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      Obese and Non-obese Polycystic Ovarian Syndrome: Comparison of Clinical, Metabolic, Hormonal Parameters, and their Differential Response to Clomiphene

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          Abstract

          Objective:

          To study the clinical, metabolic, hormonal parameters, and differential response to clomiphene among the obese and non-obese PCOS (polycystic ovarian syndrome).

          Design:

          Prospective observational study.

          Setting:

          Infertility OPD, a government hospital.

          Sample Size:

          About 164 women with PCOS-related infertility.

          Study Groups:

          Obese PCOS group [body mass index (BMI) ≥23 kg/m 2) and non-obese PCOS group (BMI <23 kg/m 2).

          Results:

          Of the total 164 PCOS women, 124 (75.61%) were in the obese group with BMI ≥23 kg/m 2 and 40 (24.39%) were in the non-obese PCOS group. The prevalence of menstrual irregularity, hypertension, insulin resistance (IR), metabolic syndrome, endometrial hyperplasia, and clomiphene resistance in the PCOS women were 82.34%, 3.66%, 59.76%, 24.39%, 7.93%, and 53.7%, respectively. The Ferriman–Gallwey score, menstrual irregularity, IR [fasting insulin and Homeostatic Model Assessment of Insulin Resistance (HOMA-IR)], metabolic syndrome, deranged lipid profile, and clomiphene resistance were statistically more common in the obese PCOS group ( P < 0.05). Hypertension, deranged blood sugar profile, testosterone, androstenedione levels, and endometrial hyperplasia were more common in obese PCOS group but the results were not statistically significant. No significant differences were found in the luteinizing hormone (LH), follicle-stimulating hormone (FSH), LH–FSH ratio, and 17-hydroxyprogesterone (17-OHP) levels between the two groups.

          Conclusion:

          Obese PCOS have a higher risk of adverse outcomes like hypertension, IR, metabolic syndrome, and endometrial hyperplasia. So, targeting obesity in PCOS women will not only help to prevent adverse outcomes but also improve responsiveness to clomiphene citrate.

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          Most cited references22

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          Polycystic Ovary Syndrome

          New England Journal of Medicine, 352(12), 1223-1236
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            Prevalence of insulin resistance in the polycystic ovary syndrome using the homeostasis model assessment.

            To determine the prevalence of insulin resistance (IR) in a large population of patients with the polycystic ovary syndrome (PCOS). Prospective, case-control. University medical center. Two hundred seventy-one PCOS patients and 260 eumenorrheic, non-hirsute, control women. History and physical examination and blood sampling. Total T, free T, DHEAS, sex hormone-binding globulin, and fasting glucose and insulin levels; homeostatic model assessment values for IR (HOMA-IR) and percent beta-cell function (HOMA-%beta-cell). Patients with PCOS and controls differed significantly in all parameters studied, except fasting glucose. Because the HOMA-IR and HOMA-%beta-cell values were variably associated with race, age, and body mass index, the HOMA-IR and HOMA-%beta-cell values were then adjusted for these cofounders. After adjustment, 64.4% of PCOS patients were noted to be insulin resistant, and 2.6% had beta-cell dysfunction. Compared with PCOS patients without IR (n = 96), patients with IR (n = 174) were more obese and had higher beta-cell function. In patients with PCOS, the prevalence of IR was 64% according to the HOMA-IR measurement, after adjustment. Patients with IR were more clinically affected. Although IR is a common abnormality in PCOS, it does not seem to be a universal feature.
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              Insulin and hyperandrogenism in women with polycystic ovary syndrome.

              Polycystic ovary syndrome (PCOS) is a very common endocrine disorder characterized by chronic anovulation, clinical and/or biochemical hyperandrogenism, and/or polycystic ovaries. But most experts consider that hyperandrogenism is the main characteristic of PCOS. Several theories propose different mechanisms to explain PCOS manifestations: (1) a primary enzymatic default in the ovarian and/or adrenal steroidogenesis; (2) an impairment in gonadotropin releasing hormone (GnRH) secretion that promotes luteal hormone (LH) secretion; or (3) alterations in insulin actions that lead to insulin resistance with compensatory hyperinsulinemia. However, in the past 20 years there has been growing evidence supporting that defects in insulin actions or in the insulin signalling pathways are central in the pathogenesis of the syndrome. Indeed, most women with PCOS are metabolically insulin resistant, in part due to genetic predisposition and in part secondary to obesity. But some women with typical PCOS do not display insulin resistance, which supports the hypothesis of a genetic predisposition specific to PCOS that would be revealed by the development of insulin resistance and compensatory hyperinsulinemia in most, but not all, women with PCOS. However, these hypotheses are not yet appropriately confirmed, and more research is still needed to unravel the true pathogenesis underlying this syndrome. The present review thus aims at discussing new concepts and findings regarding insulin actions in PCOS women and how it is related to hyperandrogenemia. Copyright © 2009 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Indian J Endocrinol Metab
                Indian J Endocrinol Metab
                IJEM
                Indian Journal of Endocrinology and Metabolism
                Wolters Kluwer - Medknow (India )
                2230-8210
                2230-9500
                Mar-Apr 2019
                : 23
                : 2
                : 257-262
                Affiliations
                [1]Department of Obstetrics and Gynaecology, Post Graduate Institute of Medical Education and Research, Chandigarh, India
                [1 ]Department of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh, India
                Author notes
                Address for correspondence: Dr. Shalini Gainder, House No. 201, Top Floor, Dr. Mukherjee Nagar, Delhi - 110 009, India. E-mail: shalini_gainderyahoo.com; gsachdeva25@ 123456gmail.com
                Article
                IJEM-23-257
                10.4103/ijem.IJEM_637_18
                6540884
                31161114
                6db5bad0-056c-420d-b1ac-d74744857941
                Copyright: © 2019 Indian Journal of Endocrinology and Metabolism

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

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                Categories
                Original Article

                Endocrinology & Diabetes
                body mass index,hypertension clomiphene,metabolic syndrome,polycystic ovarian syndrome

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