Cortisol (hydrocortisone, compound F) is the most potent glucocorticoid synthesized from cholesterol. Cortisol is found in the blood either as free Cortisol, or bound to corticosteroid-binding globulin (CBG). Cortisol production has an ACTH-dependent circadian rhythm with peak levels in the early morning and a nadir at night. The factors controlling this circadian rhythm are not completely defined. Serum levels are highest in the early morning and decrease throughout the day. In the metabolic aspect, Cortisol promotes gluconeogenesis, liver glycogen deposition, and the reduction of glucose utilization. Immunologically, Cortisol functions as an important anti inflammatory, and plays a role in hypersensitivity, immunosuppression, and disease resistance. It has also been shown that plasma Cortisol levels elevate in response to stress. Abnormal Cortisol levels are seen with a variety of different conditions: with adrenal tumors, prostate cancer, depression, and schizophrenia. Elevated Cortisol levels and lack of diurnal variation have been identified in patients with Cushing’s disease
|Quantity||96 Tests (12×8 breakable strip wells)|
|Standard range||20-400 ng/ml|
|Analytical Sensitivity||20 ng/ml|
|Sample volume||25 µl/well|
The SDi Cortisol ELISA Kit is intended for the quantitative measurement of Cortisol in human serum or plasma.
The SDi Cortisol kit is a solid phase competitive ELISA. The samples and Cortisol enzyme conjugate are added to the wells coated with anti-Cortisol monoclonal antibody. Cortisol in the patient’s sample competes with a Cortisol enzyme conjugate for binding sites. Unbound Cortisol and Cortisol enzyme conjugate is washed off by washing buffer. Upon the addition of the substrate, the intensity of color is inversely proportional to the concentration of Cortisol in the samples. A standard curve is prepared relating color intensity to the concentration of the Cortisol.
Storage and Stability
Product should be stored at 2-8 °C. Product is stable for 24 months from the date of manufacturing.
For research use only. Not for use in diagnostic procedures.
1. Chernow B, Alexander R, Smallridge RC, Thompson WR, Cook D, Beardsley D, Fink MP, Lake R, Fletcher JR: Hormonal responses to graded surgical stress. Arch Intern Med 147:1273-1278, 1987.
2. Crapo L: Cushing’s syndrome: A review of diagnostic tests. Metabolism 28:955-977, 1979.
3. Lee PDK, Winter RJ, Green OC: Virilizing adrenocortical tumors in childhood. Eight cases and a review of the literature. Pediatrics 76:437-444, 1985.
4. Leisti S, Ahonen P, Perheentupa J: The diagnosis and staging of hypocortisolism in progressing autoimmune adrenalitis. Pediatr Res 17:861-867, 1983.
5. Stewart PM, Seckl JR, Corrie J, Edwards CRW, Padfield PL: A rational approach for assessing the hypothalamo-pituitary-adrenal axis. Lancet 5:1208-1210, 1988.
6. Watts NB, Tindall GT: Rapid assessment of corticotropin reserve after pituitary surgery. JAMA 259:708-711, 1988.
7. Schlaghecke R, Kornely E, Santen RT, Ridderskamp P: The effect of long-term glucocorticoid on pituitary-adrenal responses to exogenous corticotropin-releasing hormone. New Engl J Med 326:226-230, 1992.
8. Tiertz, N. W. , Text book of Clinical Chemistry, Saunders, 1968