Hirsutism laboratory findings

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:

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Overview

It is important to carry out various biochemical tests to determine the cause of hirsutism that is necessary to make an informed decision for the best options for treatment.

Laboratory Findings

The laboratory findings

• Testosterone, total and free:
  • The most important assay is the level of serum testosterone. If the total serum testosterone level is normal, measure the free serum level because hyperandrogenism (and insulin resistance, if present) decreases sex steroid-binding globulin, such that the unbound, biologically active testosterone moiety may be elevated even if the total level is unremarkable. Extremely high testosterone levels are likely to be associated with adrenal or ovarian tumors, whereas idiopathic and benign etiologies result in very mild elevations. Indeed, in idiopathic hirsutism, the results from testing androgen levels are often normal. In some of these women, hirsutism is thought to be caused by increased skin sensitivity to androgen or by increased skin 5-alpha-reductase activity. A total serum testosterone level > 200ng/mL suggest an androgen producing tumor.

• Dehydroepiandrosterone sulfate (DHEAS):
  • An elevated testosterone level does not indicate the gland of origin. Accordingly, measurement of elevated plasma levels of DHEAS, an androgen synthesized almost exclusively by the adrenal cortex, can indicate excess adrenal function. Elevations in both testosterone and DHEAS suggest an adrenal origin, whereas an isolated testosterone elevation indicates an ovarian source. DHEAS > 700microgram/microliter suggests an androgen producing adrenal tumor.
• Dexamethasone suppression:
  • Dexamethasone-mediated suppression of androgens is observed in healthy women who do not have hirsutism and in those with congenital adrenal hyperplasia (CAH) and idiopathic hirsutism.
• Adrenocorticotropin stimulation:
  • An ACTH-stimulation test (250 mcg for 30 min) can help differentiate between CAH and idiopathic hirsutism because CAH produces abnormal findings (elevations in metabolic precursors of cortisol).
  • Hirsutism caused by CAH is due to 1 of 3 cortisol biosynthetic defects, ie, 21-hydroxylase deficiency, 3 3 β -hydroxysteroid dehydrogenase, or 11-β -hydroxylase deficiency.
  • 17-hydroxyprogesterone levels should be also obtained because 21-hydroxylase deficiency is responsible for the majority of cases of CAH (approximately 90%) and 17-hydroxyprogesterone values of less than 7 nmol/L exclude the diagnosis, and values of greater than 45 nmol/L (in women who are nongestational) confirm 21-hydroxylase deficiency. When basal values of 17-hydroxyprogesterone are between 7 and 45 nmol/L, an ACTH-stimulated concentration of greater than 45 nmol/L is also diagnostic.
• Cortisol suppression:
  • PCOS and adrenal and ovarian tumors are associated with normal suppression of cortisol by dexamethasone, whereas cortisol levels in patients with Cushing syndrome are not suppressed.

• Serum prolactin or FSH:
  • Women with hirsutism and amenorrhea of unknown cause should have a serum prolactin or FSH test to evaluate for either a prolactinoma or ovarian failure.
• Serum LH: Ratio of LH:FSH > 3 significant for PCOS.
• Diabetes screening:
  • Women with hirsutism, PCOS, obesity, or acanthosis nigricans may have insulin resistance, and screening for diabetes and hyperlipidemia is recommended.
• Prostate-specific antigen (PSA):
  • Ultrasensitive assays can detect PSA in women and is a potential marker for androgen excess. Studies thus far, however, have not shown a good correlation with the change in androgen levels after treatment. ^{null 11}