Adrenal atrophy laboratory findings

Jump to navigation Jump to search

Adrenal atrophy Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Adrenal atrophy from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Adrenal atrophy laboratory findings On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Adrenal atrophy laboratory findings

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Adrenal atrophy laboratory findings

CDC on Adrenal atrophy laboratory findings

Adrenal atrophy laboratory findings in the news

Blogs on Adrenal atrophy laboratory findings

Directions to Hospitals Treating Adrenal atrophy

Risk calculators and risk factors for Adrenal atrophy laboratory findings

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2]

Overview

The labs include random cortisol, serum ACTH, aldosterone and renin, potassium and sodium, ACTH stimulation test and CRH stimulation test.

Laboratory findings

The labs to be run should include:

In the first line, the serum cortisol level is expected to be from 10 to 20 mcg/dL (275 to 555 nmol/L) in the morning (6 AM) and the morning cortisol levels, lower than 3 mcg/dL (80 nmol/L) are highly suggestive for a form of adrenal insufficiency, including adrenal atrophy. On the other hand, the salivary cortisol concentration above 5.8 ng/mL (16 nmol/L) excludes adrenal insufficiencies, and concentrations below 1.8 ng/mL (5 nmol/L) is highly suggestive for adrenal atrophy or other forms of adrenal insufficiency. However, in order to check the functionality of the Hypothalamic Pituitary Adrenal Axis the entire axis must be tested by ACTH stimulation test and CRH stimulation test. In primary adrenal insufficiency, the 8 AM plasma ACTH concentration is high, sometimes as high as or higher than 4000 pg/mL (880 pmol/L). The mineralocorticoids, including aldosterone level are low in adrenal atrophy but the renin level are usually higher than the normal range, due to the absence of negative feedback. As a result, low sodium and high potassium levels may occur in patients. Potassium levels higher than 5.5 to 6.5 mmol/L may yield to cardiac arrhythmia or arrest. The ACTH stimulation test consists of injecting a small amount of synthetic ACTH, and the amount of [[cortisol] (and sometimes aldosterone) that the adrenals produce in response is then measured. A normal response to the high-dose (250 mcg as an intravenous [IV] bolus) ACTH stimulation test is a rise in serum cortisol concentration after either 30 or 60 minutes to a peak of ≥18 to 20 mcg/dL (500 to 550 nmol/L). The low-dose (1 mcg as an IV bolus) ACTH stimulation test criteria for a normal cortisol response after 20 or 30 minutes are more variable: 17 to 22.5 mcg/dL (400 to 620 nmol/L). Normal response strongly rules out adrenal atrophy and other forms of secondary adrenal insufficiency should be considered.[1][2]

References

  1. Abdu TA, Elhadd TA, Neary R, Clayton RN (March 1999). "Comparison of the low dose short synacthen test (1 microg), the conventional dose short synacthen test (250 microg), and the insulin tolerance test for assessment of the hypothalamo-pituitary-adrenal axis in patients with pituitary disease". J Clin Endocrinol Metab. 84 (3): 838–43. doi:10.1210/jcem.84.3.5535. PMID 10084558.
  2. Husebye ES, Perheentupa J, Rautemaa R, Kämpe O (May 2009). "Clinical manifestations and management of patients with autoimmune polyendocrine syndrome type I". J Intern Med. 265 (5): 514–29. doi:10.1111/j.1365-2796.2009.02090.x. PMID 19382991.

Template:WH Template:WS