DHEA-S (Dehydroepiandrosterone Sulfate)

Create a Free Account to View Prices

Turnaround Time: Within 1 day
CPT Code:


Test Type: 0.8 mL Serum
Stability Time:



Room temperature

14 days


14 days


14 days

Freeze/thaw cycles

Stable x3

Reference Range:

See table.1,2



Male (μg/dL)

Female (μg/dL)

0 to 30 d

Not established

Not established

1 to 12 m



1 to 4 y



5 to 8 y



9 to 11 y



12 to 14 y



15 to 19 y



20 to 24 y



25 to 34 y



35 to 44 y



45 to 54 y



55 to 64 y



65 to 74 y



≥75 y






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.

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.3 In rare cases, interference due to extremely high titers of antibodies to streptavidin and ruthenium can occur.3 The test contains additives that minimize these effects.

DHEA-S is a steroid hormone which is produced from the precursor cholesterol in the zona reticularis and broad fascia of the adrenal cortex.1 The determination of elevated DHEA-S values is an important aid in the diagnosis of hirsutism and virilism.2,4 In addition to a differential diagnosis of hirsutism and virilism, further indications for this parameter are all forms of androgenization, hyperprolactinemia, polycystic ovarian syndrome, and the exclusion of an androgen-producing tumor of the adrenal cortex.2 DHEA-S exhibits only a weak androgenic activity but can be metabolized to more active androgens, such as androstenedione and testosterone, which can indirectly cause hirsutism and virilism.2,5

From 7 years of age onwards, an increase in DHEA-S levels is observed which then gradually after the age of 30 begins to fall again.6 Only elevated DHEA-S concentrations are of clinical importance; other factors which can be responsible for DHEA-S excess production are genetic enzyme defects of the adrenal cortex (adrenogenital syndrome),7 hyperplasia of the adrenal cortex, as well as androgen-producing tumors.2

The rate of secretion of DHEA-S into the blood stream is only slightly more than the rate observed for DHEA. As a consequence of the DHEA-S half-life of approximately one day, the DHEA-S level is, however, about a thousand-fold greater.8 DHEA-S is relatively strongly bound to albumin, only a small portion is nonprotein bound, and none appears to be bound to sex hormone-binding globulin (SHBG).9 Due to its high concentration and low inter- and intra-day variability, DHEA-S is an excellent indicator of adrenal cortex androgen production.8,10

Together with testosterone, DHEA-S assays represent the assay of choice for initial screening tests to determine whether androgen values are elevated in hirsutism. Approximately 84% of the women suffering from hirsutism exhibit elevated androgen levels.11 The main purpose of this is to exclude the presence of androgen-producing tumors (from the adrenal cortex or the ovaries).7

1. Gronowski AM, Landau-Levine M. Reproductive endocrine function. In: Burtis CA, Ashwood ER, eds. Tietz Textbook of Clinical Chemistry. 3rd ed. Philadelphia, Pa: WB Saunders; 1999:1601-1641, chapter 45.

2. Goldfien A, Monroe SE. Ovaries. In: Greenspan FS, Baxter JD, eds. Basic and Clinical Endocrinology. 4th ed. Norwalk, Conn: Appleton & Lange;1994:419-470,chap 10.

3. DHEA-S on Elecsys 1010/2010 and Modular Analytics E170, package insert 2006-11, V 11, Indianapolis, Ind: Roche Diagnostics; 2006.

4. Hatch R, Rosenfield RL, Kim MH, Tredway D. Hirsutism: Implications, etiology, and management. Am J Obstet Gynecol. 1981 Aug 1; 140(7):815-830. PubMed 7258262

5. Mooradian AD, Morley JE, Korenman SG. Biological actions of androgens. Endocr Rev. 1987 Feb, 8(1):1-28. PubMed 3549275

6. Zappulla F, Ventura D, Capelli M, et al. Gonadal and adrenal secretion of dehydroepiandrosterone sulfate in prepubertal and pubertal subjects. J Endocrinol Invest. 1981 Apr-Jun; 4(2):197-202. PubMed 6268694

7. Ziegler R. Endokrinologische Erkrankungen. In: Schettler G, ed.Innere Medizin. Stuttgart, Germany: Ausgabe Thieme; 1987: 434-437.

8. Haning RV. Using DHEAS to monitor androgen disorders. Contemp Ob/Gyn.1981; 18(9):117-131.

9. Longcope C. Dehydroepiandrosterone metabolism. J Endocrinol. 1996 Sep; 150(Suppl):S125-S127. PubMed 8943796

10. Lobo RA, Paul WL, Goebelsmann U. Dehydroepiandrosterone sulfate as an indicator of adrenal androgen function. Obstet Gynecol. 1981 Jan; 57(1):69-73. PubMed 6450345

11. Lobo RA, Paul WL, Goebelsmann U. Serum levels of DHEAS in gynecologic endocrinopathy and infertility. Obstet Gynecol. 1981 May; 57(5):607-612. PubMed 6261197

Collection Details:

Patient Preparation:

Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample.

Collection Instructions:

This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R). It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample.

Red-top tube or gel-barrier tube.

If a red-top tube is used, transfer separated serum to a plastic transport tube.