Cortisol

Methodology: 
Electrochemiluminescence immunoassay (ECLIA)
Use: 
This test is used to establish the diagnosis of:
  • Adrenocortical insufficiency
  • Addison's disease
  • Adrenocortical hypersecretion
  • Cushing's syndrome
Malfunction of the organs in the hypothalamic-pituitary-adrenal cortex axis will result in alteration of the cortisol levels.
Specimen Requirements: 

Type: Serum

Container/Tube: Red-top tube or gel-barrier tube
  • If a red-top tube is used, transfer the separated serum to a plastic transport tube. Blood should be drawn between 8 a.m. and and 4 p.m.to evaluate baseline diurnal variation.

Sample Volume: 0.8 mL

Minimum Volume: 0.3 mL (Repeat testing is not possible with this specimen volume.)

Storage: Refrigerate specimens after collection.

Stability (collection to time of analysis/testing): 
  • Ambient: 14 days
  • Refrigerated: 14 days
  • Frozen: 14 days
  • Freeze/Thaw cycles: Stable (x3)
Rejection Criteria:
  • Citrate plasma specimen
  • Improper labeling
Reference Values: 

Reference Intervals

  • 2.3 - 19.4 μg/dL
    • A.M.: 6.2 - 19.4 μg/dL
       
    • P.M.: 2.3 - 11.9 μg/dL
CPT Code (s): 
82533 (per specimen)
Notes: 

UFHPL Test #: 28045

UFHPL Epic order code: LAB61

Cortisol (hydrocortisone) is the most prominent glucocorticosteroid, and it is essential for the maintenance of several body functions. Like other glucocorticosteroids, cortisol is synthesized from the common precursor cholesterol in the zona fasciculata of the cortex of the adrenal gland. For the transport of cortisol in blood, about 90% of cortisol is bound to corticosteroid-binding globulin (CBG) and to albumin. Only a small amount of cortisol circulates unbound in blood and is free to interact with its receptors.3

The most important physiological effects of cortisol are the increase of blood glucose levels (enhancement of gluconeogenesis, catabolic action) and its anti-inflammatory and immunosuppressive action.3

Synthesis and secretion of cortisol by the adrenal gland are controlled by a negative feedback mechanism within the hypothalamus-pituitary-adrenal cortex-axis. If the cortisol level is low, corticotropin-releasing hormone (CRH) is secreted by the hypothalamus, which causes the pituitary to release adrenocorticotropic hormone (ACTH). This stimulates the synthesis and secretion of cortisol by the adrenal gland. Cortisol itself acts in a negative feedback mechanism on the pituitary gland and the hypothalamus. In addition, stress is followed by increased cortisol secretion.3

Serum cortisol concentrations normally show a diurnal variation.3 Maximum concentrations are usually reached early in the morning and then concentrations decline throughout the day to an evening level that is about half of the morning concentration; therefore, for interpretation of results, it is important to know the collection time of the serum sample.

The cortisol status of a patient is used to diagnose the function or malfunction of the adrenal gland, the pituitary, and the hypothalamus.4,5 Thereby, cortisol serum concentrations are used for monitoring several diseases with an overproduction (eg, Cushing syndrome)6,7 or underproduction (eg, Addison disease) of cortisol and for monitoring several therapeutic approaches (eg, dexamethasone suppression therapy in Cushing syndrome and hormone replacement therapy in Addison disease).

Footnotes

  1. Cortisol (Serum) on Elecsys 1010/2010 and Modular Analytics E170. Package insert 2005-02, V 10. Indianapolis, Ind: Roche Diagnostics; 2005.
  2. Miyachi Y. Pathophysiology and diagnosis of Cushing'ssyndrome. Biomed Pharmacother. 2000 Jun; 54(Suppl 1):S113-117. PubMed 10915006
  3. Aron DC, Tyrell JB. Glucocorticoids and adrenal androgens. In: Greenspan FS, Baxter JD, eds. Basic and Clinical Endocrinology. 4th ed. Norwalk, Conn: Appleton and Lange;1994:307-346.
  4. Hasinski S. Assessment of adrenal glucocortoid function. Which tests are appropriate for screening? Postgrad Med. 1998 Jul; 104(1):69-72. PubMed 9676562
  5. Rosalki SB. Biochemical testing of adrenocortical function. Int J Clin Pract. 1998 Apr-May; 52(3):189-191. PubMed 9684436
  6. Newell-Price J, Trainer P, Besser M, Grossman A. The diagnosis and differential diagnosis of Cushing's syndrome and pseudo-Cushing's states. Endocr Rev. 1998 Oct; 19(5):647-672. PubMed 9793762
  7. Ross RJ, Trainer PJ. Endocrine investigation: Cushing's syndrome. Clin Endocrol (Oxf). 1998 Aug; 49(2):153-5. PubMed 9828897

References

  • Bravo EL. Physiology of the adrenal cortex. Urol Clin North Am. 1989 Aug; 16(3):433-437 (review). PubMed 2665269
  • Kirkman S, Nelson DH. Alcohol-induced pseudo-Cushing's disease: A study of prevalence with review of the literature. Metabolism. 1988 apr; 37(4):390-394 (review). PubMed 2833680
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