Dehydroepiandrosterone (DHEA) Sulfate
| Dehydroepiandrosterone (DHEA) Sulfate | | | |
| Number | | 004697 |
| CPT | | 82627 |
| Synonyms | | DHEA-S ; DHEA-SO4 ; DHEA Sulfate |
| Special Instructions | | See the Endocrine Appendix for instructions on multiple specimen testing. |
| Specimen | | Serum |
| Volume | | 1 mL |
| Minimum Volume | | 0.4 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. |
| Storage Instructions | | Refrigerate |
| Reference Interval | | See table.1,2
| Age | Male
(μg/dL) | Female
(μg/dL) | | 1-7 d | 91-376 | 73-367 | | 8-15 d | 37-224 | 44-247 | | 1-3 y | <30 | <79 | | 4-6 y | <186 | <38 | | 7-8 y | <94 | <68 | | 9-10 y | <75 | <160 | | 11 y | <152 | <98 | | 12 y | <344 | <177 | | 13 y | <242 | <167 | | 14 y | <286 | 32-301 | | 15 y | 59-310 | 39-288 | | 16 y | 47-357 | 58-354 | | 17 y | 102-341 | 97-399 | | 18-19 y | 108-441 | 145-395 | | 20-29 y | 280-640 | 65-380 | | 30-39 y | 120-520 | 45-270 | | 40-49 y | 95-530 | 32-240 | | 50-59 y | 70-310 | 26-200 | | 60-69 y | 42-290 | 13-130 | | >69 y | 28-175 | 17-90 | | Tanner Stage | | I | <87 | <65 | | II & III | <151 | <175 | | IV | 75-282 | 57-230 | | V | 121-368 | 76-378 |
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| Use | | Work up women with infertility, amenorrhea, or hirsutism, to identify the source of excessive androgen; aid in the evaluation of androgen excess (hirsutism and/or virilization), including Stein-Leventhal syndrome and adrenocortical diseases, including congenital adrenal hyperplasia and adrenal tumor. DHEA-S is not increased with hypopituitarism. It is low in Addison disease. |
| Methodology | | Immunochemiluminometric assay (ICMA) |
| Additional Information | | DHEA sulfate is the major steroid of the fetal adrenal. DHEA-S is the principal adrenal androgen and is secreted together with cortisol under the control of ACTH and prolactin. DHEA-S is elevated with hyperprolactinemia. Elevated levels may be found in the adrenogenital syndrome3 or adrenocortical neoplasms or hyperplasias. In females and children, DHEA excess causes masculinization. Increased 3-α-androstanediol glucuronide indicates excessive androgen in peripheral tissues. Persistent anovulation, the polycystic ovary, or Stein-Leventhal syndrome is characterized by increases of circulating levels of testosterone, androstenedione, dehydroepiandrosterone, and DHEA-S. 17-hydroxyprogesterone and DHEA-S are only mildly increased compared to cases of adrenal hyperplasia. Patients with androgen-producing adrenal tumors also have moderate increases of 17-KS. Testosterone is derived from ovaries, adrenals, and the peripheral tissues. Increased DHEA with normal testosterone provides evidence for an adrenal cause of excessive androgen. Low levels are found in amniotic fluid in Down syndrome.4 |
| Footnotes | | - Soldin SJ, Godwin ID, Bailey J, et al, “Serum Dehydroepiandrosterone Sulfate in a Normal Pediatric Population,” Clin Chem, 1993, 39:1171.
- Tietz NW, ed, Clinical Guide to Laboratory Tests, 3rd ed, Philadelphia, PA: WB Saunders Co, 1995, 198.
- Pintor C, Genozanni AR, Carboni G, et al, “Adrenal Androgens and Pubertal Development in Physiological and Pathological Conditions,” Adrenal Androgens, Genozanni AR, Thiossen JH, and Seiteri PK, eds, New York, NY: Raven Press, 1985, 816-90.
- Cuckle HS, Wald NJ, Densem JW, et al, “Second Trimester Amniotic Fluid Oestriol, Dehydroepiandrosterone Sulphate, and Human Chorionic Gonadotropin Levels in Down Syndrome,” Br J Obstet Gynaecol, 1991, 98(11):1160-2
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| References | | DiGeorge AM, “The Endocrine System,” Nelson Textbook of Pediatrics, 13th ed, Behrman RE, Vaughan VC III, and Nelson WE, eds, Philadelphia, PA: WB Saunders Co, 1987, 1176-244. Droegemueller W, Herbst AL, Mishell DR, et al, Comprehensive Gynecology, St Louis, MO: Mosby-Year Book Inc, 1987. Elin RJ, “Reference Intervals and Laboratory Values of Clinical Importance,” Cecil Textbook of Medicine, 18th ed, Volume 2, Wyngaarden JB and Smith LH, eds, Philadelphia, PA: WB Saunders Co, 1988, 2394-404. Imperato-McGinley J, “Disorders of Sexual Differentiation,” Cecil Textbook of Medicine, 18th ed, Volume 2, Wyngaarden JB and Smith LH Jr, eds, Philadelphia, PA: WB Saunders Co, 1988, 1390-404. Meites S, Pediatric Clinical Chemistry: Reference (Normal) Values, 3rd ed, Washington, DC: American Association of Clinical Chemistry Press, 1989, 119-20. Pang SY, Legido A, Levine LS, et al, “Adrenal Androgen Response to Metyrapone, Adrenocorticotropin, and Corticotropin-Releasing Hormone Stimulation in Children With Hypopituitarism,” J Clin Endocrinol Metab, 1987, 65(2):282-9. Siegel SF, Finegold DN, Lanes R, et al, “ACTH Stimulation Tests and Plasma Dehydroepiandrosterone Sulfate Levels in Women With Hirsutism,” N Engl J Med, 1990, 323(13):849-54. Speroff L, Glass RH, and Kase NG, Clinical Gynecologic Endocrinology and Infertility, 4th ed, Baltimore, MD: Williams & Wilkins 1989. Weykamp CW, Penders TJ, Schmidt NA, et al, “Steroid Profile for Urine: Reference Values,” Clin Chem, 1989, 35(12):2281-4. |
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