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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Moderately impaired renal function increases morning cortisol and cortisol levels at dexamethasone suppression test in patients with incidentally detected adrenal adenomas

Posted on June 26, 2015 by MaryO
Clin Endocrinol (Oxf). 2015 May 23. doi: 10.1111/cen.12823. [Epub ahead of print]
Olsen H1, Mjöman M2.

Author information

Abstract

OBJECTIVE:

Patients with incidentally detected adrenal adenomas may have subclinical hypercortisolism. We hypothesized that impaired renal function could lead to increased cortisol levels in these patients.

DESIGN:

Descriptive retrospective study of consecutive patients.

PATIENTS:

A total of 166 patients with incidentally detected unilateral adrenal adenomas were examined during 2008-2013.

MEASUREMENTS:

Levels of cortisol, ACTH and cortisol at 1 mg overnight dexamethasone suppression test (DST) were measured. The estimated glomerular filtration rate (eGFR) was calculated using the MDRD equation.

RESULTS:

Renal function was normal, mildly impaired, moderately impaired or severely impaired (eGFR >90, 60-90, 30-60 and 15-30 ml/min/1·73 m2 ) in 34, 54, 10 and 1% of the patients, respectively. Patients with normal and mildly impaired renal function had similar cortisol levels. Patients with moderately impaired renal function, compared to all the patients with eGFR >60 ml/min/1·73 m2 , exhibited increased cortisol (541 vs 456 nmol/l, P = 0·02), increased cortisol at DST (62 vs 37 nmol/l, P = 0·001), but similar ACTH levels (4·1 vs 2·9 pmol/l, P = 0·21). Patients with moderately impaired renal function thus exhibited cortisol at DST ≥50 nmol/l, more often than patients with eGFR >60 ml/min/1·73 m2 (76% vs 30%, P = 0·000), while the prevalence of ACTH below 2 pmol/l was similar (24% vs 31%, P = 0·51).

CONCLUSIONS:

Moderately impaired renal function increases cortisol and cortisol at DST in patients with adrenal adenomas, while mildly impaired renal function has no such effect. Cortisol level at DST ≥50 nmol/l therefore seems to have low specificity in diagnosing subclinical adrenal hypercortisolism, and an additional criterion, for example low ACTH, is required.

© 2015 John Wiley & Sons Ltd.

PMID:
26010731
[PubMed – as supplied by publisher]

From http://www.ncbi.nlm.nih.gov/pubmed/26010731

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Multiple aberrant hormone receptors in Cushing’s Syndrome

Posted on June 26, 2015 by MaryO
Eur J Endocrinol. 2015 May 13. pii: EJE-15-0200. [Epub ahead of print]
Multiple Aberrant Hormone Receptors in Cushing’s Syndrome.
El Ghorayeb N1, Bourdeau I2, Lacroix A3.

Author information

Abstract

The mechanisms regulating cortisol production when ACTH of pituitary origin is suppressed in primary adrenal causes of Cushing’s syndrome include diverse genetic and molecular mechanisms. These can lead either to constitutive activation of the cAMP system and steroidogenesis or to its regulation exerted by the aberrant adrenal expression of several hormone receptors, particularly G-protein coupled hormone receptors (GPCR) and their ligands.

Screening for aberrant expression of GPCR in BMAH and unilateral adrenal tumors of patients with overt or subclinical CS demonstrates the frequent co-expression of several receptors. Aberrant hormone receptors can also exert their activity by regulating the paracrine secretion of ACTH or other ligands for those receptors in BMAH or unilateral tumors.

The aberrant expression of hormone receptors is not limited to adrenal Cushing’s syndrome but can be implicated in other endocrine tumors including primary aldosteronism and Cushing’s disease. Targeted therapies to block the aberrant receptors or their ligands could become useful in the future.

PMID:
25971648
[PubMed – as supplied by publisher]

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California Doctors – So far

Posted on June 19, 2015 by MaryO

california

 

The doctors listed here have been recommended to Cushing’s Help by other patients as being helpful to them.  These physicians are familiar with the symptoms and treatment of Cushing’s Disease (pituitary) and Cushing’s Syndrome. Your primary care physician may be able to order very basic screening tests. Some of these doctors may require a referral and/or an abnormal test result prior to scheduling an appointment.

Cushing’s Help does not endorse any particular physician. Choosing a particular physician and substantiating his/her expertise is the responsibility of the individual patient.

To recommend your own doctor for this list, please fill out this form.

This list is a continuing resource as new doctors are added, edited OR removed.  

These doctors are also available on this map.  Please add yourself and/or your doctor

California

Beverly Hills

Cohan, Pejman 

Specialty: Neuroendocrine 

Location: 150 N Robertson Blvd # 210
Beverly Hills, CA

Phone: 310-657-3030

Patient Comment: He’s been my Endo for 15 years. Only sees neuroendocrine patients

Freemont

Kunwar, Sandeep

Specialty: Neurosurgeon

Hospital: Washington Hospital

Location: Freemont, CA

Hospital: UCSF

Location: San Francisco, CA

Website: http://www.ucsfhealth.org/sandeep.kunwar

Patient Comments: And dr kunwar at ucsf was my very skilled surgeon. I didn’t have to see his endo preop

I also had my surgery done with Dr. Kunwar at Washington Hospital in Fremont (East Bay). He does a few days a week in Fremont and the rest in SF. This is my third recurrence and I would definitely recommend him

Srinivasan, Lakshmi

Specialty: Endocrinologist

Hospital: Palo Alto Medical Foundation

Location: Freemont, CA

Patient Comments: My endo is Dr. Lakshmi Srinivasan at Palo Alto Medical Foundation in Fremont. She is fantastic–takes a lot of time during every appt and is very attentive and responsive to email and calls.

Los Angeles

Friedman, Theodore

Specialty: Cushing’s, Growth Hormone Deficient, Hypopituitary, adrenal, thyroid, fatigue

Address: 1125 S. Beverly Drive. Suite 730

Location: Los Angeles, CA

Hospital: Charles Drew

Website: http://goodhormonehealth.com

Patient Comments:  I am a Dr Friedman patient, he is wonderful.

 Orange

Linskey, Mark 

Specialty: Neurosurgeon 

Hospital: UCI

Location: Orange, CA

Website: http://www.ucirvinehealth.org/find-a-doctor/l/mark-linskey/

Patient Comment: The pit surgery was done by both Linskey and Bhendarkar and I am doing well post op, they are very diligent in their care. If I have to have another surgery for Cushing’s I will definitely use this team again.

Bhandarkar, Naveem

Specialty: ENT

Hospital: UCI

Location: Orange/Irving, CA

Website: http://www.ent.uci.edu/faculty/naveen-d-bhandarkar-md

Patient Comment: The pit surgery was done by both Linskey and Bhendarkar and I am doing well post op, they are very diligent in their care. If I have to have another surgery for Cushing’s I will definitely use this team again.

San Francisco

Kunwar, Sandeep

Specialty: Neurosurgeon

Hospital: Washington Hospital

Location: Freemont, CA

Hospital: UCSF

Location: San Francisco, CA

Website: http://www.ucsfhealth.org/sandeep.kunwar

Patient Comments: And dr kunwar at ucsf was my very skilled surgeon. I didn’t have to see his endo preop

I also had my surgery done with Dr. Kunwar at Washington Hospital in Fremont (East Bay). He does a few days a week in Fremont and the rest in SF. This is my third recurrence and I would definitely recommend him

More coming soon!

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“My feet are killing me!” An unusual presentation of Cushing’s syndrome

Posted on June 19, 2015 by MaryO

Adverse effects of steroid excess on bone metabolism are well established but presentation of Cushing’s syndrome with metabolic bone disease is reported to be uncommon. We describe a case of Cushing’s syndrome presenting with pathological fractures probably present for 8 years before diagnosis.

A 33 year old nurse first sustained spontaneous stress fractures of her metatarsals in 1994, with repeated fractures occurring up to 2002. In 2001 she developed hypertension, acute lumbar back pain and gained weight.

In 2002 she was admitted to hospital with chest/back pain. Lumbar spine X-ray showed new fracture of L3,old fractures of L4/5,with fractured ribs on CXR. Isotope bone scan revealed multiple hot spots. MRI showed collapse of T8 with features consistent with malignant disease. The primary malignancy was sought and a left-sided 1.5 centimetre thyroid nodule detected.

Suspicious cytology prompted thyroid lobectomy revealing follicular variant of papillary carcinoma. T8 biopsy revealed chronic infection with Propionobacteria rather than metastatic carcinoma. Despite antibiotic therapy further spontaneous vertebral fractures developed. Bone densitometry revealed Z scores of minus 2.4 at L2-4, minus 2.5 and 2.9 at the hips.

Referral to our centre prompted investigations for Cushing’s syndrome. Serum potassium was 4.1 millimols per litre, androgens, calcitonin and urinary catecholamines all normal. TSH was suppressed by T4 therapy. Urinary free cortisol values were raised,(563-959 nanomols per 24hours) with loss of diurnal rhythm in cortisol secretion (9am 429-586,midnight 397-431 nanomols per litre)and no suppression on low or high dose dexamethasone. Abdominal CT showed a 3.5 centimetre adrenal mass. These findings were consistent with adrenal dependent Cushing’s syndrome. Risedronate and metyrapone were commenced before adrenalectomy, completion thyroidectomy and ablative radioiodine.
Comment: Cushing’s syndrome may present with spontaneous fractures in both axial and appendicular skeleton in the absence of marked clinical features. This case demonstrates the importance of thorough investigation of unexplained fractures.

LM Albon, JD Rippin & JA Franklyn

From http://www.endocrine-abstracts.org/ea/0005/ea0005p26.htm

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