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      Influence of hsCRP Parameter on the Occurrence of Metabolic Syndrome in Patients with Polycystic Ovary Syndrome

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          Abstract

          PCOS (polycystic ovary syndrome) is a common endocrine disorder that affects 8–13% of women of reproductive age. Increased body weight and insulin resistance may be associated with chronic inflammation, which increases the risk of cardiovascular complications. CRP (C-reactive protein) tests may be use to assess persistent inflammation. Elevated CRP levels may be associated with insulin resistance and type 2 diabetes. Determination of hsCRP, highly sensitive C-reactive protein, can be used to assess cardiovascular risk in women with PCOS. In this study, 120 women between the ages of 18 and 42 were divided into two groups: patients with polycystic ovary syndrome (n = 80) and regular menstruating women in whom PCOS was excluded (n = 40). Lipid and carbohydrate metabolism parameters and hsCRP levels were assessed, followed by receiver operating characteristic (ROC) analysis for hsCRP, where metabolic syndrome was the dependent variable. For hsCRP, the cutoff point was 1.44 (mg/dL). Sensitivity for the cutoff point was 0.913 and specificity was 0.691. The area under the curve (AUC) was 0.851 (p < 0.000). The closer the AUC value is to unity, the better the predictive ability of the studied variable. There was also a statistically significant correlation between hsCRP levels and the presence of metabolic syndrome.

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          Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association

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            Inflammation and insulin resistance.

            Over a hundred years ago, high doses of salicylates were shown to lower glucose levels in diabetic patients. This should have been an important clue to link inflammation to the pathogenesis of type 2 diabetes (T2D), but the antihyperglycemic and antiinflammatory effects of salicylates were not connected to the pathogenesis of insulin resistance until recently. Together with the discovery of an important role for tissue macrophages, these new findings are helping to reshape thinking about how obesity increases the risk for developing T2D and the metabolic syndrome. The evolving concept of insulin resistance and T2D as having immunological components and an improving picture of how inflammation modulates metabolism provide new opportunities for using antiinflammatory strategies to correct the metabolic consequences of excess adiposity.
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              A comprehensive definition for metabolic syndrome.

              The metabolic syndrome refers to the co-occurrence of several known cardiovascular risk factors, including insulin resistance, obesity, atherogenic dyslipidemia and hypertension. These conditions are interrelated and share underlying mediators, mechanisms and pathways. There has been recent controversy about its definition and its utility. In this article, I review the current definitions for the metabolic syndrome and why the concept is important. It identifies a subgroup of patients with shared pathophysiology who are at high risk of developing cardiovascular disease and type 2 diabetes. By considering the central features of the metabolic syndrome and how they are related, we may better understand the underlying pathophysiology and disease pathogenesis. A comprehensive definition for the metabolic syndrome and its key features would facilitate research into its causes and hopefully lead to new insights into pharmacologic and lifestyle treatment approaches.
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                Journal
                BIOMID
                Biomedicines
                Biomedicines
                MDPI AG
                2227-9059
                July 2023
                July 10 2023
                : 11
                : 7
                : 1953
                Article
                10.3390/biomedicines11071953
                10377555
                37509592
                0ee61aed-2504-4d65-98c2-5f32f3136905
                © 2023

                https://creativecommons.org/licenses/by/4.0/

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