Part of the Group

DHEA

Key Features and Values

– Same sample type can be used across all assays to simplify inclusion into routine serology work-up
– Ready to use reagents reduces hands-on time for assay preparation
– Long shelf life cost-effective solution by reducing wastage due to expired kits
– Suitable for inclusion on automated plate systems simplifies scale-up of test volume
– Supported by a complete panel of assays for supporting treatment monitoring of several forms of hormonal dysfunctions

Product Description

Competitive immunoenzymatic colorimetric method for the quantitative determination of Dehydroepiandrosterone (DHEA) concentration in human serum or plasma.
DHEA kit is intended for laboratory use only.

Scientific Description
Dehydroepiandrosterone (DHEA) is a C19 steroid secreted by the adrenal cortex and in smaller quantities by the gonads.  DHEA is a precursor in testosterone and various estrogens biosynthesis.  The physiologic role of DHEA is not-well defined, because of a lot of ascertained in vivo and in vitro effects, for example the prevention and regression of colon tumor, spontaneous and inducted, in rodents.  Some studies showed a decrease in the DHEA production in women with risk for the breast cancer.  In animal models DHEA showed a role in the therapeutic action against diabetes, obesity and cardiovascular pathologies, and unclear roles in immunology, in lipid metabolism (also cholesterol) and in the nervous system.
Seric levels of DHEA are relatively high in foetal and neonatal age, decreased during childhood and increased again during puberty until 30 years.  No DHEA variations have been observed during pregnancy or menstrual cycle.  Seric levels of DHEA are 100-1000 times lower than the levels of DHEA sulphate (DHEAS).
The measurement of seric levels of DHEA is a marker for adrenal androgen synthesis.  Abnormal low levels of DHEA can be observed in the hypoadrenalism, while elevated levels can be observed in various pathologies such as the surrenalic adenomas, 21-hydroxylase and 3b-hydroxysteroid dehydrogenase deficiency and in some cases of female hirsutism.
Publications

1. Dorfman RI, Shipley, RA, Adrogens, John Wiley and Sons, New York, 1956, pp. 116-128.
2. Pang S, Riddick L, Hirsutism, IN Lifshitz (ed), Pediatric Endocrinology, A Clinical Guide, second edition, Marcel Dekker Inc., New York 1990, pp259-291
3. De Peretti E, Forest MG, Pattern of plasma dehydroepiandrosterone sulfate levels ih humans from birth to adulthood: evidence for testicular
production, J Clin Endocrinol Metab, 47, 572-577 (1978)
4. Lashansky G, Saenger P, Fishman K, Gautier T, Mayes D, Berg G, Di Martino-Nardi J, Reiter E. Normative data for adrenal steroidogenesis in a healthy pediatric population: age and sex-related changes after adrenocorticotropin stimulation, J Clin Endocrinol Metab, 73, 674-686 (1991)
5. Zurnoff B, Roenfeld RS, Stain GW, Levin J, Fukushima DK, Sex differences in twenty-four hour mean plasma concentration of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) and the DHEA to DHEAS ratio in normal adults, J Clin Endocrinol Metab 51, 330-333 (1980)
6. Pang S, Lerner A, Stoner E, Oberfield S, Engle I, New M, Late-onset adrenal steroid 3’-hydroxysteroid dehydrogenase deficiency: a cause of hirsutism in pubertal and postpubertal women, J Clin Endocrinol Metab 60, 428-439 (1985)
7. Lee PDK, Winter RJ, and Gree OC, Virilizing adrenocortical tumors in childhood: eight cases and a review of the literature, Pediatrics, 76, 437-444 (1985)
8. Tietz NW, Textbook of clinical chemistry, 2nd ed. Philadelphia WB Saunders, 1994

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Code: DKO124
Clinical Area:
Incubation: 60+20 min
Sensitivity: N/A
Specificity: N/A
Classification: IVD, CE
Number of Tests: 96
Sample Type: Serum/Plasma
Sample Volume: 25 μL
Assay Range: 0.5 – 30 ng/mL