Webinar: Diagnosis and Management of Acromegaly: A Clinical Update

Posted on July 19, 2015 by MaryO

Presented by
Lisa Nachtigall, MD
Co-director Neuroendocrine Clinical Center
Massachusetts General Hospital

Register Here

After registering you will receive a confirmation email with details about joining the webinar.

Contact us at webinar@pituitary.org with any questions or suggestions.

Date: Monday, July 27, 2015
Time: 2:00 PM – 3:00 PM Pacific Daylight Time

Presenter Bio
Lisa B. Nachtigall, MD, is an Associate Professor of Medicine at Harvard Medical School, the clinical co-director of the Neuroendocrine Clinical Center at Massachusetts General Hospital and course director in Clinical Neuroendocrine at Harvard Medical School.

Dr. Nachtigall earned her medical degree from New York University (NYU) School of Medicine in New York City. She completed her internship and residency in internal medicine at Bellevue Hospital Center/NYU school of Medicine, and a clinical fellowship in endocrinology and metabolism, as well as a research fellowship in reproductive endocrinology at Massachusetts General Hospital/Harvard Medical School.

Dr. Nachtigall’s work has been published in the New England Journal of Medicine, the Journal of Clinical Endocrinology and Metabolism, Neurosurgery, Pituitary, and the Clinical Endocrinology among others. She serves on the editorial board of Pituitary and as an ad hoc reviewer for many endocrine journals. Dr Nachtigall has been a presenter at national and international medical conferences, and she is currently an investigator on several clinical studies of acromegaly and pituitary tumors.

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7 health conditions that are responsible for making you fat

Posted on July 18, 2015 by MaryO

Cushing’s syndrome: Cushing’s syndrome or hypercortisolism is a condition caused when the adrenal glands produce too much cortisol. This leads to a buildup of fat in the face, upper back and abdomen. Cushing’s syndrome can also be a side-effect of certain medications.

Read the other 6 at 7 health conditions that are responsible for making you fat | Read Health Articles & Blogs at TheHealthSite.com.

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Lowest cortisol levels found in women with overweight, mild obesity

Posted on July 18, 2015 by MaryO

Women with overweight and class I obesity appear to have the lowest cortisol levels, while more significant obesity appears to be associated with higher cortisol levels, according to recent findings.

In the cross-sectional study, Karen K. Miller, MD, of Massachusetts General Hospital, and colleagues evaluated 60 premenopausal women aged 18 to 45 years: 28 with overweight or obesity, 18 with anorexia nervosa and 21 healthy controls at normal weight. Overweight was defined as BMI 25 to 29.9 kg/m2, and obesity was classified as class I (30-34.9 kg/m2) and class II (35-39 kg/m2).

Anorexia nervosa was classified based on DSM-IV criteria, which includes extreme fear of weight gain, body image dysmorphia, weight that is 85% of ideal body weight and cessation of menstruation for 3 consecutive months. Participants were asked to collect 24-hour urine samples, in addition to 11 p.m. and 7 a.m. salivary samples within 1 week of an inpatient hospital visit. For each sample, researchers assessed creatinine clearance, and urinary free cortisol/creatinine clearance was calculated for each specimen to account for the decreased creatinine and filtered cortisol linked to anorexia nervosa.

During the inpatient visit, participants underwent placement of an IV catheter and fasting blood was sampled every 20 minutes from 8 p.m. to 8 a.m. Fasting cortisol and cortisol binding globulin concentrations were measured at 8 a.m. Participants were asked to take 5 g of oral dexamethasone every 6 hours for 48 hours to decrease endogenous disparities in cortisol levels.

The researchers found that with the exception of dexamethasone-suppression-CRH testing, all cortisol measures exhibited a U-shaped association with BMI, most notably urinary free cortisol/creatinine clearance (P = .0004) and mean overnight serum cortisol (P < .0001).

The lowest cortisol levels were seen in the overweight-class I obesity range, and these were also associated with visceral fat tissue and total fat mass. Participants with anorexia nervosa had higher mean cortisol levels than participants with overweight or obesity. Attenuated inverse relationships were seen between lean mass and some measures of cortisol, and most measures of cortisol were inversely related to posterior-anterior spine and total hip bone mineral density.

According to the researchers, these findings have not determined the precise nature of the relationship between cortisolemia, hypothalamic-pituitary-adrenal activation and adiposity.

“The [hypothalamic-pituitary-adrenal] axis activation associated with obesity and excess adiposity raises the question of whether hypercortisolemia contributes to increased adiposity in the setting of caloric excess, whether increased adiposity drives [hypothalamic-pituitary adrenal] activation, or whether the relationship between hypercortisolemia and adiposity is bidirectional,” the researchers wrote. – by Jennifer Byrne

Disclosure: The researchers report no relevant financial disclosures.

From http://www.healio.com/endocrinology/obesity/news/online/%7B73cac1c4-af30-4f24-89e3-86f50d05aaa2%7D/lowest-cortisol-levels-found-in-women-with-overweight-mild-obesity

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Food-dependent Cushing syndrome: a new entity of organic hypercorticism

Posted on July 9, 2015 by MaryO
Matejka G, et al. Rev Med Interne. 1996.

Abstract

Diagnosis of Cushing’s syndrome is quite difficult in endocrinology. Spontaneous Cushing’s syndrome is usually divided into two subgroups, one which is dependent on corticotropin (ACTH) and another one which is not.

In the first class are Cushing’s disease, the ectopic corticotropin syndrome and the rare ectopic corticotropin-releasing hormone (CRH) syndrome; these ACTH-dependent Cushing’s syndrome have usually diffusely enlarged adrenal glands.

In the second class are cortisol producing unilateral adrenocortical adenomas or carcinomas, and the recent Cushing’s syndrome with food dependent periodic hormonogenesis.

This food dependent Cushing’s syndrome is an ACTH-independent Cushing’s syndrome with multinodular enlargement of both adrenal glands. Pathogenesis is an aberrant adrenal sensitivity to physiologic secretion of gastric inhibitory peptide (GIP). Ectopic expression of GIP receptors on adrenal cells involve pathologic food induced cortisol secretion.

Food dependent Cushing’s syndrome is a new cause of Cushing’s syndrome. Food induced cortisol secretion may have to be explored in the ACTH-independent Cushing’s syndrome.

PMID

8758532 [PubMed – indexed for MEDLINE]

Full text

Full text from provider (Elsevier Science) Article in French.

From http://www.ncbi.nlm.nih.gov/m/pubmed/8758532/

Biography of a Food-Dependent Cushing’s patient

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The low-dose dexamethasone suppression test: a reevaluation in patients with Cushing’s syndrome

Posted on July 9, 2015 by MaryO

J Clin Endocrinol Metab. 2004 Mar;89(3):1222-6.

Findling JW1, Raff H, Aron DC.

Abstract

Low-dose dexamethasone suppression testing has been recommended for biochemical screening when Cushing’s syndrome is suspected. The criterion for normal suppression of cortisol after dexamethasone is controversial.

To assess diagnostic utility (sensitivity), we report the results of low-dose dexamethasone suppression testing in 103 patients with spontaneous Cushing’s syndrome. There were 80 patients with Cushing’s disease (78%), 13 with the ectopic ACTH syndrome (13%), and 10 with cortisol-producing adrenocortical adenomas (10%). Fourteen (18%) of 80 patients with Cushing’s disease suppressed serum cortisol to less than 5 micro g/dl (<135 nmol/liter) after the overnight 1-mg test, whereas six patients (8%) actually showed suppression of serum cortisol to less than 2 micro g/dl (<54 nmol/liter). In addition, the 2-d, low-dose dexamethasone suppression test yielded false-negative results in 38% of patients when urine cortisol was used and 28% when urinary 17-hydroxycorticosteroids were used. Serum cortisol after the 1-mg test correlated with baseline urinary free cortisol (r = 0.705, P < 0.001), plasma ACTH level (r = 0.322, P = 0.001), and urinary free cortisol after the 2-d test (r = 0.709, P = 0.001).

This study provides evidence that low-dose dexamethasone may suppress either plasma cortisol or urinary steroids to levels previously thought to exclude Cushing’s syndrome and that these tests should not be used as the sole criterion to exclude the diagnosis of endogenous hypercortisolism.

PMID:
15001614
[PubMed – indexed for MEDLINE]

From http://www.ncbi.nlm.nih.gov/pubmed/15001614

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