Idiopathic hirsutism: Is it really idiopathic or is it misnomer?

Table 1 Overview of pathogenetic mechanisms in idiopathic hirsutism

Suggested/Established mechanisms	How to contribute to hirsutism
Functional hyperandrogenism	Milder forms of ovarian and adrenal androgen hypersecretion
5α-reductase activity	Leading to increased DHT level which is a potent androgen
Androgen receptors	Some forms of AR variances leads to increased receptor activity
Aromatase enzyme (dys)function	Decreased aromatase activity leads to relative hyperandrogenemia at tissue level and possibly in the circulation
Local androgen production	Pilocebaceous unit locally produce increased amount of androgens
Insulin resistance	Althouhg its role in IH is not clearly established as seen in PCOS, concomitant hyperinsulinemia may contribute to hyperandrogenism

DHT: Dihydrotestosterone; AR: Androgen receptor; IH: İdiopathic hirsutism; PCOS: Polycystic ovary syndrome.