Deducing factors that precipitate Idiopathic hirsutism
Hirsutism – characterized by excessive terminal hair growth, can be caused by various factors. Predisposing factors for such male-pattern hair growth include – polycystic ovary syndrome (PCOS), non-classic congenital adrenal hyperplasia, adrenal or ovarian tumors, or idiopathic causes. Idiopathic hirsutism refers to hirsutism with normal ovulatory function, serum androgen levels, and ovarian morphology, wherein the exact cause is unknown. Androgens play a crucial role in stimulating body hair growth, so any form of increased androgen effect should be present in patients with hirsutism, regardless of normal serum androgen levels. Prior evidence suggests that patients with idiopathic hirsutism have relatively higher serum androgen levels (relative hyperandrogenemia) than healthy individuals within normal limits. Hence, the notion of idiopathic hirsutism truly being idiopathic remains questionable.
In addition, higher steroid sulphatase and 17-beta hydroxysteroid dehydrogenase mRNA expressions seem to impact the local androgen metabolism in women with idiopathic hirsutism. These findings suggest that increased local androgen production in pilosebaceous units in some patients may lead to hirsutism without ovulatory dysfunction, even if the adrenals or ovaries do not secrete excessive androgens.
Given the relative hyperandrogenemia and possible increase in local androgen synthesis in patients with idiopathic hirsutism, we propose renaming idiopathic hirsutism as "normoandrogenic hirsutism" – as it does not appear to be idiopathic in its pathogenesis. In fact, it could represent an early-stage hyperandrogenic disorder, such as PCOS.
Prospective follow-up of patients with idiopathic hirsutism is warranted to shed more light on this hypothesis. These findings are essential because gaining an in-depth understanding of the pathogenesis of idiopathic hirsutism may lead to new therapeutic approaches.
Source: Unluhizarci K, Hacioglu A, Taheri S, et al. World J Clin Cases. 2023;11(2):292-298. doi:10.12998/wjcc.v11.i2.292
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