Androgens are part of normal female physiology. When they are secreted
in excess or when they cause unwanted symptoms such as hirsutism and
male-pattern baldness, the term hyperandrogenism is used. In many hype
randrogenic women, there is no well-defined hormonal abnormality, but
the women are simply on one end of a normal spectrum of androgen secre
tion and cutaneous androgen sensitivity. To be active in the skin, tes
tosterone must be converted to dihydrotestosterone by the enzyme 5 alp
ha-reductase. Androgen sensitivity is determined, in part, by 5 alpha-
reductase activity in the skin. This is a localized phenomenon, and th
ere is no generalized increase in 5 alpha-reductase activity in these
women. Dihydrotestosterone can be converted to glucuronide and sulfate
conjugates, including androstanediol glucuronide. These androgen conj
ugates have been proposed to be serum markers of cutaneous androgen me
tabolism, but recent evidence indicates that they arise from adrenal p
recursors and are more likely to be markers of adrenal steroid product
ion and metabolism. Antiandrogens (androgen receptor blockers) are the
best medical treatment of cutaneous hyperandrogenism. 5 alpha-Reducta
se inhibitors have recently been approved for the treatment of benign
prostatic hyperplasia, and research is currently underway to determine
their effectiveness in treating hirsutism and male-pattern baldness.