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In 2005, 4 million cases of PCOS were reported in the US, costing $4.36 billion in healthcare costs. In 2016 out of the National Institute Health's research budget of $32.3 billion for that year, 0.1% was spent on PCOS research. Among those aged between 14-44, PCOS is conservatively estimated to cost $4.37 billion per year.

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Signs and symptoms of PCOS include irregular or no menstrual periods, heavy periods, excess body and facial hair, acne, pelvic pain, difficulty getting pregnant, and patches of thick, darker, velvety skin. This metabolic, endocrine and reproductive disorder is not universally defined, but the most common symptoms are irregular or irregular absent periods, ovarian cysts, enlarged ovaries, excess androgen, weight gain and hirsutism [2] Associated conditions include type 2 diabetes, obesity, obstructive sleep apnea, heart disease, mood disorders, and endometrial cancer. This disease is related to the number of follicles per ovary each month growing from the average range of 6 to 8 to double, triple or more. it is important to distinguish between PCOS (the syndrome) and a woman with PCO (polycystic ovaries): to have PCOS, a woman must have at least two of these three symptoms (PCO, anovulation/oligoovulation and hyperandrogenism). This means that a woman can have PCOS (displaying anovulation and hyperandrogenism) without having PCO. At the same time, having polycystic ovaries does not relate necessary with the presence of PCOS.

Associated conditions

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Many individuals aren't under the impression that the first warning sign is usually a change in appearance. But there are also manifestations of mental health problems, such as anxiety, depression, and eating disorders. [3]

A diagnosis of PCOS suggests an increased risk of the following:

In 2005, 4 million cases of PCOS were reported in the US, costing $4.36 billion in healthcare costs.[4] In 2016 out of the National Institute Health's research budget of $32.3 billion for that year, 0.1% was spent on PCOS research.[5]Among those aged between 14-44, PCOS is conservatively estimated to cost $4.37 billion per year.[6]

As opposed to women in the general population, women with PCOS experience higher rates of depression and anxiety. International guidelines and Indian guidelines suggest psychosocial factors should be considered in women with PCOS, as well as screenings for depression and anxiety.[7]Globally, this aspect has been increasingly focused on because it reflects the true impact of PCOS on the lives of patients. Research shows that PCOS adversely impacts a patient's quality of life. [8]

Not all women with PCOS have difficulty becoming pregnant. But for some women with PCOD may have difficulty getting pregnant since their body does not produce the hormones necessary for regular ovulation.[9] PCOD might also increase the risk of miscarriage or premature delivery. However, it is possible to have a normal pregnancy. Including medical care and a healthy lifestyle to follow.

The condition was first described in 1935 by American gynecologists Irving F. Stein, Sr. and Michael L. Leventhal, from whom its original name of Stein–Leventhal syndrome is taken.[10][11] Stein and Leventhal first described PCOS as an endocrine disorder in the United States, and since then, it has become recognized as one of the most common causes of oligo ovulatory infertility among women. [12]

Environment

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PCOS may be related to or worsened by exposures during the prenatal period, epigenetic factors, environmental impacts (especially industrial endocrine disruptors,[13] such as bisphenol A and certain drugs) and the increasing rates of obesity.[13][14][15][16][17][18][19][excessive citations] Along with PCOS appearing to be inherited as a complex genetic trait that is characterized by both androgen excess and ovulatory dysfunction.[20]


The genetic component appears to be inherited in an autosomal dominant fashion with high genetic penetrance but variable expressivity in females; this means that each child has a 50% chance of inheriting the predisposing genetic variant(s) from a parent, and, if a daughter receives the variant(s), the daughter will have the disease to some extent.[21][22][23][24] The genetic variant(s) can be inherited from either the father or the mother, and can be passed along to both sons (who may be asymptomatic carriers or may have symptoms such as early baldness and/or excessive hair) and daughters, who will show signs of PCOS.[22][24] The phenotype appears to manifest itself at least partially via heightened androgen levels secreted by ovarian follicle theca cells from women with the allele.[23] The exact gene affected has not yet been identified.[25][21][26] In rare instances, single-gene mutations can give rise to the phenotype of the syndrome.[27] Current understanding of the pathogenesis of the syndrome suggests, however, that it is a complex multigenic disorder.[28]

Due to the scarcity of large-scale screening studies, the prevalence of endometrial abnormalities in PCOS remains unknown, though women with the condition may be at increased risk for endometrial hyperplasia and carcinoma as well as menstrual dysfunction and infertility.

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References

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  1. ^ Azziz, Ricardo (01 August 2005). "Health Care-Related Economic Burden of the Polycystic Ovary Syndrome during the Reproductive Life Span". The Journal of Clinical Endocrinology & Metabolism. 90. {{cite journal}}: Check date values in: |date= (help)
  2. ^ "What We Talk About When We Talk About PCOS". www.vice.com. Retrieved 2022-01-19.
  3. ^ "What We Talk About When We Talk About PCOS". www.vice.com. Retrieved 2022-01-19.
  4. ^ Azziz R, Marin C, Hoq L, Badamgarav E, Song P (August 2005). "Health care-related economic burden of the polycystic ovary syndrome during the reproductive life span". The Journal of Clinical Endocrinology and Metabolism. 90 (8): 4650–4658. doi:10.1210/jc.2005-0628. PMID 15944216.
  5. ^ "RCDC Estimates of Funding for Various Research, Condition, and Disease Categories (RCDC)". NIH. NIH. Retrieved 3 December 2018.
  6. ^ Azziz R (March 2006). "Controversy in clinical endocrinology: diagnosis of polycystic ovarian syndrome: the Rotterdam criteria are premature". The Journal of Clinical Endocrinology and Metabolism. 91 (3): 781–785. doi:10.1210/jc.2005-2153. PMID 16418211.
  7. ^ Chaudhari, Aditi P.; Mazumdar, Kaustubh; Mehta, Pooja Deepak (2018). "Anxiety, Depression, and Quality of Life in Women with Polycystic Ovarian Syndrome". Indian Journal of Psychological Medicine. 40 (3): 239–246. doi:10.4103/IJPSYM.IJPSYM_561_17. ISSN 0253-7176. PMC 5968645. PMID 29875531.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  8. ^ Chaudhari, Aditi P.; Mazumdar, Kaustubh; Mehta, Pooja Deepak (2018). "Anxiety, Depression, and Quality of Life in Women with Polycystic Ovarian Syndrome". Indian Journal of Psychological Medicine. 40 (3): 239–246. doi:10.4103/IJPSYM.IJPSYM_561_17. ISSN 0253-7176. PMC 5968645. PMID 29875531.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  9. ^ "Erase the Dread and Stigma of PCOD". Matria. Retrieved 2022-01-19.
  10. ^ Imaging in Polycystic Ovary Disease at eMedicine
  11. ^ Polycystic Ovarian Syndrome at eMedicine
  12. ^ Barry JA, Azizia MM, Hardiman PJ (1 September 2014). "Risk of endometrial, ovarian and breast cancer in women with polycystic ovary syndrome: a systematic review and meta-analysis". Human Reproduction Update. 20 (5): 748–758. doi:10.1093/humupd/dmu012. PMC 4326303. PMID 24688118.
  13. ^ a b Palioura E, Diamanti-Kandarakis E (December 2013). "Industrial endocrine disruptors and polycystic ovary syndrome". Journal of Endocrinological Investigation. 36 (11): 1105–1111. doi:10.1007/bf03346762. PMID 24445124. S2CID 27141519.
  14. ^ Hoeger KM (May 2014). "Developmental origins and future fate in PCOS". Seminars in Reproductive Medicine. 32 (3): 157–158. doi:10.1055/s-0034-1371086. PMID 24715509.
  15. ^ Harden CL (2005). "Polycystic ovaries and polycystic ovary syndrome in epilepsy: evidence for neurogonadal disease". Epilepsy Currents. 5 (4): 142–146. doi:10.1111/j.1535-7511.2005.00039.x. PMC 1198730. PMID 16151523.
  16. ^ Rasgon N (June 2004). "The relationship between polycystic ovary syndrome and antiepileptic drugs: a review of the evidence". Journal of Clinical Psychopharmacology. 24 (3): 322–334. doi:10.1097/01.jcp.0000125745.60149.c6. PMID 15118487. S2CID 24603227.
  17. ^ Hu X, Wang J, Dong W, Fang Q, Hu L, Liu C (November 2011). "A meta-analysis of polycystic ovary syndrome in women taking valproate for epilepsy". Epilepsy Research. 97 (1–2): 73–82. doi:10.1016/j.eplepsyres.2011.07.006. PMID 21820873. S2CID 26422134.
  18. ^ Abbott DH, Barnett DK, Bruns CM, Dumesic DA (2005). "Androgen excess fetal programming of female reproduction: a developmental aetiology for polycystic ovary syndrome?". Human Reproduction Update. 11 (4): 357–374. doi:10.1093/humupd/dmi013. PMID 15941725.
  19. ^ Rutkowska A, Rachoń D (April 2014). "Bisphenol A (BPA) and its potential role in the pathogenesis of the polycystic ovary syndrome (PCOS)". Gynecological Endocrinology. 30 (4): 260–265. doi:10.3109/09513590.2013.871517. PMID 24397396. S2CID 5828672.
  20. ^ Azziz, Ricardo; Marin, Catherine; Hoq, Lalima; Badamgarav, Enkhe; Song, Paul (2005-08-01). "Health Care-Related Economic Burden of the Polycystic Ovary Syndrome during the Reproductive Life Span". The Journal of Clinical Endocrinology & Metabolism. 90 (8): 4650–4658. doi:10.1210/jc.2005-0628. ISSN 0021-972X.
  21. ^ a b Legro RS, Strauss JF (September 2002). "Molecular progress in infertility: polycystic ovary syndrome". Fertility and Sterility. 78 (3): 569–576. doi:10.1016/S0015-0282(02)03275-2. PMID 12215335.
  22. ^ a b Crosignani PG, Nicolosi AE (2001). "Polycystic ovarian disease: heritability and heterogeneity". Human Reproduction Update. 7 (1): 3–7. doi:10.1093/humupd/7.1.3. PMID 11212071.
  23. ^ a b Strauss JF (November 2003). "Some new thoughts on the pathophysiology and genetics of polycystic ovary syndrome". Annals of the New York Academy of Sciences. 997 (1): 42–48. Bibcode:2003NYASA.997...42S. doi:10.1196/annals.1290.005. PMID 14644808. S2CID 23559461.
  24. ^ a b Hamosh A (12 September 2011). "POLYCYSTIC OVARY SYNDROME 1; PCOS1". OMIM. McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine. Archived from the original on 16 July 2015. Retrieved 15 November 2011.
  25. ^ Diamanti-Kandarakis E, Kandarakis H, Legro RS (August 2006). "The role of genes and environment in the etiology of PCOS". Endocrine. 30 (1): 19–26. doi:10.1385/ENDO:30:1:19. PMID 17185788. S2CID 21220430.
  26. ^ Amato P, Simpson JL (October 2004). "The genetics of polycystic ovary syndrome". Best Practice & Research. Clinical Obstetrics & Gynaecology. 18 (5): 707–718. doi:10.1016/j.bpobgyn.2004.05.002. PMID 15380142.
  27. ^ Draper N, Walker EA, Bujalska IJ, Tomlinson JW, Chalder SM, Arlt W, et al. (August 2003). "Mutations in the genes encoding 11beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to cause cortisone reductase deficiency". Nature Genetics. 34 (4): 434–439. doi:10.1038/ng1214. PMID 12858176. S2CID 22772927.
  28. ^ Ehrmann DA (March 2005). "Polycystic ovary syndrome". The New England Journal of Medicine. 352 (12): 1223–1236. doi:10.1056/NEJMra041536. PMID 15788499.
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