PCOS and amenorrhea
Polycystic Ovarian Syndrome (PCOS) is a complicated syndrome which is characterized with on-going multiple follicles development in ovaries which produce high concentration of androgens (male hormones), particularly testosterone. Severe hormonal disbalance in PCOS ovaries is the main cause of menstrual dysfunctions – oligomenorrhea (rare periods) and/or amenorrhea (absence of periods).
The frequency of Polycystic Ovarian Syndrome in female population in reproductive age is about 6-8% and about 30-35% of obese women with Polycystic Ovarian Syndrome have secondary amenorrhea.
PCOS and amenorrhea – HORMONES
PCOS well known clinical triad include:
1) elevated Luteinizing Hormone (LH) and androgens (male hormones, mainly testosterone) with normal or low Follicle-Stimulating Hormone (FSH);
2) menstrual dysfunctions – mainly oligomenorrhea and amenorrhea with oligoovulation (rare ovulations) or anovulation (absence of ovulation);
3) polycystic appearing ovaries with multiple on-growing small and/or medium follicles.
In PCOS women the increased androgens’ production provokes high LH levels and decreased levels of FSH – this hormonal condition prevents ovaries to produce healthy mature egg (so called “dominant egg”) once per menstrual cycle. Without dominant egg production, ovaries produce multiple small follicles which swell with fluid and form into multiple cysts. Every time an egg is trapped within the follicle (because of anovulation), another cyst forms and as a result the ovary swells, sometimes reaching the size of a grapefruit. Increased androgens further arrest follicular development and result in anovulation. Without ovulation, progesterone is no longer produced, whereas estrogen levels remain normal.
In polycystic ovaries the multiple follicles produce large amounts of estradiol, which inhibits FSH release thereby preventing further follicular development.
Main cause of amenorrhea during Polycystic Ovarian Syndrome is elevated levels of androgens (hyperandrogenemia) which could also cause obesity, hirsutism (unwanted hair on face and body), acne and infertility. Sometimes hyperandrogenia could also develop voice change (deepening voice) and clitoral enlargement.
During PCOS amenorrhea could be discovered in severe cases with severely increased concentrations of androgens, obesity, insulin insensitivity and genetic predispositions.
Obese clients with Polycystic Ovarian Syndrome are more likely to be anovulatory, have symptoms of excess androgens and more often have amenorrhea. Excess adipose tissue increases peripheral conversion of androgens to estrone, which inhibits ovulation at hypothalamus level.
Polycystic Ovarian Syndrome is recognized as a high risk for insulin resistance – especially in women with different levels of obesity. Insulin resistance is associated with diabetes type 2, in which insulin levels are normal or high but the body cannot use this hormone efficiently. About 40-50% of clients with PCOS could have pre-diabetes or diabetes. Amenorrhea in these cases is also pretty common.
Anti-Mullerian Hormone (AMH) could be also involved in PCOS development. As AMH is involved in regulating the progression of follicles into growth phase, the abnormalities in AMH production (concentration) could be an important triggering factor for PCOS development.
In many but not all cases of Polycystic Ovarian Syndrome, insulin insensitivity, amenorrhea and obesity are observed. Combination of tree mentioned symptoms usually decreases the success rate of PCOS treatment (including infertility treatment).
Scientists discovered that about 20-23% of ovulating women could have symptoms of polycystic ovaries on ultrasound. It was also noted that about 70-75% women suffering from anovulation could also have polycystic ovaries. But in these mentioned situations women not always develop PCOS and/or amenorrhea. Only combination of polycystic ovaries, hyperandrogenia and oligomenorrhea could be the cause for following PCOS and amenorrhea.
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