Female Hirsutism: Pathophysiological Considerations and Therapeutic Implications*

Abstract
INTRODUCTION FEMALE HIRSUTISM may be defined as excessive hair growth in anatomical sites where such growth is considered a secondary male characteristic. Although this disorder can be a symptom of a number of endocrine diseases such as polycystic ovarian disease (PCO) or Cushing's syndrome, most patients present with no obvious abnormalities of endocrine function. The term that has been applied to this condition is idiopathic or simple hirsutism. Idiopathic hirsutism shows no clinical differences from other types of hirsutism. However, it is generally not associated with other signs of hyperandrogenism such as virilization of the external genitalia, deepening of the voice, breast atrophy, or development of a male-type muscle bulk. Although racial differences have been noted in the occurrence of this disorder (Mediterranean women being more subjected to abnormal hair growth), no such differences have been found in androgenic steroids (1). Starting with the concept that hair follicles as well as sebaceous glands are androgen-dependent structures (2), idiopathic hirsutism has been found to be a condition of local hyperandrogenization that involves increases in hair growth, sweat and sebum secretion, and total skin collagen content (3).