or (4) P pulmonale.[33]

We planned to exclude from the study any ECGs with intraventricular conduction defects and delays (IVCDs) or bundle-branch block (BBB), as both IVCDs and BBB affect the QRS patterning, and may impact the accuracy of ECG criteria for LVH.[32] However, none was found in our patient cohort.

Statistical Analysis

Values are presented as mean value ± standard error (±SE). Statistical significance was accepted at a P-value<0·05. The distribution of normality of continuous variables was assessed graphically by histograms and statistically by the nonparametric Kolmogorov–Smirnov test. Comparisons between control and patient groups were made by the unpaired t-test or the Mann–Whitney U tests for normally or non-normally distributed variables, respectively. Correlations between categorical variables were estimated by the chi-square test or by Fisher's exact test, as appropriate. In the patient population, independent variables (ECG indices, SBP, DBP, age, gender, BMI, duration of the disease, lipids, fasting glucose, morning cortisol, CDC) associated with the presence of ECG-LVH and ECG-RVH were evaluated by univariate and multiple logistic regression analysis because those variables were dichotomous, and QTc and QTcd by univariate and multiple linear regression analysis because those variables were continuous. In the total population, independent variables (ECGs indices, SBP, DBP, age, gender and BMI) associated with the presence of LVH and RVH were evaluated by univariate and multiple logistic regression analysis, and QTc and QTcd by univariate and multiple regression analysis. Analysis of variance (anova) with Bonferroni correction and the Kruskal–Wallis test with Conover-Inman correction were used for multiple group comparison for normally and non-normally distributed variables. Analysis was performed using spss (version 16·01; SPSS, Inc., Chicago, IL, USA) for Windows XP (Microsoft Corp.).


The metabolic and CV features of the patients with CD are shown in Table 1. The median value of 'CD duration' was 3 years (range <1–39 years). No correlation was found between CD duration and any of the parameters studied.

On analysis of the previous medical history of the patients, we noted that 16 patients had a history of CVD: three with deep vein thrombosis, two with stroke, four with angina pectoris, three with myocardial infarction and four with cardiac failure, while one more patient had a single episode of atrial fibrillation.

Patients with CD had a longer QTcd (P < 0·001), more prevalent ECG indices of LVH (P < 0·001) and RVH (P = 0·001), higher SBP (P < 0·001) and DBP (P < 0·001) values, but a shorter QTcmin (P = 0·004), compared to the control group (Table 2).

The differences between controls and patients subgroups with (A) CVD, with and without hypertension, (B) hypertension only and (C) without CVD or hypertension are shown in Table 2. QTcd was prolonged in all the subgroups (P < 0·001), and no relevant difference was seen in QTc, QTcd, ECG-LVH or ECG-RVH between these groups besides the fact that QTcd was more prolonged in subgroup B compared to subgroup C. It is of note that patients of subgroup C still had a prolonged QTcd compared to the controls, despite the fact that they were younger (P = 0·02; Table 2). In this specific group, no patient had DM, although one had IFG and another IGT. In addition, there was a statistically significant difference between the groups regarding sex (women: A: 56%, B: 78%, C: 100%, P = 0·01).

In 44 (56%) patients, the QTcd value was more than >50 ms and in 5 (6·3%) more than >80 ms (maximal value 87 ms). Interestingly, in six out of seven patients on treatment with drugs associated with prolonged QT, QTcd value was >50 ms (85·7%) but only in one >80 ms (14·3%). When the subgroups of patients with QTcd ≥50 ms or <50 ms were compared, there was a higher prevalence of ECG-LVH (P = 0·004) and ECG-RVH (P = 0·01) in the first subgroup. By contrast, only 2/42 (4·8%) subjects from the control group had a QTcd >50 s, and all were <60 ms. Hence, the sensitivity of QTcd >50 ms to identify a patient with CD was 50·6%, the specificity 95·2%, the positive predictive value (PPV) 95·6% and the negative predictive value 53·3%. However, there was no difference in ECG-LVH or ECG-RVH prevalence between the subgroups of QTcd ≥80 ms and <80 ms.

With regard to the drug history, 28 patients were on no medication, while the remaining patients were on treatment for oedema and/or hypertension (diuretics, potassium-sparing diuretics, aldosterone antagonists, β-adrenoceptor blockers, calcium antagonists, angiotensin-converting enzyme inhibitors), potassium replacement, nitrates, anticoagulants, aspirin, statins and fibrates, sulphonylureas, metformin or insulin, analgesics, psychiatric drugs or drugs for digestive problems. However, only seven patients were on treatment with drugs generally accepted or weakly associated with prolonged QT, namely sotalol, hydrochlorthiazide, sertraline, clomipramine, imipramine, chlorpromazide or fluoxetine. All these patients were women, and all were included in the hypertension-only subgroup. The only differences that were observed when this group was excluded from analysis were that the QTcd in the hypertensive group was reduced and the difference between patients with CVD alone and HTN alone was no longer significant (Table 2). As no other difference was observed in the results, we have included those seven patients in the final analysis.

Seventy-one of the 79 patients had records of plasma potassium levels; the mean level was 3·8 ± 0·68 mm (range: 2·6–5 mm). Fifty-seven (80%) patients had normal potassium levels (median value: 3·9 mm; range: 3·5–5 mm), while 14 had low potassium levels (median value: 3·2 mm; range: 2·6–3·4 mm). No difference was found in the QTcd between these groups (normal potassium: 52·34 ± 2·15 ms vs low potassium: 51·66 ± 5·57 ms, P = 0·90) or in QTc (normal potassium: 392·11 ± 3·11 ms vs low potassium: 388·21 ± 8·10 ms, P = 0·60). In the low-potassium group, six patients (42·9%) had QTcd >50 ms and two patients (14·3%) had QTcd >80 ms, while in the normal-potassium group 35 (61·4%) had QTcd >50 ms and three patients (5·3%) had QTcd >80 ms; these difference were not statistically significant (P = 0·24 and 0·25, respectively). Furthermore, no correlation was found between potassium levels and QTcd or QTc in the whole group of patients or in each subgroup of potassium levels.

Regarding the comparison between female and male patients with CD, no significant difference was found in any of the parameters studied. Men had QTcd 51·38 ± 3·09 ms vs women 51·82 ± 2·29 ms (P = 0·92) and QTc 391·11 ± 3·39 ms vs 391·8 ± 3·13 ms, respectively (P = 0·92). Interestingly, the accepted difference between women and men in QT interval was seen only in the control group in QTcd with men having 15·46 ± 1·87 ms vs women 23·1 ± 2·63 ms (P = 0·02) but not in QTc with men having 385·77 ± 6·28 ms vs 398·79 ± 4·44 ms, respectively (P = 0·11).

Seventy-one patients were Caucasian.[22] To control for racial differences, a group of 71 Caucasian patients with CD was compared to the control population (only Caucasian), and similar results were observed as for the total group (data not shown).

In the patient population, univariate analysis showed that the presence of ECG-LVH (b = 9·78, P = 0·03) and ECG-RVH (b = 12·48, P = 0·002) were predictors of QTcd. However, multivariate analysis revealed that only ECG-LVH (b = 11·20, P = 0·02) remained a predictor of QTcd. In univariate analysis, only CDC (OR = 1·004, CI = 1·0–1·007, P = 0·04) was a predictor of ECG-LVH, while only triglycerides levels (OR = 3·14, CI = 1·23–7·99, P = 0·02) were a predictor of ECG-RVH.

In the total population of controls and patients, univariate analysis showed that the presence of CD (b = 30·99, P < 0·001), SBP (b = 0·37, P < 0·001), DBP (b = 0·57, P < 0·001), ECG-LVH (b = 2431, P < 0·001) and ECG-RVH (b = 21·44, P < 0·001) were predictors of QTcd. However, in multivariate analysis only the presence of CD (b = 24·05, P < 0·001) and ECG-LVH (b = 10·51, P = 0·02) remained predictors of QTcd (Table 3). In the multivariate analysis, only DBP remained a predictor of ECG-LVH and ECG-RVH (Table 3).


In this study, analysis of the baseline ECG characteristics of patients with CD at diagnosis demonstrated that QTcd but not QTc was strongly associated with CD along with the well established association of LVH with QTcd. In addition, hypercortisolaemia was found to be associated with the presence of LVH, implying an interplay of CS pathophysiology with ECG characteristics before the introduction of any therapy. As CD is associated with an increased risk of CVD and mortality, ECG features might represent an easily assessable CV-risk marker present early in the natural history of CD.

We found a high prevalence of hypertension and CVD in CD, in accordance with previous studies[2,26] in addition to a deleterious metabolic profile.[2,23] The presence of these factors may well contribute to the increased morbidity and mortality seen in untreated CD and emphasise the need for early and effective intervention to treat the disease. We did not find any clear relationship between these risk factors and the degree of hypercortisolaemia, but we were dealing with a population of patients with homogeneously increased levels of cortisol. Interestingly, the duration of the disease in this study did not predict any ECG abnormality implying that the presence of these risk factors is not a function of the length of excessive glucocorticoid exposure.[3,34] Nevertheless, it is important to note that many of these risk factors may remain present even years after the cure of CD, suggesting that continued vigilance is required in monitoring their presence and in initiating treatment.[6,35]

In terms of ECG features, a direct comparison of the patient group and controls revealed prolonged QTcd and ECG features of LVH in patients with CD. However, the significant difference in QTcd remained present even in patients without overt CVD or hypertension, suggesting that the conventional risk factors alone could not explain, on their own, all of the cardiac morbidity in CS. It is also of note that QTc was not as sensitive as QTcd in revealing any difference among the subgroups studied. Regression analysis confirmed the well-known association between QTcd and LV mass.[36,37] On the other hand, it has been previously suggested that the relationship between prolonged QTc and future cardiac mortality may be attributed to ventricular electrical instability and abnormal repolarization,[38] while increased QTcd reflects electrical inhomogeneity as a result of myocardial ischaemia, ventricular hypertrophy or dilatation, autonomic neuropathy, peripheral vascular disease or hypertension.[9–14,17,18,39] However, in our study, only a single female patient had a history of a cardiac dysrhythmia. Hence, our findings support the studies that dispute the validity of QT interval as an indicator of repolarization abnormalities,[8] but are in keeping with more recent evidence suggesting its role as predictor of CV risk[10] not always related to electrical disturbances.[9–19] There was no direct correlation between QTcd and the degree of hypercortisolaemia, but this may again reflect the rather uniform increase in hypercortisolaemia in the study population. However, the fact that prolonged QTcd could be predicted by a diagnosis of CD in the total population or by LVH that is affected by the degree of hypercortisolaemia suggests that there may be a direct impact of hypercortisolaemia on QTcd. If this speculation is valid, it may be of even greater clinical significance considering the large number of patients on glucocorticoids for medical reasons; the increasingly diagnosed cases with subclinical CS and mild hypercortisolaemia may also need to be treated even in the face of normal or treated conventional risk factors.[40] It is of note that despite the recent debate regarding the clinical validity of QTcd, this is the feature of ECG that was found abnormal in this specific patient population and not QTc.[8,41] The real significance of the better diagnostic value of QTcd over QTc found in CD in this study cannot be explained because the debates regarding the clinical significance of these CV risk markers have not been resolved. However, it has been documented that patients with an increased QTcd, which may mirror discrepant repolarization characteristics in different areas of the heart, show increased CV mortality and morbidity and that both prolongation of the QT interval and QTcd dispersion independently affected the prognosis of CV mortality and cardiac fatal and nonfatal morbidity.[42]

A QTcd >80 ms, which has been considered indicative of cardiac mortality,[16,30] was seen only in 6·3% of the patients. However, we found that the lower established threshold (>50 ms)[19] was observed in 56% of patients and was related to both ECG-LVH and ECG-RVH, demonstrating high specificity and PPV. Finally, while severe hypercortisolism may be associated with hypokalaemic alkalosis,[43] the fact that no difference was observed in QTcd or QTc between patients with normal or low potassium levels implies that prolonged QTcd is a distinct feature of CD independent of potassium levels. Furthermore, the known differences in women and men in QTcd was not seen in patients with CD as in the normal population.

Finally, the recent findings of a specific effect of the glucocorticoids acting on mineralocorticoid and/or glucocorticoid receptor have to be considered along with the results of this study on LVH and RVH prevalence. Indeed, in adults, treatment with mineralocorticoid receptor antagonists results in a reduction in cardiac hypertrophy and an increase in survival rate,[44,45] mainly because of a decrease in cardiac fibrosis.[46] However, the research in this area is ongoing, and the role of glucocorticoids acting through the cardiac mineralocorticoid receptor remains controversial.[47,48]

This study has a number of limitations, principally because of the retrospective recruitment of patients with CD. Some of the patients were on drugs that could influence QTcd; however, since this study focused on patients with CD who may be under variable pharmacological treatment for several years before their diagnosis and thus this is considered a more representative group of patients as seen in clinical practice. Indeed, the findings persisted even if such patients were excluded. Indeed, the fact that hypercortisolaemia per se seems to be associated with a prolonged QTcd suggests that particular caution is required in such patients when drugs known to alter this parameter are administered. Another limitation was the fact that patient and control groups were from different national backgrounds. We also used a different national group for our control population for logistic reasons, but as similar changes were seen when the small number of non-Caucasian patients were excluded from the analysis, it seems highly unlikely that national identity can account for these marked changes.[24]

In conclusion, a detailed comparison of the ECG features of a group of patients with CD and a BMI-matched control group showed ECG abnormalities along with the expected increase in cardiac risk factors. However, certain of these changes appeared to be specific to this disorder as they correlated directly or indirectly with the hypercortisolaemia independent of any known risk factors. We suggest that hypercortisolaemia per se can be cardiotoxic, and this needs to be considered when assessing the need for therapy even in cases of mild hypercortisolaemia. Prolonged QTc dispersion is classically considered to increase the risk of serious dysrhythmias such as torsades de pointes;[49–51] this may be further increased by certain drugs included in the therapeutic armamentarium of CD, while the effects of others such as somatostatin analogues and ketoconazole are under investigation (;;[49] these findings should be borne in mind when considering pharmacotherapy.


Monday, May 16, 2011

Helpful Hints for Dealing with Cushing's

Hint For... What to do

Add Your Helpful Hints for Dealing with Cushing's


Adrenal Crisis

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Adrenal Crisis, getting medical attention

Before any crisis occures, contact the local ambulance service that would come to your home and/or work and find out if they have a protocol to treat you. My ambulance service could not give me the shot I needed even tho I not only had a medic alert bracelet, but a file of life on my refridgerator with physician instructions etc.

After my advent, we had to bring it to the governing body's attention for change, and now ambulance personel are approved to use information like the file of life or the Medic Alert bracelet to treat anyone with not only in Adrinal crisis but anyone with documented medical information.

You could help a lot of other people besides yourself. You may need the help of your physican.

Kim Pulsipher/Dr. Dan

Emergency Kit

Contact list: Primary and secondary.

Charged cell phone, all the time.

Directions for how to help. Print out info at

Medic alert bracelet or pendant. See what others have on theirs here.

Always carry a medical identification card that states the type of medication and the proper dose needed in case of an emergency.

Never omit medication. If unable to retain medication due to vomiting, notify the health care provider.

If there are places that you go often, be sure that those people know that you may have a problem. For a child, inform all of his/her teachers and other staff.


Body and Skin

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Brown Spots

I have quite a few brown "age spots" on my face,  I accidentally discovered a way to camouflage them when I got a sample of Vaseline Healthy Body Glow. It "tans" your skin. In my case it made the skin dark enough to match the brown spots so they don't show up as much.

I've noticed that there are now lots of similar products on the market and I'm sure that they will all work as well.

~ MaryO


Bones and Muscles

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Water aerobics for people with arthritis is really helping. I do that twice a week.

~ MaryO


Since I can't take my arthritis meds anymore, I've gone back on a combo pill of glucosamine/chondroitin. This only works for osteoarthritis, so if you have any rheumatoid, it won't work at all.

I was interested to see that The National Institutes of Health (NIH) is currently running a study of Glucosamine and Chondroitin Sulfate and Dr. Jason Theodosakis is heading this up.

There's more info on "Dr Theo" on Power Surge.

Dr Theo outlined the complete plan in his Power Surge transcripts, saying that it wasn't enough just to take the pills.

His plan is:

  1. Have a thorough consultation with a physician.

  2. Take glucosamine and chondroitin sulfates to repair damaged joints.

  3. Improve your biomechanics to counteract stress to your joints.

  4. Exercise regularly. (But the right kinds!)

  5. Eat a healthful, joint-preserving diet

  6. Maintain your ideal body weight.

  7. Fight depression.

  8. Use traditional medicine as necessary.

  9. Maintain a positive attitude.

~ MaryO


Question: Will the glucosamine/chondroitin that supposedly helps arthritis help with the pain and stiffness of steroid withdrawal? Is there any harm in trying it?

Answer: Glucosamine and chondroitin are chemical components of cartilage, tendons, ligaments, and other connective tissues that form the joints and muscle attachments. Some people with arthritic joint pain appear to benefit from taking these chemicals as dietary supplements (supplements because they are in a normal diet that contains meat). I am unaware of any report of their effect on the musculoskeletal symptoms of steroid withdrawal. However, I see no reason to anticipate any more risk for their use in this setting than in any other.

~ David Orth MD


Top 10 healthiest foods for spring

  1. Asparagus. Rich in vitamins A and C, calcium, iron and folate (the world's most common vitamin deficiency), asparagus has been prized for its culinary and medicinal purposes since ancient times.

  2. Green beans. Harvested while still immature when the inner bean is just beginning to form, they are one of the few bean varieties that can be eaten fresh..

  3. Spring Chinook salmon. The health benefits of eating fatty, cold-water fish are widely known, but salmon contains the highest volume of omega-3 fatty acids, essential for maintaining good heart health.

  4. Spinach. A Mediterranean favorite since the 16th century, spinach is a rich source of vitamin A (for cardiovascular health) and vitamin K (for bone health).

  5. Apricots. The true fruits of spring, apricots were first discovered in China and have been cultivated for more than 3,000 to 4,000 years. They are also rich with beta-carotene and lycopene, two carotenoids important in reducing the artery-clogging LDL cholesterol and maintain a healthy heart.

  6. Spring onions. Onions have been the subject of new research linking them to lower incidence of certain cancers. They also provide vitamins A and C, calcium and iron.

  7. Green peas. Green peas are a rich source of folate and a wide range of B vitamins, essential for the proper metabolism of fats, proteins and carbohydrates.

  8. Basil. A popular herb that can enhance the flavors of your favorite pasta sauce or spring salad, basil is a wonderful source of vitamin A.

  9. Avocados. Previously avoided by dieters due to their high fat content, avocados have made a comeback as a great source of heart-healthy monounsaturated fats to help lower cholesterol. By volume, avocados are also 50 percent higher in potassium than bananas.

  10. Spring greens. Choose from arugula, romaine, mesclun, bok choy and watercress to mustard, collard and dandelion greens. All are rich in lutein, beta-carotene, vitamin C, folate, minerals and fiber and excellent for digestion.



Nutrition for Patients with Cushing Syndrome (National Institutes of Health, Clinical Center) - PDF File

~ NIH, National Institutes of Health, Clinical Center

Diet / Exercise

Question: While my cortisol levels are still high, is there anything I can do with my diet or exercise to keep my weight from increasing and loosing more strength? Is protein intake important?

Answer: With excessive cortisol levels, diet and exercise are important to keep from gaining weight and losing more muscle strength. A nutritious diet with a multivitamin supplement is recommended, usually the diet should not exceed 1000 to 1200 calories per day. It is important that the balanced diet contain adequate protein, however excessive protein intake probably will not make much difference in muscle strength since excessive cortisol causes protein (muscle) breakdown. Since patients are usually treated soon after diagnosis, no studies have evaluated the effect of a high protein diet.

Regarding exercise, the best type of exercise is that which is not stressful to the skeletal system. For example, swimming and bicycle riding are good exercises. Jogging and lifting weights are probably not a good idea since this does place stress on the skeleton (bones). Additionally, a calcium supplement is important. The recommended amount of approximately 1500 mg of elemental calcium per day can be achieved by taking 4 Tums Ultra or 3 tablets OsCal 500.

~ Mary Lee Vance MD


I choose to just eat salt like it's a candy. I have a little container of plain sea salt (you don't want the iodized stuff) and I lick my finger and just dip it! Gross I know... but it's cured many a headache. My sodium remains low... but it never ceases to amaze me how salt will taste good, and then just stop tasting good. That's how i know I've had enough.

~ ADDflower


Question: My Cushing's has been cured for about 3 years, but my muscle strength is still not like it used to be. I work out at a gym regularly, but is there anything else that I can do to try and recover my strength?

Answer: Deterioration of muscle function is a common consequence of Cushing's syndrome. The majority of patients recover full muscle strength and performance after cure of their Cushing's syndrome. Physical therapy and a high protein diet have both been shown to improve muscle strength in patients with steroid-induced muscle damage. After cure, most patients recover normal muscle strength within 1-2 years.

~ James Findling MD

Muscle fatigue and weakness

From the message boards

Question: A really big problem for me (and seems like a lot of people) is the muscle weakness and fatigue. Does anyone have any tricks that work for them?

Answer: One thing that has helped me is eating more salt. Of course if your blood pressure is really high already, you shouldn't do this. But mine runs pretty low and I have a hard time keeping my liquids....I am in the bathroom constantly. This is something Dr. F recommended after finding that I have low aldosterone and renin. Also, I am taking vitamins and iron. It seems to help sometimes and sometimes I am as fatigued as can be, but I figure it can't hurt. Hope this helps!

~ Mertie

Answer: If you are cyclical, it is SUPER important to chart. Part of the problem is that for some folks a Low symptom is another person's High. After awhile you should be able to see a pattern showing itself.

And yes, when I'm low like that, I did eat salt out of the shaker (I even have 5 different flavored salts, I know, i'm a whacko!)

But when I'm in a Low, I haven't found a way to pop out of it, or force a High. It's something I'm working on though.

....If I eat lots of pasta or bread, I have lots of muscle aches and pains. A big bowl of mac'n'cheese will make me feel like I'm having a fibro flair most days

~ vinesqueen

Answer: You're right. I choose to just eat salt like it's a candy. I have a little container of plain sea salt (you don't want the iodized stuff) and I lick my finger and just dip it! Gross I know... but it's cured many a headache. My sodium remains low... but it never ceases to amaze me how salt will taste good, and then just stop tasting good. That's how i know I've had enough.

~ ADDflower

Answer: One thing to try to find is Sea Salt to replace your normal salt with in the house. It is better for you than regular table salt.

I crave salt and sugar. I can't get enough of either one.

I need to pick up some DHEA and try it out, it is a precursor hormone and I hear people say it help them feel better.

I can't seem to find any way to feel better lately, so I am working on a strategy also. I'm back to taking Flintstones vitamins with Iron and an extra Vitamin B6 also.

~ LisaMK

Add your suggestion on the message boards


Question: I have osteoporosis due to Cushing's. Will this improve over time?

Answer: A recent study has shown substantial improvements in bone density within several years after the successful cure of patients with pituitary Cushing's. Bones have the best possible chance for recovery when the replacement steroid dosage is as low as possible. If you are on replacement therapy following surgery, you should be working with your doctor to taper the steroid dose at a rapid , but tolerable rate.

Bones can also benefit from a healthy diet and intake of at least 1 gram of calcium per day. Exercise has also been shown to be beneficial, but is best started under the supervision of a physician. Most patients with osteoporosis can undertake exercise such as walking or swimming without risk of injury. Exercise that is weight bearing, such as weight lifting, or exercise that involves a risk of falling, such as skiing, would not be advisable unless under the direction of a physician or physical therapist.

~ David Orth MD


Question: Following surgery for Cushing's, I have had a lot of swelling in my hands, feet and face. Is there anything that can be done to help this problem and is it anything to be concerned about?

Answer: Swelling, or edema, may often accompany Cushing's syndrome. Following surgical treatment of Cushing's, some patients will continue to experience edema for some time following the surgery. This may be related to the frequent need for steroid therapy following curative surgery. This is really nothing serious, but can be uncomfortable. I usually treat patients with a water pill or decrease the dose of steroids.

~ James Findling MD


Eyes, Ears, Nose,
Sinus, Throat

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Heart and blood

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Sleep and Fatigue

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For insomnia try Bach Rescue Sleep. Two sprays on the tongue really seem to help. It is available in most health type stores and markets.



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Read ~ Susan's bio


What pointed me in the cushing's disease direction were the symptoms such as buffalo hump; hair growth on specific areas; weight gain around my neck, face, abdomen, chest and back; my pituitary adenoma and the last results from my test that showed high levels of cortisol.

Read ~ Gina's bio


Get a copy of ALL your lab test results and copies of imaging reports and the actual images....on CD and films.

Read ~ Gina's bio


It is absolutely critical for your physical and emotional health for you to have a doctor with expertise and experience with Cushing's! Inexperienced doctors all too often misdiagnose, insult and frustrate, preventing prompt and proper diagnosis. Misdiagnosis can be lethal!

Obviously, it is also crucial for you to have a surgeon with experience in order to minimize the likelihood of errors that can lead to complications or death. Wouldn't you prefer someone who performs the surgery 5 days per week over someone who may have done it a total of 5 times in his or her career?

On the other hand, doctors with experience are most likely to be more thorough and precise in recommending and offering the proper tests and treatments, and more aware of the subtle nuances and possible complications of the syndrome, learning from each Cushing's patient s/he treats, to the benefit of others.

Investigate your insurance, and if necessary (and possible), change your coverage in order to be able to afford to go to doctors who are Cushing's experts. Because Cushing's is often caused by a tumor, some insurance (including United Health Care) covers Cushing's related medical expenses including travel to facilities they consider "cancer centers for excellence" if you need to travel over 100 miles to these experts. United Health Care covers medical expenses with no co-pay, including travel, lodging and meals for myself and a travel companion so that I am able to afford the best medical care possible from doctors who are experienced with Cushing's.

~ Judi


The most important advice I have to give is this:


2) If you have kids, think twice before eating disorder treatment. I went into the program with pain and a method of coping. I came out with an eating disorder psyche, bad experiences, and a truckload of pills that were making me crazy.


• the cortisol goes up with too much of any protein, fat or carbs. I eat small turkey/cheese sandwiches at every meal (enough to be full, but well balanced).

• I use stevia instead of sugar because its natural (health food aisle.)

• alcohol really hurts now, so only a little wine occassionally.

• lots of yogurts.

• every couple days a mixture of senna laxative and stool softener (not too often)

4) Remember the squeekiest wheel gets the grease.

~ Magdalena's bio



On the Message Boards

Sex Drive

Question: Since having Cushing's, my sex drive is next to nothing. Is this common, will this problem remain forever or get better? Is there anything that can help?

Answer: A decrease in libido or sex drive is common in patients with Cushing's. Several factors influence a person's sex drive.

In women, regular menstrual periods or adequate estrogen and progesterone replacement is important.

In men, if the testosterone level is low, this indicates the need for testosterone replacement. In pituitary dependent Cushing's, once the normal pituitary gland has recovered, the adrenal glands should be producing an adequate amount of both cortisol and male hormones (important in women for sex drive).

If a woman has had 1 adrenal gland removed, the other adrenal should make an adequate amount of male hormones once the entire pituitary adrenal axis has recovered (this may take several months as well). In the situation of bilateral adrenalectomy, there is loss of adrenal male hormone production. If the ovaries are functioning normally, male hormones are also produced and this should provide an adequate amount for normal libido.

If a woman does not have normal menstrual function and requires estrogen and progesterone replacement, sometimes a small dose of testosterone is added to improve libido. A common preparation is Estratest.

~ Mary Lee Vance MD



On the Message Boards

Sex Drive

Question: Since having Cushing's, my sex drive is next to nothing. Is this common, will this problem remain forever or get better? Is there anything that can help?

Answer: A decrease in libido or sex drive is common in patients with Cushing's. Several factors influence a person's sex drive.

In women, regular menstrual periods or adequate estrogen and progesterone replacement is important.

In men, if the testosterone level is low, this indicates the need for testosterone replacement. In pituitary dependent Cushing's, once the normal pituitary gland has recovered, the adrenal glands should be producing an adequate amount of both cortisol and male hormones (important in women for sex drive).

If a woman has had 1 adrenal gland removed, the other adrenal should make an adequate amount of male hormones once the entire pituitary adrenal axis has recovered (this may take several months as well). In the situation of bilateral adrenalectomy, there is loss of adrenal male hormone production. If the ovaries are functioning normally, male hormones are also produced and this should provide an adequate amount for normal libido.

If a woman does not have normal menstrual function and requires estrogen and progesterone replacement, sometimes a small dose of testosterone is added to improve libido. A common preparation is Estratest.

~ Mary Lee Vance MD



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Help Yourself