Unluhizarci Kursad, Hacioglu Aysa, Taheri Serpil, Karaca Zuleyha, Kelestimur Fahrettin
Department of Endocrinology, Erciyes University Medical School, Kayseri 38039, Turkey.
Department of Medical Biology, Erciyes University Medical School, Kayseri 38039, Turkey.
World J Clin Cases. 2023 Jan 16;11(2):292-298. doi: 10.12998/wjcc.v11.i2.292.
Hirsutism, which is characterized by excessive growth of terminal hair in a male pattern, may result from various causes including polycystic ovary syndrome (PCOS), non-classic congenital adrenal hyperplasia, adrenal or ovarian tumors or it may be idiopathic. Idiopathic hirsutism is currently defined as hirsutism associated with normal ovulatory function, normal serum androgen levels and normal ovarian morphology, however, the pathogenesis of idiopathic hirsutism is not clear. The androgens are the main hormones to stimulate growth of body hair, therefore, there should be any form of increased androgen effect irrespective of normal serum androgen levels in any patient with hirsutism. In accordance to this scientific truth, we have previously shown that, although within normal limits, patients with idiopathic hirsutism have relatively higher serum androgen levels (relative hyperandrogenemia) in comparison to healthy subjects which let as to think that is idiopathic hirsutism really idiopathic? In addition to relative hyperandrogenemia, we have previously shown that, in comparison to healthy subjects, women with idiopathic hirsutism demonstrated higher expression of steroid sulphatase and 17-beta hydroxysteroid dehydrogenase mRNA both in the subumbilical region and arm skin, which contributes to local androgen metabolism. Those results support the idea that, in some patients, although the adrenals or ovaries do not secrete increased amount of androgens leading to hyperandrogenemia, pilocebaceous unit locally produce increased amount of androgens leading to hirsutism without ovulatory dysfunction. Upon the demonstration of relative hyperandrogenemia and possible increase in local androgen synthesis in patients with idiopathic hirsutism, we think that idiopathic hirsutism is not idiopathic and it may be named as "normoandrogenic hirsutism". Furthermore, it may not be a different entity but may be an early stage of hyperandrogenic disorders such as PCOS. Clinically, this can be find out by following-up patients with idiopathic hirsutism prospectively.
多毛症的特征是终毛以男性模式过度生长，其可能由多种原因引起，包括多囊卵巢综合征（PCOS）、非经典先天性肾上腺皮质增生、肾上腺或卵巢肿瘤，也可能是特发性的。特发性多毛症目前被定义为与正常排卵功能、正常血清雄激素水平和正常卵巢形态相关的多毛症，然而，特发性多毛症的发病机制尚不清楚。雄激素是刺激体毛生长的主要激素，因此，任何多毛症患者，无论血清雄激素水平是否正常，都应该存在任何形式的雄激素作用增强。根据这一科学事实，我们之前已经表明，尽管在正常范围内，但与健康受试者相比，特发性多毛症患者的血清雄激素水平相对较高（相对高雄激素血症），这让我们思考特发性多毛症真的是特发性的吗？除了相对高雄激素血症，我们之前还表明，与健康受试者相比，特发性多毛症女性在脐下区域和手臂皮肤中类固醇硫酸酯酶和17-β羟类固醇脱氢酶mRNA的表达更高，这有助于局部雄激素代谢。这些结果支持了这样一种观点，即在一些患者中，尽管肾上腺或卵巢不分泌导致高雄激素血症的雄激素增加量，但毛囊皮脂腺单位局部产生的雄激素增加量导致多毛症且无排卵功能障碍。在证实特发性多毛症患者存在相对高雄激素血症和局部雄激素合成可能增加后，我们认为特发性多毛症并非特发性，它可能被命名为“正常雄激素性多毛症”。此外，它可能不是一个不同的实体，而是可能是诸如PCOS等高雄激素性疾病的早期阶段。临床上，这可以通过对特发性多毛症患者进行前瞻性随访来发现。
