Hirsutism (excess androgen-pattern hair growth) arises from either non-androgenic causes (e.g., acromegaly, topical irritants, certain medications) or androgenic causes involving excess androgen production or action, including polycystic ovary syndrome (the most common cause), non-classical congenital adrenal hyperplasia, androgen-secreting neoplasms, hyperprolactinemia, luteoma of pregnancy, and Cushing syndrome (distinguished by signs of hypercortisolism such as central obesity and purple striae). Management follows the mechanistic principle of reducing androgen production, increasing androgen binding, or blocking androgen action at the receptor: oral contraceptives (first-line, given the predominance of PCOS) suppress LH-driven ovarian androgen synthesis and increase sex hormone-binding globulin, while adjunct agents act by distinct mechanisms—spironolactone (androgen receptor antagonism, 5-alpha-reductase inhibition), flutamide (androgen receptor blockade), and finasteride (5-alpha-reductase inhibition)—situating this topic within the endocrinology/gynecology framework of androgen physiology.
Hirsutism has a differential diagnosis spanning non-androgenic causes (e.g., acromegaly, medication-induced, idiopathic follicular enzymatic activity) and androgen-mediated causes (e.g., polycystic o…