Cortisol ELISA


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Product Catalog No: CO368S Pack Size: 96 Tests

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Summary

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

Test Principle

The Calbiotech, Inc. Cortisol test kit is a solid phase competitive ELISA. The samples, working Cortisol-HRP Conjugate and anti-cortisol-biotin solution are added to the wells coated with streptavidin. Cortisol in the patient’s serum competes with the cortisol enzyme (HRP) 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.

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References
  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
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