The measurement of dehydroepiandrosterone sulfate (DHEA-S) is used in the diagnosis and differential diagnosis of androgen overproduction (hyperandrogenism - in combination with measurements and other steroid hormones), in the investigation of women with amenorrhea, infertility, and hypertrichosis, in the diagnosis and monitoring of congenital adrenal hyperplasia as well as in the diagnosis of premature adrenarche (early onset of androgen secretion in children).
Dehydroepiandrosterone (DHEA) has very low androgenic activity, but it serves as the major precursor for most steroid sex hormones. DHEA is secreted by the adrenal glands, and its production is controlled, at least in part, by the adrenocorticotropic hormone (ACTH). Most DHEA is secreted as dehydroepiandrosterone sulfate (DHEA-S). Both hormones are bound by albumin, but the binding of DHEA-S is much stronger. As a result, circulating DHEA-S concentrations are much higher (> 100 times) than DHEA. In most cases, the results of DHEA and DHEA-S can be used the same. In the gonads and several other tissues, mainly in the skin, some enzymes (steroid sulfatases) can convert DHEA-S to DHEA, which is then metabolized to more potent androgens and to estrogens.
During pregnancy, DHEA and DHEA-S are secreted by the fetal adrenals in large quantities and serve as precursors for the production of the placenta of the dominant estrogen in pregnancy, estriol. Within weeks after birth, levels of DHEA and DHEA-S are reduced by 80% or more and remain low until the onset of adrenarche at the age of 7-8 years in girls and 8-9 years in boys. Adrenarche, a phenomenon that is not fully understood, is characterized by a gradual increase in adrenal androgen production, progresses to adolescence but is not causally related. Early adrenarche is not associated with early adolescence or any decrease in final height or the appearance of hyperandrogenism. However, girls with early adrenarche may be at increased risk of developing polycystic ovary syndrome as adults.
Following adrenarche, DHEA and DHEA-S levels rise to a maximum level by the age of 20, approximately comparable to that observed at birth. Then levels fall over the next 40 to 60 years to about 20% of maximum levels. The clinical significance of this age-related decline is unknown. In young and elderly patients with primary adrenal insufficiency, the addition of DHEA and DHEA-S has been shown to improve mood, energy, and sexual desire.
Increased levels of DHEA and DHEA-S can cause symptoms or signs of hyperandrogenism in women. Men are usually asymptomatic, but through the peripheral conversion of androgens to estrogens, occasionally increased amounts of estrogen can occur. Most mild to moderate increases in DHEA and DHEA-S levels are idiopathic. However, large increases in DHEA and DHEA-S may be indicative of adrenal glands producing androgens. In young children, congenital adrenal hyperplasia due to beta-hydroxysteroid dehydrogenase deficiency is associated with the overproduction of DHEA and DHEA-S. Smaller increases can be observed in 21-hydroxylase deficiency (the most common form of congenital adrenal hyperplasia) and in the lack of beta-hydroxylase. In contrast, deficiency of STAR regulatory protein or 17 alpha-hydroxylase is characterized by low levels of DHEA and DHEA-S.
Many drugs and hormones can lead to lower levels of DHEA-S, such as insulin, contraceptives, corticosteroids, CNS drugs such as e.g. carbamazepine, clomipramine, imipramine, phenytoin, antilipidemic drugs (statins), dopaminergic drugs (eg levodopa/dopamine, bromocriptine), fish oil and vitamin E.
Medications that can increase DHEA-S levels include metformin, troglitazone, prolactin, danazol, calcium channel blockers (eg, diltiazem, amlodipine), and nicotine.
Laboratory test results are the most important parameter for the diagnosis and monitoring of all pathological conditions. 70%-80% of diagnostic decisions are based on laboratory tests. The correct interpretation of laboratory results allows a doctor to distinguish "healthy" from "diseased".
Laboratory test results should not be interpreted from the numerical result of a single analysis. Test results should be interpreted in relation to each individual case and family history, clinical findings, and the results of other laboratory tests and information. Your personal physician should explain the importance of your test results.
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