CPT Test code: 82533
|Minimum Volume:||0.3 mL (Note: This volume does not allow for repeat testing.)|
|Container:||Red-top tube or gel-barrier tube|
|Collection:||If a red-top tube is used, transfer separated serum to a plastic transport tube. Blood should be drawn at 8 AM and 4 PM to evaluate baseline diurnal variation (see Cortisol, AM & PM ). Morning specimen is often ordered with ACTH level.|
|Causes for Rejection:||Citrate plasma specimen; improper labeling|
|Reference Interval:||• 2.3-19.4 μg/dL
• AM: 6.2-19.4 μg/dL; PM: 2.3-11.9 μg/dL
|Use:||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.|
|Limitations:||Pregnancy, contraceptives, and estrogen therapy give rise to elevated cortisol concentrations.1 In samples from patients who have been treated with prednisolone, methylprednisolone, or prednisone, falsely elevated concentrations of cortisol may be determined.1 During metyrapone tests, 11-deoxycortisol levels are elevated.1 Falsely-elevated cortisol values may be determined due to cross reactions. Patients suffering from 21-hydroxylase-deficiency exhibit elevated 21-deoxycortisol levels and this can also give rise to elevated cortisol levels.1
The time of sample collection must be taken into account when interpreting results due to the cortisol secretion circadian rhythm. Severe stress can also give rise to elevated cortisol levels.1
In patients receiving therapy with high biotin doses (ie, >5 mg/day), no sample should be taken until at least eight hours after the last biotin administration.1 As with all tests containing monoclonal mouse antibodies, erroneous findings may be obtained from samples taken from patients who have been treated with monoclonal mouse antibodies or who have received them for diagnostic purposes.1 In rare cases, interference due to extremely high titers of antibodies to streptavidin and ruthenium can occur.1 The test contains additives, which minimize these effects.
The determination of cortisol in 24-hour urine is the method of choice for the detection of Cushing syndrome since cortisol excretion in urine is not subject to the diurnal rhythm of cortisol secretion.2
|Additional Information:||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, IN: Roche Diagnostics, 2005.
2. Miyachi Y, “Pathophysiology and Diagnosis of Cushing Syndrome,” Biomed Pharmacother, 2000, 54(Suppl 1):S113-7.PubMed 10915006
3. Aron DC, Tyrell JB, “Glucocorticoids and Adrenal Androgens,” Basic & Clinical Endocrinology, 4th ed, Greenspan FS, Baxter JD, eds, Norwalk, CT: Appleton & Lange, 1994, 307-46.
4. Hasinski S, “Assessment of Adrenal Glucocortoid Function. Which Tests Are Appropriate for Screening?” Postgrad Med , 1998, 104(1):69-72.PubMed 9676562
5. Rosalki SB, “Biochemical Testing of Adrenocortical Function,” Int J Clin Pract, 1998, 52(3):189-91.PubMed 9684436
6. Newell-Price J, Trainer P, Besser M, et al, “The Diagnosis and Differential Diagnosis of Cushing’s Syndrome and Pseudo-Cushing’s States,” Endocr Rev, 1998, 19(5):647-72.PubMed 9793762
7. Ross RJM, Trainer PJ, “Endocrine Investigation: Cushing’s Syndrome,” Clin Endocrol (Oxf), 1998, 49(2):153-5.PubMed 9828897
|References:||Bravo EL, “Physiology of the Adrenal Cortex,” Urol Clin North Am, 1989, 16(3):433-7 (review). PubMed 2665269
Kirkman S, Nelson DH, “Alcohol-Induced Pseudo-Cushing’s Disease: A Study of Prevalence With Review of the Literature,” Metabolism, 1988, 37(4):390-4 (review).PubMed 2833680