Today’s Subject: Polycystic Ovarian Syndrome (PCOS).

It is interesting the people you come across when you are learning. While I was doing my Postgrad people would ask what I was studying (Female Endocrinology), after explaining exactly what that entails their faces would light up and say “oh I suffer from such-and-such” or “my partner has this.”  Then the questions would come and I was more than happy to answer. After all, the recall of information is a great way to cement knowledge.
One of the most common questions I would get would be about Polycystic Ovarian Syndrome (PCOS), which is becoming more and more prevalent in today’s society, particularly in the first and the developing world’s.

Polycystic Ovarian Syndrome (PCOS) can also be known as hyperandrogenic anovulation, or Stein- Leventhal Syndrome is a chronic heterogeneous disorder. It is a form of chronic anovulation which is related to excess androgen.
It is associated with issues such as irregular menstrual bleeding, reduced fertility, acne, obesity, excess hair growth and insulin resistance. It is a complex condition where a females ovaries are generally larger than average and the follicles struggle to grow to maturity, or they produce an ovum capable of fertilisation and often covered in cysts. It occurs in around 5 to 10% of reproducing aged females (Melmed et al 2011).

The cause of PCOS is not completely understood, but risk of developing the condition is increased with a positive family history of chronic anovulation and androgen excess.
An overproduction of the androgen hormone is associated as a contributing factor. Androgen is predominantly a male hormone but is also produced in the female reproductive system, but when it is produced in higher than normal levels this can cause an imbalance of the female sex hormones and as a result reduces the development and the subsequent release of the antral follicle, preventing ovulation occurring.
Insulin resistance is also an issue with PCOS. Insulin is a hormone produced in the pancreas and allows cells to use glucose. In regards to insulin resistance, the body’s ability to use insulin in an effective manner becomes impaired and the pancreas releases more insulin to allow the glucose to become available to the cells. This excess in insulin causes an increase in the production of androgen which as mentioned, restricts follicle development and the ovaries ability to ovulate.
Another possible cause is inflammation within the body (Melmed et al 2011). Literature suggests that females who suffer from PCOS have a type of low grade inflammation. This low grade inflammation stimulates the polycystic ovaries to produce excess amounts of androgens, however this may very well just be a result of PCOS as opposed to a cause and more research into this area needs to be conducted.

Females who suffer from PCOS have a higher mean concentration of Luteinizing Hormone (LH) but low levels of Follicle Stimulating Hormone (FSH) compared to the levels found in healthy females (Oberg et al 2005). These elevated levels of LH increase the sensitivity of the anterior pituitary gland to Gonadotropin Releasing Hormone (GnRH) stimulation which is manifested by the increase in LH pulse amplitude and frequency. This suggests the GnRH secretion is a causative factor. There is also a notable reduction in progesterone.
With the increase of LH pulse amplitude and frequency it also has an impact on increase circulating steady-state levels of oestrogens.
The increase in androgen levels as well as the LH pulse amplitude this has an effect on FSH levels. The levels of FSH remains constantly low with excess LH secretion. FSH is continuously stimulated but not to a point where full follicle maturation and ovulation can occur. Even though the follicle does not reach full maturation, its lifespan can be extended by several months, but in the form of follicular cysts. These cysts vary in size and are formed when follicles reach a certain size, some 2-10 mm and others as large as 15 mm (Melmed et al 2011). Hyperplastic theca cells will often luteinize in response to the higher levels of LH and surround these follicles. With an accumulation of follicles, this allows for an increase and a constant production of steroids in response to the steady-state levels of gonadotropins. These follicles will result in atresia but are replaced by new follicles which are limited to a similar growth potentials. This produces the consistent FSH production as well as increase in androgen levels.
Insulin resistance is a major factor in the pathophysiology of PCOS. However research shows that this is selective in the female population.
Insulin decreases the secretion of sex hormone-binding globulin (SHBG) which increases the availability of active androgens. Insulin directly increases the production of LH as well as androgens by activating its own receptors on the ovaries and the pituitary gland. Insulin binding to the anterior pituitary gland causes the release of LH hormone. The result is hyperandrogenism.

Other hormones have an impact as a result of PCOS. LH and FSH have been mentioned in depth but testosterone, dehydroepiandrosterone, and progesterone also deserve a quick mention.
Testosterone is primary a male sex hormone responsible for male sexual characteristics, but is also important in minimal amounts in the female reproductive system. In PCOS sufferers total testosterone levels of free and total testosterone are higher than in their healthy female counterparts. This excess of testosterone can be responsible for irregular or supressed menstruation and ovulation in sufferers.
Dehydroepiandrosterone (DHEA) is also primary a male hormone which is also important in female reproductive system, like testosterone tends to be at greater levels in females who suffer with PCOS.
Progesterone is crucial in the female reproductive system particularly in ovulation. If progesterone levels are low, then ovulation does not occur. Levels of progesterone in females who suffers PCOS tend to be a lot lower than healthy females.

PCOS occurs in around 5 to 10% of reproductive aged females. PCOS can be designed as the ppresence of hyperangrogenism and chronic anovulation in the absence of a specific adrenal or pituitary disease. Disease manifestations of PCOS and hyperandrogenism include hirsutism or the male pattern growth of hair on females such as the upper lip, chest, chin, abdomen and back. Acne which is related to hyperandrogenism particularly in adolescence females. Those with severe acne in adolescence as well as those who suffer well into adulthood should be tested for PCOS. Chronic anovulation such as amenorrhea or irregular menstrual bleeding is usually accompanied with infertility. However around 20% (Melmed et al 2011) of PCOS suffers do not suffer any form of menstrual abnormalities. Most PCOS suffers will experience menstrual abnormalities since menarche.
Significant weight gain is also a manifestation of the condition due in part to the excess oestrogen production. Diabetes risk due to insulin resistance, and as a result of diabetes, cardiovascular disease becomes a risk.

Although PCOS is condition that affects 5 to 10% of the female population whom are of reproductive age, there is still a great deal which research has not yet covered or is yet to make conclusions.
We do know that PCOS is the most common form of chronic ovulation which is associated with androgen excess, but there are many theories into the causative factors which need to be explored.

Aly Curd



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