Hyperandrogenism in PCOS contributed from ovary and adrenal glands
clinically manifests as hirsutism, acne, and alopecia. In PCOS, LH hypersecretion over
FSH occurs due to increased frequency of pulsatile secretion of gonadotropin-releasing
hormone. In contrast to an associated deficiency in FSH, excess LH promotes ovarian
androgen production, or FSH resistance harms follicular development. In PCOS
women, LH:FSH ratio alteration leads to ovarian theca cell proliferation, which leads
to elevated steroidogenesis and, eventually, hyperandrogenism. There are 5 types of
androgen in women: Dehydroepiandrosterone Sulfate (DHEAS), Androstenedione
(A4), Testosterone (T), Dehydroepiandrosterone (DHEA), and Dihydrotestosterone
(DHT). Among these androgens, testosterone and DHT are more active than others.
Androgen is also secreted from the adrenal gland in small amounts. By the enzyme
aromatase, testosterone converts to estradiol, both of which coordinate the function of
reproductive function in women. Excess of androgen from the ovary causes ovarian
follicular changes, leading to anovulation and menstrual irregularities. Not only the
development but the progression of PCOS is also influenced by hyperandrogenism.
Complications of PCOS, such as type 2 diabetes, hypertension, and obesity, also occur
by hyperandrogenism, increasing insulin resistance. Thus, it is important to address this
hyperandrogenism clinically to stop the progression and complications of PCOS.
Keywords: Hyperandrogenemia, Insulin resistance, Lifestyle modifications, Metformin, Nonalcoholic fatty liver disease, Polycystic ovary syndrome.
