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Androgen Conjugates: Physiology and Clinical Significance

Departments of Medicine and Physiology/Biophysics, Dalhousie University Halifax, Nova Scotia B3J 1B6, Canada

Correspondence: Address correspondence to: Roger S. Rittmaster, M.D., Suite 809, Gerard Hall, 5303 Morris Street, Halifax, Nova Scotia B3J1B6, Canada. Reprints of this article are not available.

Abstract

I. Introduction and Definitions: HIRSUTISM in women is characterized by increased androgen production from the ovaries and/or adrenal glands and enhanced sensitivity of the skin to circulating androgens (1). Frequently these problems coexist. Serum levels of testosterone, androstenedione, and dehydroepiandrosterone sulfate (DHEAS) have been used as markers of overproduction of androgens or their precursors and are often elevated in hirsute women. It has been more difficult to find markers of skin sensitivity to androgens.

Skin sensitivity to androgens is modulated by the enzyme 5-reductase, which converts testosterone to dihydrotestosterone (DHT), the active androgen in the skin (2). Serum DHT levels, however, have not usually correlated with the presence or the degree of hirsutism. DHT is rapidly metabolized to other compounds, including androstanediol, androsterone, and their glucuronide and sulfate conjugates. Over the past decade, physiological and clinical studies have suggested that androstanediol glucuronide, and possibly other androgen conjugates, may be biochemical markers of cutaneous androgen metabolism and action. Other studies have suggested that these androgen conjugates arise primarily from adrenal precursors and may be a marker of adrenal hyperandrogenism. The purpose of this review is to critically appraise the data concerning the physiological significance of androgen conjugates and to address the following question: "Are androgen conjugates a reflection of cutaneous androgen metabolism or is their correlation with hirsutism an epiphenomenon caused by the overproduction of androgen precursors in hirsute women?"

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