Journal articles: 'Polycystic ovary syndrome Pathophysiology'

1

Mauvais-Jarvis, Pierre, and Claire Bricaire. "Pathophysiology of polycystic ovary syndrome." Journal of Steroid Biochemistry 33, no. 4 (October 1989): 791–94. http://dx.doi.org/10.1016/0022-4731(89)90494-9.

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Taketani, Yuji. "Pathophysiology of Polycystic Ovary Syndrome." Hormone Research 33, no. 2 (1990): 3–4. http://dx.doi.org/10.1159/000181556.

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Tsilchorozidou, Tasoula, Caroline Overton, and Gerard S. Conway. "The pathophysiology of polycystic ovary syndrome." Clinical Endocrinology 60, no. 1 (January 2004): 1–17. http://dx.doi.org/10.1046/j.1365-2265.2003.01842.x.

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Whitaker, Kristin Nadine. "Polycystic Ovary Syndrome." Journal of Pharmacy Practice 24, no. 1 (November 30, 2010): 94–101. http://dx.doi.org/10.1177/0897190010384632.

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Polycystic ovary syndrome is the most common endocrine disorder in women of reproductive age. It affects 6% to 7% of the population and is characterized by hyperandrogenism and ovarian dysfunction. Women with the disorder often present with insulin resistance and obesity, making it importance for health care providers to monitor closely for signs and symptoms of metabolic syndrome and type 2 diabetes. Treatments are targeted toward improving insulin tolerance, reducing signs and symptoms of hyperandrogenism (hirsutism, anovulation, etc), restoring normal menstrual cycle function, and restoring fertility. Major treatment should include weight management through diet and exercise, regardless of body mass index and might include concurrent drug therapy. It is important that pharmacists understand the underlying pathophysiology of the disease and the available treatments, in addition to the importance of reducing risk of metabolic syndrome/type 2 diabetes, and cardiovascular disease in these patients.

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Guzick, David. "Polycystic ovary syndrome: Symptomatology, pathophysiology, and epidemiology." American Journal of Obstetrics and Gynecology 179, no. 6 (December 1998): S89—S93. http://dx.doi.org/10.1016/s0002-9378(98)70238-8.

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Platt, Terrie H. "Polycystic ovary syndrome: Diagnosis and management." Women’s Healthcare: A Clinical Journal for NPs 10, no. 5 (October 12, 2022): 08–42. http://dx.doi.org/10.51256/whc102208.

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The author reviews prevalence, pathophysiology, assessment and diagnostic considerations, and treatment options for polycystic ovary syndrome to help nurse practitioners recognize it and provide evidence-based patient counseling and management.

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Cunningham, Priscilla. "Pathophysiology, diagnosis and treatment of polycystic ovary syndrome." Nursing Standard 31, no. 39 (May 24, 2017): 44–51. http://dx.doi.org/10.7748/ns.2017.e10595.

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Spritzer, Poli, Carolina Barone, and Fabiana Oliveira. "Hirsutism in Polycystic Ovary Syndrome: Pathophysiology and Management." Current Pharmaceutical Design 22, no. 36 (November 11, 2016): 5603–13. http://dx.doi.org/10.2174/1381612822666160720151243.

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C., Muhas, Nishad K. M., Ummunnoora K. P., Jushna K., Saheera K. V., and Dilsha K. P. "POLYCYSTIC OVARY SYNDROME (PCOS)–AN OVERVIEW." International Journal of Current Pharmaceutical Research 10, no. 6 (November 30, 2018): 5. http://dx.doi.org/10.22159/ijcpr.2018v10i6.30969.

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Polycystic ovary syndrome (PCOS) is one of most common female endocrine disorder that affects 6-15% of the female population. Women with PCOS have a hormonal imbalance and metabolism problems that may affect their overall health and appearance. Androgen excess and insulin resistance are currently recognized to be responsible for much of the phenotypic presentation, though insulin resistance is far from universally present. It is characterized by irregular menstrual cycle, acne and also associated with type-2 diabetes mellitus and cardiovascular disease. Efficient management of PCOS provides a prospective window of opportunity to avoid the risk of associated complications. Treatment is broadly aimed at tackling (IR), effects of hyperandrogenism, irregular menstruation, and infertility. This review article mainly deals with the etiology, pathophysiology, diagnosis and management of Polycystic ovary syndrome.

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Soni, Abhishek, Shivali Singla, and Sachin Goyal. "POLYCYSTIC OVARY SYNDROME: PATHOGENESIS, TREATMENT AND SECONDARY ASSOCIATED DISEASES." Journal of Drug Delivery and Therapeutics 8, no. 5 (September 6, 2018): 107–12. http://dx.doi.org/10.22270/jddt.v8i5.1892.

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Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women of reproductive age. It is characterized by hyperandrogenism, polycystic ovaries, and chronic anovulation along with insulin resistance, hyperinsulinemia, abdominal obesity, hypertension, and dyslipidemia as frequent metabolic traits (metabolic syndrome) that culminate in serious long-term consequences such as type 2 diabetes mellitus, endometrial hyperplasia, and coronary artery disease. It is one of the most common causes of anovulatory infertility. A complete understanding of the underlying Pathophysiology of PCOS is still lacking. Because of the heterogeneity of this disorder, there are most likely multiple underlying pathophysiologic mechanisms. Pathogenesis of PCOS is explaining as alteration in gonadotropin-releasing hormone secretion results in increased luteinizing hormone (LH) secretion. An alteration in insulin secretion and insulin action results in hyperinsulinemia and insulin resistance. A defect in androgen synthesis that results in increased ovarian androgen production.Treatment of PCOS include maintaining a normal endometrium, antagonizing the actions of androgens on target tissues, reducing insulin resistance (when present), and correcting anovulation. Women with polycystic ovary syndrome (PCOS) are at higher risk for several other health conditions as Insulin Resistance, Metabolic Syndrome, Type 2 Diabetes, Obesity, Heart Disease and High Blood Pressure (Cardiovascular Disease)

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Barnes, Randall. "Pathophysiology of Ovarian Steroid Secretion in Polycystic Ovary Syndrome." Seminars in Reproductive Medicine 15, no. 02 (May 1997): 159–68. http://dx.doi.org/10.1055/s-2007-1016297.

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Carmina, Enrico, and R. A. Lobo. "Adrenal hyperandrogenism in the pathophysiology of polycystic ovary syndrome." Journal of Endocrinological Investigation 21, no. 9 (October 1998): 580–88. http://dx.doi.org/10.1007/bf03350783.

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Hu, Cong, Bo Pang, Zhanchuan Ma, and Huanfa Yi. "Immunophenotypic Profiles in Polycystic Ovary Syndrome." Mediators of Inflammation 2020 (March 19, 2020): 1–10. http://dx.doi.org/10.1155/2020/5894768.

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Polycystic ovary syndrome (PCOS) a long-known endocrinopathy and one of the most common endocrine-reproductive-metabolic disorders in women, which can lead to infertility. Although the precise etiology remains unclear, PCOS is considered as a complex genetic trait, with a high degree of heterogeneity. Besides, hormones and immune cells, including both innate and adaptive immune cells, are reportedly a cross talk in PCOS. Chronic low-grade inflammation increases autoimmune disease risk. This proinflammatory condition may, in turn, affect vital physiological processes that ultimately cause infertility, such as ovulation failure and embryo implantation. Here, we review the accumulating evidence linking PCOS with inflammatory status providing an overview of the underlying hormone-mediated dysregulation of immune cells. We mainly focus on the correlational evidence of associations between immune status in women and the increased prevalence of PCOS, along with the specific changes in immune responses. Further recognition and exploration of these interactions may help elucidate PCOS pathophysiology and highlight targets for its treatment and prevention.

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Rajska, Anna, Magdalena Buszewska-Forajta, Dominik Rachoń, and Michał Jan Markuszewski. "Metabolomic Insight into Polycystic Ovary Syndrome—An Overview." International Journal of Molecular Sciences 21, no. 14 (July 9, 2020): 4853. http://dx.doi.org/10.3390/ijms21144853.

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Searching for the mechanisms of the polycystic ovary syndrome (PCOS) pathophysiology has become a crucial aspect of research performed in the last decades. However, the pathogenesis of this complex and heterogeneous endocrinopathy remains unknown. Thus, there is a need to investigate the metabolic pathways, which could be involved in the pathophysiology of PCOS and to find the metabolic markers of this disorder. The application of metabolomics gives a promising insight into the research on PCOS. It is a valuable and rapidly expanding tool, enabling the discovery of novel metabolites, which may be the potential biomarkers of several metabolic and endocrine disorders. The utilization of this approach could also improve the process of diagnosis and therefore, make treatment more effective. This review article aims to summarize actual and meaningful metabolomic studies in PCOS and point to the potential biomarkers detected in serum, urine, and follicular fluid of the affected women.

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Aftab, Mansoor, Muhammad Inzamam, and Shahid Latif. "Polycystic Ovary Syndrome: An Update on Management Strategies." Pakistan Journal of Medical and Health Sciences 16, no. 4 (April 30, 2022): 654–57. http://dx.doi.org/10.53350/pjmhs22164654.

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In the reproductive years of a female, she often comes up with a common disorder known as polycystic ovary syndrome also called as PCOS. In this disorder the level of androgen, male hormone, increases above the normal level that causes ovulatory dysfunctioning. Moreover, this disorder also causes severe metabolic anomalies, specifically weight gain and insulin resistance which is a well-known attribute of the pathophysiology of PCOS. PCOS leaves adverse impacts upon the ovarian cycle and fertility of women. This review paper encapsulates possible treatments present for PCOS in females by discussing current and potentially available options. Keywords: Obesity, polycystic ovary syndrome, hirsutism, therapeutic approach.

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Ruddenklau, Amy, and Rebecca E. Campbell. "Neuroendocrine Impairments of Polycystic Ovary Syndrome." Endocrinology 160, no. 10 (July 2, 2019): 2230–42. http://dx.doi.org/10.1210/en.2019-00428.

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Abstract Polycystic ovary syndrome (PCOS) is a prevalent and distressing disorder of largely unknown etiology. Although PCOS defined by ovarian dysfunction, accumulating evidence supports a critical role for the brain in the ontogeny and pathophysiology of PCOS. A critical pathological feature of PCOS is impaired gonadal steroid hormone negative feedback to the GnRH neuronal network in the brain that regulates fertility. This impairment is associated with androgen excess, a cardinal feature of PCOS. Impaired steroid hormone feedback to GnRH neurons is thought to drive hyperactivity of the neuroendocrine axis controlling fertility, leading to a vicious cycle of androgen excess and reproductive dysfunction. Decades of clinical research have been unable to uncover the mechanisms underlying this impairment, because of the extreme difficulty in studying the brain in humans. It is only recently, with the development of preclinical models of PCOS, that we have begun to unravel the role of the brain in the development and progression of PCOS. Here, we provide a succinct overview of what is known about alterations in the steroid hormone–sensitive GnRH neuronal network that may underlie the neuroendocrine defects in clinical PCOS, with a particular focus on those that may contribute to impaired progesterone negative feedback, and the likely role of androgens in driving this impairment.

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Pasquali, Renato. "Contemporary approaches to the management of polycystic ovary syndrome." Therapeutic Advances in Endocrinology and Metabolism 9, no. 4 (February 7, 2018): 123–34. http://dx.doi.org/10.1177/2042018818756790.

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Polycystic ovary syndrome (PCOS) is a common disorder in women in their reproductive years and is characterized by androgen excess, ovulatory dysfunction, and polycystic ovarian morphology. It is also associated with several metabolic abnormalities, particularly insulin resistance and obesity, which play an important role in the pathophysiology of PCOS and, in particular, negatively influence ovarian function and fertility. This review article summarizes the available treatment for women with PCOS. Specifically, current and potentially new therapies are discussed.

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Boqun, Xu, Dai Xiaonan, Cui YuGui, Gao Lingling, Dai Xue, Chao Gao, Diao Feiyang, et al. "Expression of SET Protein in the Ovaries of Patients with Polycystic Ovary Syndrome." International Journal of Endocrinology 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/367956.

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Background. We previously found that expression of SET gene was up-regulated in polycystic ovaries by using microarray. It suggested that SET may be an attractive candidate regulator involved in the pathophysiology of polycystic ovary syndrome (PCOS). In this study, expression and cellular localization of SET protein were investigated in human polycystic and normal ovaries.Method. Ovarian tissues, six normal ovaries and six polycystic ovaries, were collected during transsexual operation and surgical treatment with the signed consent form. The cellular localization of SET protein was observed by immunohistochemistry. The expression levels of SET protein were analyzed by Western Blot.Result. SET protein was expressed predominantly in the theca cells and oocytes of human ovarian follicles in both PCOS ovarian tissues and normal ovarian tissues. The level of SET protein expression in polycystic ovaries was triple higher than that in normal ovaries(P<0.05).Conclusion. SET was overexpressed in polycystic ovaries more than that in normal ovaries. Combined with its localization in theca cells, SET may participate in regulating ovarian androgen biosynthesis and the pathophysiology of hyperandrogenism in PCOS.

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Wallach, Edward E., Richard P. Buyalos, and C. Terence Lee. "Polycystic ovary syndrome: pathophysiology and outcome with in vitro fertilization." Fertility and Sterility 65, no. 1 (January 1996): 1–10. http://dx.doi.org/10.1016/s0015-0282(16)58017-0.

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Yuliadha, Asti, and Rohmaningtyas Hidayah Setyaningrum. "Psikoneuroimunologi Depresi pada Polycystic Ovary Syndrome (PCOS)." Smart Medical Journal 5, no. 1 (April 20, 2022): 38. http://dx.doi.org/10.13057/smj.v5i1.43238.

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Introduction: Polycystic ovary syndrome (PCOS) is heterogeneous, complex endocrine disorder with unknown etiology, affecting 4%−18% of reproductive age women and associated with reproductive, metabolic and psychological dysfunction. Along with physical disorders, many mental disorders are also associated with PCOS, about 40% of women with PCOS have depression. This literature review aims to explore how PCOS can lead to depression in term of psychoneuroimmunology aspects.Method: Literature review was conducted through search engine from Google Scholar and Clinical Key with keywords “Polycystic ovary syndrome”, “depression”, “psychoneuroimmunology”, “distress”, and “inflammation” from 2015-2020.Result: The important role of the HPG axis in the pathophysiology of mood disorder has concluded that high comorbidity between depression and PCOS are caused by hyperandrogenism and insulin resistance mediated by low grade chronic inflammation. The activation of HPA by stress exerts an inhibitory effect on the female reproductive system. CRH can inhibit GnRH secretion from the hypothalamus. The anti-reproductive action of CRH in the ovaries of women with high psychosocial stress lead to early ovarian failure. In addition, the pathophysiology of depression and mental stress in PCOS is associated with various changes including high activity of pro-inflammation markers and the body's immune system during stress, it has also been linked to increased cortisol levels, increased sympathetic activity and decreased serotonin levels in the central nervous system.Result: There’s close relationship between PCOS and depression in terms of psychoneuroimmunology aspects, by HPG axis role. Comprehensive management of depression is improving outcome strategy in women with PCOS by involving CLP.Keywords: Polycystic ovary syndrome (PCOS), Depression, Psychoneuroimmunology, HPG axis

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Yuliadha, Asti, and Rohmaningtyas Hidayah Setyaningrum. "Psikoneuroimunologi Depresi pada Polycystic Ovary Syndrome (PCOS)." Smart Medical Journal 5, no. 1 (April 20, 2022): 38. http://dx.doi.org/10.13057/smj.v5i1.43238.

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Introduction: Polycystic ovary syndrome (PCOS) is heterogeneous, complex endocrine disorder with unknown etiology, affecting 4%−18% of reproductive age women and associated with reproductive, metabolic and psychological dysfunction. Along with physical disorders, many mental disorders are also associated with PCOS, about 40% of women with PCOS have depression. This literature review aims to explore how PCOS can lead to depression in term of psychoneuroimmunology aspects.Method: Literature review was conducted through search engine from Google Scholar and Clinical Key with keywords “Polycystic ovary syndrome”, “depression”, “psychoneuroimmunology”, “distress”, and “inflammation” from 2015-2020.Result: The important role of the HPG axis in the pathophysiology of mood disorder has concluded that high comorbidity between depression and PCOS are caused by hyperandrogenism and insulin resistance mediated by low grade chronic inflammation. The activation of HPA by stress exerts an inhibitory effect on the female reproductive system. CRH can inhibit GnRH secretion from the hypothalamus. The anti-reproductive action of CRH in the ovaries of women with high psychosocial stress lead to early ovarian failure. In addition, the pathophysiology of depression and mental stress in PCOS is associated with various changes including high activity of pro-inflammation markers and the body's immune system during stress, it has also been linked to increased cortisol levels, increased sympathetic activity and decreased serotonin levels in the central nervous system.Result: There’s close relationship between PCOS and depression in terms of psychoneuroimmunology aspects, by HPG axis role. Comprehensive management of depression is improving outcome strategy in women with PCOS by involving CLP.Keywords: Polycystic ovary syndrome (PCOS), Depression, Psychoneuroimmunology, HPG axis

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Lathief, Sanam, and Lubna Pal. "Advances in Treatment Options for Polycystic Ovary Syndrome." US Endocrinology 08, no. 01 (2012): 57. http://dx.doi.org/10.17925/use.2012.08.01.57.

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Polycystic ovary syndrome (PCOS) is the most common endocrinopathy seen in women of reproductive age. Clinical concerns relating to PCOS range from ovulatory infertility and menstrual disorders to risk of diabetes and cardiovascular disease. Hormonal contraceptives have been the mainstay of the management of common PCOS symptoms, such as menstrual irregularity and clinical stigmata of androgen excess (i.e., hirsutism and acne). An appreciation of the relevance of metabolic pathways in the pathophysiology of PCOS is relatively recent, and has translated into an expansion of the therapeutic strategies available for the management of PCOS. Insulin sensitizers were one of the first metabolic modulators to be incorporated in the clinical management paradigm, albeit with mixed results. Recognizing that insulin resistance is central to the pathophysiology of PCOS, newer agents—e.g., thiazolidinediones— followed, with almost comparable efficacy to metformin. Statins and most recently incretins constitute novel therapies with distinct metabolic targets that seem to hold promise in the management of PCOS. In tandem with the expansion in pharmaceuticals, a host of complementary and alternative medical therapies have generated interest for purported promise in the management of PCOS, including vitamin D, acarbose, and myo-inositol. The therapeutic options for managing PCOS-related infertility have also expanded. Clomiphene citrate (CC) has long been the first-line strategy for ovulation induction in the setting of anovulatory infertility; however, aromatase inhibitors are fast gaining acceptance as an ovulation induction strategy, with results comparable or even better than those seen with CC. An increasing level of therapeutic sophistication is reflected in ovarian stimulation protocols judiciously using gonadotropins, gonadotropin-releasing hormone antagonists, the procedure of ovarian drilling, and assisted reproductive technologies within vitrooocyte maturation.

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Garruti, Gabriella, Raffaella Depalo, Maria Grazia Vita, Filomenamila Lorusso, Federica Giampetruzzi, Aurelia Bellomo Damato, and Francesco Giorgino. "Adipose tissue, metabolic syndrome and polycystic ovary syndrome: from pathophysiology to treatment." Reproductive BioMedicine Online 19, no. 4 (October 2009): 552–63. http://dx.doi.org/10.1016/j.rbmo.2009.05.010.

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Essah, Paulina, Kai Cheang, and John Nestler. "The Pathophysiology of Miscarriage in Women with Polycystic Ovary Syndrome. Review and Proposed Hypothesis of Mechanisms Involved." HORMONES 3, no. 4 (October 15, 2004): 221–27. http://dx.doi.org/10.14310/horm.2002.11130.

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Yesiladali, Mert, Melis G. K. Yazici, Erkut Attar, and Fahrettin Kelestimur. "Differentiating Polycystic Ovary Syndrome from Adrenal Disorders." Diagnostics 12, no. 9 (August 24, 2022): 2045. http://dx.doi.org/10.3390/diagnostics12092045.

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Although polycystic ovary syndrome (PCOS) is primarily considered a hyperandrogenic disorder in women characterized by hirsutism, menstrual irregularity, and polycystic ovarian morphology, an endocrinological investigation should be performed to rule out other hyperandrogenic disorders (e.g., virilizing tumors, non-classical congenital adrenal hyperplasia (NCAH), hyperprolactinemia, and Cushing’s syndrome) to make a certain diagnosis. PCOS and androgen excess disorders share clinical features such as findings due to hyperandrogenism, findings of metabolic syndrome, and menstrual abnormalities. The diagnosis of a woman with these symptoms is generally determined based on the patient’s history and rigorous clinical examination. Therefore, distinguishing PCOS from adrenal-originated androgen excess is an indispensable step in diagnosis. In addition to an appropriate medical history and physical examination, the measurement of relevant basal hormone levels and dynamic tests are required. A dexamethasone suppression test is used routinely to make a differential diagnosis between Cushing’s syndrome and PCOS. The most important parameter for differentiating PCOS from NCAH is the measurement of basal and ACTH-stimulated 17-OH progesterone (17-OHP) when required in the early follicular period. It should be kept in mind that rapidly progressive hyperandrogenic manifestations such as hirsutism may be due to an androgen-secreting adrenocortical carcinoma. This review discusses the pathophysiology of androgen excess of both adrenal and ovarian origins; outlines the conditions which lead to androgen excess; and aims to facilitate the differential diagnosis of PCOS from certain adrenal disorders.

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Maqbool, Mudasir, Mohmad Amin Dar, Imran Gani, and Mohammad Ishaq Geer. "Insulin Resistance and Polycystic ovary Syndrome: A Review." Journal of Drug Delivery and Therapeutics 9, no. 1-s (February 15, 2019): 433–36. http://dx.doi.org/10.22270/jddt.v9i1-s.2275.

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Polycystic Ovary Syndrome (PCOS) is the most common, yet complex, endocrine disorder affecting women in their reproductive years and is a leading cause of infertility. This disease appears to be multifactorial and polygenic in nature involving multisystem dysfunction, namely reproduction, endocrine and metabolic. Hyperandrogenism and insulin resistance appear to be central cause to the pathophysiology of the disease. The glucose and insulin metabolism pathways have been studied and debated to understand whether Insulin Resistance is due to a defect in insulin action or a primary defect in β-cell function or decreased hepatic clearance of insulin, or a combination of all these factors. Numerous studies have demonstrated that obese, normal weight and thin women with PCOS have a form of insulin resistance that is unique and intrinsic to the disorder. Moreover obese women with PCOS possess an additional burden of insulin resistance resulting from their excess adiposity. Hyperinsulinemia leads to increase in androgen production directly by acting as a co-gonadotropin, augmenting Luteinizing Hormone activity within the ovary, and indirectly by increasing serum LH pulse amplitude. Whereas Androgens may in turn contribute at least partially to the insulin resistance state linked with PCOS. In this review, we will briefly study the role of insulin resistance in polycystic ovary syndrome. Keywords: Polycystic ovary syndrome, insulin resistance, Hyperandrogenism.

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Homburg, R. "Involvement of growth factors in the pathophysiology of polycystic ovary syndrome." Gynecological Endocrinology 12, no. 6 (January 1998): 391–97. http://dx.doi.org/10.3109/09513599809012841.

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Souza, Ester Avelino de, Alyssa Venturin de Miguel, Fernanda Shinkai de Oliveira, Fernando Sabath de Oliveira Bernardes, Stella Petrazzo Fascineli, and Sofia Banzatto. "GESTATIONAL DIABETES MELLITUS: RELATIONSHIP WITH PATHOPHYSIOLOGY, HYPERANDROGENISM AND POLYCYSTIC OVARY SYNDROME." International Journal of Health Science 2, no. 39 (July 19, 2022): 2–8. http://dx.doi.org/10.22533/at.ed.1592392215073.

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Abbott, David H., Daniel A. Dumesic, and Jon E. Levine. "Hyperandrogenic origins of polycystic ovary syndrome – implications for pathophysiology and therapy." Expert Review of Endocrinology & Metabolism 14, no. 2 (February 15, 2019): 131–43. http://dx.doi.org/10.1080/17446651.2019.1576522.

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Leondires, M. P., and S. L. Berga. "Role of GnRH drive in the pathophysiology of polycystic ovary syndrome." Journal of Endocrinological Investigation 21, no. 7 (July 1998): 476–85. http://dx.doi.org/10.1007/bf03347331.

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Kandaraki, Eleni, Charikleia Christakou, and Evanthia Diamanti-Kandarakis. "Metabolic syndrome and polycystic ovary syndrome... and vice versa." Arquivos Brasileiros de Endocrinologia & Metabologia 53, no. 2 (March 2009): 227–37. http://dx.doi.org/10.1590/s0004-27302009000200014.

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The metabolic syndrome (MS) and the polycystic ovary syndrome (PCOS) appear to be interrelated, although they are distinct entities. Women with PCOS appear to be commonly affected by MS, while women with MS may display reproductive or endocrine features of PCOS. These clinical observations appear to be only partly attributable to the association of both syndromes with obesity and imply a reciprocal pathophysiologic relationship between PCOS and MS with potentially significant clinical sequelae. Adult women with MS are at a greater risk of developing cardiovascular disease; women with PCOS also appear to carry such an increased risk in their postmenopausal life. Conversely, women with MS may experience reproductive disturbances, reminiscent of PCOS, more commonly than their counterparts from the general population. This review presented the current epidemiology of MS in adults and adolescents with PCOS, as well as the limited amount of data on the prevalence of features of PCOS among women with MS or MS features. We also discuss the potential pathophysiologic mechanisms underlying the relationship between these interweaving, but distinct, syndromes.

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Briden, Lara. "Beyond the Label: A Patient-Centred Approach to Polycystic Ovary Syndrome." CAND Journal 29, no. 2 (June 28, 2022): 2–8. http://dx.doi.org/10.54434/candj.114.

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Polycystic ovary syndrome (PCOS) is the most common endocrine disorder affecting women of reproductive age. Importantly, it is not one disease with a single pathophysiology but is instead a heterogeneous syndrome with several underlying biological mechanisms. Careful diagnosis requires attention to the key symptom of androgen excess as well as the exclusion of similar disorders including hyperprolactinemia, late-onset congenital adrenal hyperplasia, and hypothalamic amenorrhea. A patient-centred approach to treatment requires further assessment of underlying drivers and mechanisms including neuroendocrine disturbance, insulin resistance, and adrenal hyperresponsiveness.

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Fadeeva, M. I., L. V. Savel'eva, and V. V. Fadeev. "Cindrom obstruktivnogo apnoe sna v praktikevracha-endokrinologa." Obesity and metabolism 7, no. 1 (March 15, 2010): 3–10. http://dx.doi.org/10.14341/2071-8713-5271.

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It is known, that sleep-disordered breathing can affect patients with various endocrine diseases. Obstructive, central and mixed types of sleep apnea syndrome are known to occur in obesity, hypothyroidism, acromegaly, diabetes mellitus, especially with diabetic neuropathy, Cushing syndrome and polycystic ovary syndrome. The pathogenic mechanisms and pathophysiology of оbstructive sleep apnea in patients with different endocrine diseases, clinical manifestations and treatment of sleep apnea are reviewed in this article.

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Andhare, R. "MULTIPLE APPROACHES IN AYURVEDA FOR PATHO-PHYSIOLOGY IN POLYCYSTIC OVARIAN SYNDROME." Journal of Medical pharmaceutical and allied sciences 10, no. 3 (July 15, 2021): 3055–58. http://dx.doi.org/10.22270/jmpas.v10i3.1158.

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The most prevalent endocrine condition in women is polycystic ovary syndrome (pcos).the clinical presentation of pcos ranges between mild menstrual dysfunction and extreme reproductive and metabolic function disruption. According to modern science, the physiology related to ovulation is controlled by hormones of hypothalamo – pituitary – ovarian axis. This axis is disturbed in pcos. According to ayurveda, patho-physiology involves vitiated doshas i.e. Vata, pitta, kapha and agni – especially dhatwagni. The pathophysiology of pcos is analysed to clarify the precise cause of the disorder in order to prepare therapy for a full cure. Multiple approaches in ayurveda for patho-physiology in polycystic ovarian syndrome. It is evident in conclusion that pcos is an enigma. There is no complete understanding of its fundamental pathophysiology as per modern science. No therapy is a panacea, as therapies have so far been targeted at the symptoms but not at the syndrome itself.

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Stener-Victorin, Elisabet, Vasantha Padmanabhan, Kirsty A. Walters, Rebecca E. Campbell, Anna Benrick, Paolo Giacobini, Daniel A. Dumesic, and David H. Abbott. "Animal Models to Understand the Etiology and Pathophysiology of Polycystic Ovary Syndrome." Endocrine Reviews 41, no. 4 (April 20, 2020): 538–76. http://dx.doi.org/10.1210/endrev/bnaa010.

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Abstract More than 1 out of 10 women worldwide are diagnosed with polycystic ovary syndrome (PCOS), the leading cause of female reproductive and metabolic dysfunction. Despite its high prevalence, PCOS and its accompanying morbidities are likely underdiagnosed, averaging > 2 years and 3 physicians before women are diagnosed. Although it has been intensively researched, the underlying cause(s) of PCOS have yet to be defined. In order to understand PCOS pathophysiology, its developmental origins, and how to predict and prevent PCOS onset, there is an urgent need for safe and effective markers and treatments. In this review, we detail which animal models are more suitable for contributing to our understanding of the etiology and pathophysiology of PCOS. We summarize and highlight advantages and limitations of hormonal or genetic manipulation of animal models, as well as of naturally occurring PCOS-like females.

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STRAUSS, JEROME F. "Some New Thoughts on the Pathophysiology and Genetics of Polycystic Ovary Syndrome." Annals of the New York Academy of Sciences 997, no. 1 (November 2003): 42–48. http://dx.doi.org/10.1196/annals.1290.005.

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Witchel, Selma Feldman, Sharon E. Oberfield, and Alexia S. Peña. "Polycystic Ovary Syndrome: Pathophysiology, Presentation, and Treatment With Emphasis on Adolescent Girls." Journal of the Endocrine Society 3, no. 8 (June 14, 2019): 1545–73. http://dx.doi.org/10.1210/js.2019-00078.

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AbstractPolycystic ovary syndrome (PCOS) is a heterogeneous disorder characterized by hyperandrogenism and chronic anovulation. Depending on diagnostic criteria, 6% to 20% of reproductive aged women are affected. Symptoms of PCOS arise during the early pubertal years. Both normal female pubertal development and PCOS are characterized by irregular menstrual cycles, anovulation, and acne. Owing to the complicated interwoven pathophysiology, discerning the inciting causes is challenging. Most available clinical data communicate findings and outcomes in adult women. Whereas the Rotterdam criteria are accepted for adult women, different diagnostic criteria for PCOS in adolescent girls have been delineated. Diagnostic features for adolescent girls are menstrual irregularity, clinical hyperandrogenism, and/or hyperandrogenemia. Pelvic ultrasound findings are not needed for the diagnosis of PCOS in adolescent girls. Even before definitive diagnosis of PCOS, adolescents with clinical signs of androgen excess and oligomenorrhea/amenorrhea, features of PCOS, can be regarded as being “at risk for PCOS.” Management of both those at risk for PCOS and those with a confirmed PCOS diagnosis includes education, healthy lifestyle interventions, and therapeutic interventions targeting their symptoms. Interventions can include metformin, combined oral contraceptive pills, spironolactone, and local treatments for hirsutism and acne. In addition to ascertaining for associated comorbidities, management should also include regular follow-up visits and planned transition to adult care providers. Comprehensive knowledge regarding the pathogenesis of PCOS will enable earlier identification of girls with high propensity to develop PCOS. Timely implementation of individualized therapeutic interventions will improve overall management of PCOS during adolescence, prevent associated comorbidities, and improve quality of life.

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Laganà, Antonio Simone, Simone Garzon, Jvan Casarin, Massimo Franchi, and Fabio Ghezzi. "Inositol in Polycystic Ovary Syndrome: Restoring Fertility through a Pathophysiology-Based Approach." Trends in Endocrinology & Metabolism 29, no. 11 (November 2018): 768–80. http://dx.doi.org/10.1016/j.tem.2018.09.001.

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Shukla, Pallavi, and Srabani Mukherjee. "Mitochondrial dysfunction: An emerging link in the pathophysiology of polycystic ovary syndrome." Mitochondrion 52 (May 2020): 24–39. http://dx.doi.org/10.1016/j.mito.2020.02.006.

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Wang, Fangfang, Jiexue Pan, Ye Liu, Qing Meng, Pingping Lv, Fan Qu, Guo-Lian Ding, et al. "Alternative splicing of the androgen receptor in polycystic ovary syndrome." Proceedings of the National Academy of Sciences 112, no. 15 (March 30, 2015): 4743–48. http://dx.doi.org/10.1073/pnas.1418216112.

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Polycystic ovary syndrome (PCOS) is one of the most common female endocrine disorders and a leading cause of female subfertility. The mechanism underlying the pathophysiology of PCOS remains to be illustrated. Here, we identify two alternative splice variants (ASVs) of the androgen receptor (AR), insertion and deletion isoforms, in granulosa cells (GCs) in ∼62% of patients with PCOS. AR ASVs are strongly associated with remarkable hyperandrogenism and abnormalities in folliculogenesis, and are absent from all control subjects without PCOS. Alternative splicing dramatically alters genome-wide AR recruitment and androgen-induced expression of genes related to androgen metabolism and folliculogenesis in human GCs. These findings establish alternative splicing of AR in GCs as the major pathogenic mechanism for hyperandrogenism and abnormal folliculogenesis in PCOS.

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Dumesic, Daniel A., Sharon E. Oberfield, Elisabet Stener-Victorin, John C. Marshall, Joop S. Laven, and Richard S. Legro. "Scientific Statement on the Diagnostic Criteria, Epidemiology, Pathophysiology, and Molecular Genetics of Polycystic Ovary Syndrome." Endocrine Reviews 36, no. 5 (October 1, 2015): 487–525. http://dx.doi.org/10.1210/er.2015-1018.

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Polycystic ovary syndrome (PCOS) is a heterogeneous and complex disorder that has both adverse reproductive and metabolic implications for affected women. However, there is generally poor understanding of its etiology. Varying expert-based diagnostic criteria utilize some combination of oligo-ovulation, hyperandrogenism, and the presence of polycystic ovaries. Criteria that require hyperandrogenism tend to identify a more severe reproductive and metabolic phenotype. The phenotype can vary by race and ethnicity, is difficult to define in the perimenarchal and perimenopausal period, and is exacerbated by obesity. The pathophysiology involves abnormal gonadotropin secretion from a reduced hypothalamic feedback response to circulating sex steroids, altered ovarian morphology and functional changes, and disordered insulin action in a variety of target tissues. PCOS clusters in families and both female and male relatives can show stigmata of the syndrome, including metabolic abnormalities. Genome-wide association studies have identified a number of candidate regions, although their role in contributing to PCOS is still largely unknown.

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Nahar, Khairun, Gazi Mahfuza, Shirin Akhter Begum, Khodeza Khatun, and Md Rafiqul Islam. "Clinical, Biochemical and Hormonal Profile of Polycystic Ovary Syndrome." Journal of National Institute of Neurosciences Bangladesh 3, no. 2 (May 26, 2018): 94–98. http://dx.doi.org/10.3329/jninb.v3i2.36773.

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Background: The polycystic ovary syndrome is a heterogenous condition, the pathophysiology of which is multifactorial. It is considered as a systemic and metabolic disorder like hyperglycemia and insulin resistance with increased risk of type II diabetes mellitus and cardiovascular diseases.Objective: The purpose of the present study was to analyze the clinical, biochemical and hormonal profile of patients PCOS and to find out correlations among them.Methodology: This cross-sectional observational study was done including 100 diagnosed cases of PCOS attending the GOPD, BSMMU Hospital. This study was done to analyze the clinical, biochemical and hormonal characteristics of PCOS patients and to observe the correlations among them.Result: The mean age of study populations was 22.7± 6.9 years and more than half of them were overweight or obese. Menstrual abnormality like oligomenorrhoea and secondary amenorrhoea was found in 95% cases and 5% were eumenorrhic. Prevalence of hirsutism and subfertility was 69% and 50% respectively. More than half (52%) of cases had LH/FSH ratio >2 which is taken to be significant. About one-third (30%) of cases had total testosterone level above the reference range with a mean value of serum testosterone 71.4±27.9 ng/dL.Conclusion: Significant positive correlation was found among increased BMI, increased LH/FSH ratio, serum testosterone and serum TSH level. Further studies are needed to corroborate our findings and to find out the clinical, biochemical and endocrinological characteristics of our women of PCOS.Journal of National Institute of Neurosciences Bangladesh, 2017;3(2): 94-98

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Majid Raheem, Noor, and Bushra Hassan Marouf. "Impact of Vitamin D Deficiency on the Pathogenesis of Polycystic Ovary Syndrome." Al-Rafidain Journal of Medical Sciences ( ISSN: 2789-3219 ) 2 (January 10, 2022): 1–7. http://dx.doi.org/10.54133/ajms.v2i.53.

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There are many metabolic and hormonal factors related to polycystic ovary syndrome (PCOS) that can be affected by vitamin D3 supplementation. To find clinical trials, in vivo studies, and in vitro studies that met the review's inclusion and exclusion criteria, we searched many databases. PCOS women's ovulation and metabolic parameters were examined in relation to the effects of vitamin D3 treatment on PCOS risk variables such as seasonal changes in body mass index, and obesity. The current review included twenty-five articles. Vitamin D3(25-hydroxy vitamin D) levels were significantly lower in the PCOS group than in the control group, and lipid profile and androgen hormone levels were significantly higher in the PCOS group, resulting in increased cardiovascular events and exaggerated hirsutism. According to the majority of research, vitamin D3 plays a beneficial role in decreasing the pathophysiology of PCOS, notably in restoring ovulation, which ultimately improves fertility. Although other studies found no effect on lipid profile, there was a minor effect on reducing cardiovascular risks. The response of patients to vitamin D3 was influenced by the dose administered and the study's methodology. In conclusion, vitamin D3 had a good effect on the pathophysiology of PCOS in the majority of investigations.

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Rudnicka, Ewa, Michał Kunicki, Anna Calik-Ksepka, Katarzyna Suchta, Anna Duszewska, Katarzyna Smolarczyk, and Roman Smolarczyk. "Anti-Müllerian Hormone in Pathogenesis, Diagnostic and Treatment of PCOS." International Journal of Molecular Sciences 22, no. 22 (November 19, 2021): 12507. http://dx.doi.org/10.3390/ijms222212507.

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Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among reproductive-aged women. It is characterized by chronic anovulation, hyperandrogenism, and the presence of polycystic ovary in ultrasound examination. PCOS is specified by an increased number of follicles at all growing stages, mainly seen in the preantral and small antral follicles and an increased serum level of Anti-Müllerian Hormone (AMH). Because of the strong correlation between circulating AMH levels and antral follicle count on ultrasound, Anti-Müllerian Hormone has been proposed as an alternative marker of ovulatory dysfunction in PCOS. However, the results from the current literature are not homogeneous, and the specific threshold of AMH in PCOS and PCOM is, therefore, very challenging. This review aims to update the current knowledge about AMH, the pathophysiology of AMH in the pathogenesis of PCOS, and the role of Anti-Müllerian Hormone in the treatment of this syndrome.

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Chen, Xinwang, Xiao Jia, Jie Qiao, Youfei Guan, and Jihong Kang. "Adipokines in reproductive function: a link between obesity and polycystic ovary syndrome." Journal of Molecular Endocrinology 50, no. 2 (January 18, 2013): R21—R37. http://dx.doi.org/10.1530/jme-12-0247.

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Polycystic ovary syndrome (PCOS) is the most common endocrinopathy associated with infertility and metabolic disorder in women of reproductive age. Dysfunction of adipose tissue has been implicated in the pathophysiology of PCOS. Increasing evidence shows that the dysregulated expression of adipokines, the secreted products of adipose tissue, plays an important role in the pathology of PCOS. Here, we review the role of several identified adipokines that may act as a link between obesity and PCOS. PCOS also reciprocally influences the profile of adipokines. Insight into the underlying mechanisms will help better understand the pathology of PCOS and identify new therapeutic targets of this syndrome.

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Balen, Adam. "The pathophysiology of polycystic ovary syndrome: trying to understand PCOS and its endocrinology." Best Practice & Research Clinical Obstetrics & Gynaecology 18, no. 5 (October 2004): 685–706. http://dx.doi.org/10.1016/j.bpobgyn.2004.05.004.

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NEACȘU, Adrian, Cătălina Diana STĂNICĂ, and Constantin Dimitrie NANU. "The conservative treatment in adolescents with the Polycystic ovary syndrome." Romanian Journal of Medical Practice 11, no. 4 (December 31, 2016): 337–41. http://dx.doi.org/10.37897/rjmp.2016.4.8.

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Polycystic ovary syndrome (PCOS) is a common endocrine and heterogeneous dysfunction, characterized by chronic anovulation and androgen excess, affecting 6-10% of women of childbearing age. It is the most common cause of anovulatory infertility. It seems that the key element in the pathophysiology of PCOS is increased insulin resistance. The correction of infertility in teens is not a priority. They can receive treatment to normalize menstrual cycles, with the reduction of symptoms and improvement of metabolic disorders. Many overweight teens have increased insulinemia, which may play a role in the development of PCOS. Standard treatment is oral estroprogestative, used to perform regular menstrual cycles. Normalize menstrual cycles can be done with oral contraceptives or oral antidiabetic agents that improve metabolic dysfunctions. An adjuvant approach of the utmost importance for teens is lifestyle modification and diet. Teen treatment should be individualized depending on a number of peculiarities that have to be taken into account: menstruation disorders, mastopathies and ovarian dystrophies, hyperandrogenism syndrome, sexually transmitted diseases and other associated disorders. In obese women with PCOS, weight loss improves hyperandrogenism, reduces metabolic disturbances, reduces insulin resistance and insulinemia, improves fertility rate, stimulates ovulation.

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Prakash, Amog, Milad Nourianpour, Abiola Senok, and William Atiomo. "Polycystic Ovary Syndrome and Endometrial Cancer: A Scoping Review of the Literature on Gut Microbiota." Cells 11, no. 19 (September 28, 2022): 3038. http://dx.doi.org/10.3390/cells11193038.

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Gut dysbiosis has been associated with polycystic ovary syndrome (PCOS) and endometrial cancer (EC) but no studies have investigated whether gut dysbiosis may explain the increased endometrial cancer risk in polycystic ovary syndrome. The aim of this scoping review is to evaluate the extent and nature of published studies on the gut microbiota in polycystic ovary syndrome and endometrial cancer and attempt to find any similarities between the composition of the microbiota. We searched for publications ranging from the years 2016 to 2022, due to the completion date of the ‘Human Microbiome Project’ in 2016. We obtained 200 articles by inputting keywords such as ‘gut microbiome’, ‘gut microbiota’, ‘gut dysbiosis’, ‘PCOS’, and ‘endometrial cancer’ into search engines such as PubMed and Scopus. Of the 200 identified in our initial search, we included 25 articles in our final review after applying the exclusion and inclusion criteria. Although the literature is growing in this field, we did not identify enough published studies to investigate whether gut dysbiosis may explain the increased EC risk in PCOS. Within the studies identified, we were unable to identify any consistent patterns of the microbiome similarly present in studies on women with PCOS compared with women with EC. Although we found that the phylum Firmicutes was similarly decreased in women with PCOS and studies on women with EC, there was however significant variability within the studies identified making it highly likely that this may have arisen by chance. Further research pertaining to molecular and microbiological mechanisms in relation to the gut microbiome is needed to elucidate a greater understanding of its contribution to the pathophysiology of endometrial cancer in patients with polycystic ovarian syndrome.

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Basu, Barnali Ray, Sanchari Chakraborty, Ankita Samaddar, Nilansu Das, and Sudip Kumar Saha. "An insight of association of insulin resistance with polycystic ovary syndrome." Indian Journal of Clinical Anatomy and Physiology 8, no. 4 (March 15, 2022): 248–54. http://dx.doi.org/10.18231/j.ijcap.2021.055.

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Polycystic ovary syndrome (PCOS), a multifaceted condition, often has salient features like insulin resistance (IR). Abnormal alternation in insulin synthesis and function usually alters PCOS expressivity by deviating molecular and biochemical activity underlying this pathophysiology.This review intends to unveil the molecular basis of the genetic polymorphism of IR and its correlation with PCOS. It also highlights the existing methods of IR estimation. Searching of different articles using keywords including PCOS, IR, and polymorphism in various databases was performed to illustrate the review article.POCS, and IR are complex and multifactorial conditions in terms of the contributing factors, their interactions, and expressivity. Further studies on diversified genotype responses to environmental and ethnic variances are required for precise understanding.Insulin resistance (IR) and polycystic ovary syndrome (PCOS) are intricately interacted conditions that abnormally alter functions from genetic to organ system level. Complex gene-environment interactions make it difficult to understand the etiology and manifestation, and so diagnosis and management approaches of the heterogeneous pathophysiology are not foolproof. Further studies on genetic susceptibility related to ethnic distribution are essential for the implementation of personalized treatment of IR and PCOS.

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Zoltán, Kun Imre, Kun Ildikó, and Kolcsár Melinda. "Current aspects of polycystic ovary syndrome I: definition, pathophysiology, clinical manifestations, diagnosis and complications." Bulletin of Medical Sciences 91, no. 1 (July 1, 2018): 5–18. http://dx.doi.org/10.2478/orvtudert-2018-0011.

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Abstract Polycystic ovary syndrome (PCOS) is the most frequent endocrine disease among women with childbearing potential, the best-known cause of hirsutism, with a hypothesized prevalence of 8-22%. The first part of the paper discusses the conceptional evolution of the syndrome, from its description in 1935 by Stein and Leventhal till today. It describes the changes in the criteria systems, emphasizing that the Rotterdam criteria, proposed in 2003 by the European Society for Human Reproduction and Embryology/American Society for Reproductive Medicine, are still valid today. This system basically differs from earlier (1990) NIH-criteria in one aspect: it introduced two newer phenotypes, one without hyperandrogenism and the other with ovulatory cycles, so it distinguishes 4 phenotypes. The etiology and pathogenesis of PCOS is heterogeneous, multifactorial, poorly understood. We present the 3 leading hypotheses (1 - hypothalamo-hypophyseal disturbances, 2 – primary enzyme disorders in ovarian, or ovarian/adrenal steroidogenesis, resulting primarily in hyperactivity of 17alpha-hydroxylase/17,20-lyase, 3 – insulin resistance-hyperinsulinism and other metabolic dysfunctions). We emphasize the role of genetically determined hyperandrogenism, that of insulin resistance-hyperinsulinism and the importance of reinforcing each other. Subsequently, the aggravating aspects of the frequently associated metabolic syndrome are discussed, and then the effects of the mentioned pathological processes on the endocrine and other organ structures participating in the regulation of sexual functions. We stress the hypothetical role of perinatal and pubertal androgen exposition in the pathogenesis of PCOS. The mechanisms of anovulation and those of the endometrial lesions are discussed, too. The clinical manifestations, the paraclinical and laboratory examinations, the positive and differential diagnosis and the complications are also presented. We intend to deal with the therapeutic aspects of PCOS in an upcoming paper.

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Journal articles on the topic 'Polycystic ovary syndrome Pathophysiology'

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