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      Increased risk of type 2 diabetes in patients with systemic lupus erythematosus: A nationwide cohort study in Taiwan

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          Abstract

          Data on the risk of developing diabetes in patients with systemic lupus erythematosus (SLE) are limited and have yielded mixed results. We conducted a nationwide cohort study to investigate the risk of subsequent type 2 diabetes in patients with SLE compared with matched non-SLE controls.

          Data were collected from the Taiwan National Health Insurance Research Database. Adult patients newly diagnosed with SLE between 2003 to 2010 were identified as the study cohort. The non-SLE group was matched for age, gender, and date of initial diagnosis as the comparison cohort.

          A total of 6159 SLE patients (87.90% female, mean age 38.79 years) were identified during this period. Of these, 206 (3.34%) developed type 2 diabetes. The 3-year incidence of type 2 diabetes was significantly higher in the SLE cohort than in the control group (130.26 vs 101.18 cases per 10,000 person-years), with an adjusted hazard ratio of 1.22 (95% confidence interval [CI] 1.04–1.44), after adjusting for age, gender, underlying comorbidities, and monthly income. Stratified analyses showed that women with SLE and low-income SLE patients (monthly income < 20,000 New Taiwan Dollar) had a higher risk of type 2 diabetes than non-SLE controls, with adjusted hazard ratios of 1.21 (95% CI 1.01–1.45) and 1.36 (95% CI 1.10–1.69), respectively.

          Patients with newly diagnosed SLE had a 22% increased risk of developing type 2 diabetes during the 3-year follow-up period compared with matched controls.

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          Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin.

          Type 2 diabetes affects approximately 8 percent of adults in the United States. Some risk factors--elevated plasma glucose concentrations in the fasting state and after an oral glucose load, overweight, and a sedentary lifestyle--are potentially reversible. We hypothesized that modifying these factors with a lifestyle-intervention program or the administration of metformin would prevent or delay the development of diabetes. We randomly assigned 3234 nondiabetic persons with elevated fasting and post-load plasma glucose concentrations to placebo, metformin (850 mg twice daily), or a lifestyle-modification program with the goals of at least a 7 percent weight loss and at least 150 minutes of physical activity per week. The mean age of the participants was 51 years, and the mean body-mass index (the weight in kilograms divided by the square of the height in meters) was 34.0; 68 percent were women, and 45 percent were members of minority groups. The average follow-up was 2.8 years. The incidence of diabetes was 11.0, 7.8, and 4.8 cases per 100 person-years in the placebo, metformin, and lifestyle groups, respectively. The lifestyle intervention reduced the incidence by 58 percent (95 percent confidence interval, 48 to 66 percent) and metformin by 31 percent (95 percent confidence interval, 17 to 43 percent), as compared with placebo; the lifestyle intervention was significantly more effective than metformin. To prevent one case of diabetes during a period of three years, 6.9 persons would have to participate in the lifestyle-intervention program, and 13.9 would have to receive metformin. Lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk. The lifestyle intervention was more effective than metformin.
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            Prevention of Type 2 Diabetes Mellitus by Changes in Lifestyle among Subjects with Impaired Glucose Tolerance

            New England Journal of Medicine, 344(18), 1343-1350
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              Type 2 diabetes: principles of pathogenesis and therapy.

              Type 2 diabetes mellitus has become an epidemic, and virtually no physician is without patients who have the disease. Whereas insulin insensitivity is an early phenomenon partly related to obesity, pancreas beta-cell function declines gradually over time already before the onset of clinical hyperglycaemia. Several mechanisms have been proposed, including increased non-esterified fatty acids, inflammatory cytokines, adipokines, and mitochondrial dysfunction for insulin resistance, and glucotoxicity, lipotoxicity, and amyloid formation for beta-cell dysfunction. Moreover, the disease has a strong genetic component, but only a handful of genes have been identified so far: genes for calpain 10, potassium inward-rectifier 6.2, peroxisome proliferator-activated receptor gamma, insulin receptor substrate-1, and others. Management includes not only diet and exercise, but also combinations of anti-hyperglycaemic drug treatment with lipid-lowering, antihypertensive, and anti platelet therapy.
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                Author and article information

                Contributors
                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MD
                Medicine
                Lippincott Williams & Wilkins (Hagerstown, MD )
                0025-7974
                1536-5964
                23 December 2022
                23 December 2022
                : 101
                : 51
                : e32520
                Affiliations
                [a ] Department of Allergy, Immunology and Rheumatology, Chi-Mei Medical Center, Yung Kang District, Tainan City, Taiwan
                [b ] Department of Nephrology, Chi-Mei Medical Center, Yung Kang District, Tainan City, Taiwan
                [c ] Department of Medical Research, Chi-Mei Medical Center, Yung Kang District, Tainan City, Taiwan.
                Author notes
                * Correspondence: Yeong-Jang Lin, Department of Allergy, Immunology and Rheumatology, Chi-Mei Medical Center, 901 Jung-Hua Road, Yung Kang District, Tainan City 710, Taiwan (e-mail: linyeongjang@ 123456gmail.com ).
                Article
                00127
                10.1097/MD.0000000000032520
                9794330
                36595866
                1a4f0886-633d-4f47-9a36-e7ab29a73e01
                Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 19 October 2022
                : 9 December 2022
                : 9 December 2022
                Categories
                6900
                Research Article
                Observational Study
                Custom metadata
                TRUE

                diabetes,hazard ratio,national health insurance research database,systemic lupus erythematosus

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