Abstract
Polycystic ovarian syndrome (PCOS) is the most prevalent endocrine disorder affecting females. It is a common cause of menstrual irregularities and infertility during reproductive age. Genetic and hormonal factors play crucial role in the pathogenesis of PCOS. Low level of progesterone in PCOS causes overstimulation of immune system that produces more estrogen which leads to various autoantibodies. Different autoantibodies have been documented in PCOS, for example, anti-nuclear (ANA), anti-thyroid, anti-spermatic, anti-SM, anti-histone, anti-carbonic anhydrase, anti-ovarian, and anti-islet cell antibodies. There is an association between PCOS and autoimmune diseases such as ANA and anti-TPO that have been documented in systemic lupus erythematosus and Hashimoto thyroiditis, respectively, and it is suspected that there are autoantibodies that might affect the long term clinical management of these patients. Therefore fluctuating levels of autoantibodies in different PCOS patients give us the way to open new chapter for future research on molecular level. This may lead to discovery of better treatment options for PCOS in near future.
Highlights
In women polycystic ovarian syndrome (PCOS) was first described in 1935, by Stein and Leventhal [1, 2]
Hypothalamus secretes gonadotrophin releasing hormone (GnRH) which binds its receptors on secretory cells of adenohypophysis [10, 11]
The level of progesterone is decreased in PCOS which cannot suppress GnRH/luteinizing hormone (LH) pulse frequency in PCOS; increased estrogen secretion may lead to autoantibodies, for example, anti-nuclear, anti-thyroid, and anti-islet cell antibodies [16]
Summary
In women polycystic ovarian syndrome (PCOS) was first described in 1935, by Stein and Leventhal [1, 2]. In Pakistan about 5%– 10% of women were affected by PCOS in 2009 [6]. PCOS can affect females and males but with less frequency. Men do not have ovaries but underlying defects (high levels of androgens and low level steroid binding globulin) and clinical features of PCOS can be seen in males and they are referred to as SteinLeventhal syndrome (Figure 1) [13,14,15]. The level of progesterone is decreased in PCOS which cannot suppress GnRH/LH pulse frequency in PCOS; increased estrogen secretion may lead to autoantibodies, for example, anti-nuclear, anti-thyroid, and anti-islet cell antibodies [16]. Kerchner et al detected depression in 40% of women of PCOS and the incidence of suicide is increased up to 7-fold in PCOS (Figure 1) [23, 24]
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