Polycystic ovary syndrome: evolution of a concept.
Despite improved diagnostic facilities and advanced in vitro studies, the primary causes of the polycystic ovary syndrome (PCOS) have not been resolved. In addition to certain enzyme deficiencies causing a PCOS-like state, current evidence indicates altered functions of 5 alpha-reductase and cytochrome P450c17 alpha in PCOS patients as a group. However, it is not obvious if these are primary or secondary to the abnormal hormonal milieu. The relation of insulin-like growth factors (IGFs) to PCOS is of particular interest in view of the occurrence of IGF-II mRNA in the granulosa cells and the ability of IGF-I to regulate the granulosa cell and thecal-interstitial cell functions. In obese PCOS patients, the levels of sex hormone binding globulin and IGF-binding protein-1 are subnormal in serum, and fasting increases them. Fasting also suppresses high insulin and IGF-I concentrations in the same women. Growth hormone, regulated by insulin and probably by IGF-I, appears to be decreased in PCOS patients. Follicular growth, characteristically arrested in PCOS, is regulated by growth hormone to some extent, and growth hormone treatment has been found to improve the ovarian response to gonadotropins in some but not all anovulatory patients. In addition to the administration of growth hormone itself, therapeutic measures modulating the growth hormone-ovarian axis are being studied. High serum luteinizing hormone levels are typical of PCOS. These are often associated with infertility and early pregnancy loss. Lowering of the luteinizing hormone levels by a gonadotropin-releasing hormone analogue in combination with gonadotropins improves the outcome of pregnancies as compared with those achieved by clomiphene citrate. The use of the former regimen in PCOS patients may result in ovarian hyperstimulation. Ovarian electrocautery has proved to be effective in restoring cyclicity of ovarian function with a concomitant fall in luteinizing hormone and androgen levels. Interestingly, an increase in serum insulin secretion has been noted. It remains to be elucidated if this therapy, followed by decreased luteinizing hormone, is effective in reducing the elevated risk of miscarriages in women with PCOS.
Ruutiainen
K
K
Department of Obstetrics and Gynecology, Turku University Central Hospital, Finland.
Seppälä
M
M
D000022:Abortion, Spontaneous / Q000209:etiology; D005260:Female; D013006:Growth Hormone / Q000502:physiology; D006801:Humans; D007247:Infertility, Female / Q000209:etiology; D007333:Insulin Resistance; D007334:Insulin-Like Growth Factor I / Q000502:physiology; D007986:Luteinizing Hormone / Q000097:blood; D009765:Obesity / Q000150:complications; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000150:complications / Q000503:physiopathology / Q000628:therapy; D011247:Pregnancy
D007334:Insulin-Like Growth Factor I; D007986:Luteinizing Hormone; D013006:Growth Hormone