Asst. Prof. Dr. Rehab Jasem Mohammed &
Zahraa Emad Hussien
Department of chemistry, College of Education for Pure Sciences, University of Karbala, Iraq.
Polycystic ovarian syndrome (PCOS) is one of the most common endocrine disorders that affect women in their childbearing age. Globally, the incidence of this syndrome varies, ranging from 6% to 20%, depending on the diagnostic criteria applied (1). PCOS is a hormonal disorder that leads to an increase in the male hormone (androgen) and rises luteinizing hormone/ follicle-stimulating hormone ratio in females of reproductive age. Symptoms include irregular menstruation, ovarian cysts, infertility, excessive hair growth on the face and other places (hirsutism), acne and ovarian immaturity (2). Over the years, it turned from a disease into a syndrome. The cause or causes of PCOS remain unknown. Given its heterogeneous clinical symptoms, several causes are involved in the expansion of PCOS. The main clinical feature for diagnosing PCOS is hyperandrogenism (3). Statistics indicate that 80 per cent or more of females with PCOS show signs or symptoms of hyperandrogenism, including hirsutism, acne or alopecia (4). Also, one of the reasons that contribute to causing this disorder is the disruption of the regulation of the neuroendocrine gland that contributes to the production of androgens in the ovaries (5). Environmental factors also contribute to causing PCOS, as well as environmental factors that lead to a change in the action of insulin; obesity, weight gain cause endocrine disorders, insulin resistance, hyperinsulinemia and insulin resistance are among the main pathological factor in the development of PCOS. The metabolic and reproductive abnormalities of PCOS are mainly caused by lifestyle and diet (6). Also, genetic factors may be a cause of PCOS, as suggested by many studies that have been conducted on the possibility of PCOS revealed a high heritability of metabolic and endocrine features (7, 8).
References
1-Yildiz, B. O., Bozdag, G., Yapici, Z., Esinler, I., &Yarali, H. (2012). Prevalence, phenotype and cardiometabolic risk of polycystic ovary syndrome under different diagnostic criteria. Human reproduction, 27(10), 3067-3073.
2-Legro, R. S. (2008, January). New directions in polycystic ovary syndrome. In Seminars in reproductive medicine (Vol. 26, No. 01, pp. 003-004). © Thieme Medical Publishers.
3- Rojas, J., Chávez, M., Olivar, L., Rojas, M., Morillo, J., Mejías, J., … &Bermúdez, V. (2014). Polycystic ovary syndrome, insulin resistance, and obesity: navigating the pathophysiologic labyrinth. International journal of reproductive medicine, 2014.
4-Sirmans, S. M., & Pate, K. A. (2013). Epidemiology, diagnosis, and management of polycystic ovary syndrome. Clinical epidemiology, 1-13.
5- Goodarzi, M. O., Dumesic, D. A., Chazenbalk, G., &Azziz, R. (2011). Polycystic ovary syndrome: etiology, pathogenesis and diagnosis. Nature reviews endocrinology, 7(4), 219-231.
6- Diamanti-Kandarakis, E., Kandarakis, H., &Legro, R. S. (2006). The role of genes and environment in the etiology of PCOS. Endocrine, 30, 19-26.
7-Franks, S., Webber, L. J., Goh, M., Valentine, A., White, D. M., Conway, G. S., … & McCarthy, M. I. (2008). Ovarian morphology is a marker of heritable biochemical traits in sisters with polycystic ovaries. The Journal of Clinical Endocrinology & Metabolism, 93(9), 3396-3402.
8-Legro, R. S., Driscoll, D., Strauss III, J. F., Fox, J., &Dunaif, A. (1998). Evidence for a genetic basis for hyperandrogenemia in polycystic ovary syndrome. Proceedings of the National Academy of Sciences, 95(25), 14956-14960.
