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Aim: This study evaluated the levels of anti-insulin antibodies (AIAs) and the influence of some antidiabetic medications on AIA in diabetes mellitus (DM) patients with retinopathy. Patient & methods: An observational cross-sectional study. Results: A lower titer of AIA IgG was observed in the diabetic retinopathy (DR) and DM-only study categories compared with the control group [DR = 86 (5-560), DM-only = 50 (5-500), versus control = 200 (7-565); p = 0.017]. Taking nifedipine and metformin were negatively correlated (r = -0.32, p = 0.04) with the levels of AIA IgE in the DR group. Conclusion: A decreased titer of circulating AIAs was observed in the DR study category, suggesting that AIA may not contribute to the pathogenesis of DR.
Diabetic retinopathy (DR) is the main reason people lose their sight in countries with few resources. Anti-insulin antibodies, or AIAs, help the body fight off infections and may play a role in the development of DR. The study looked at how much AIA was in DR patients and how some diabetes drugs affected AIA levels. There was a negative link between nifedipine and one AIA (IgE) in people with DR, but a positive link between metformin and another AIA (IgG). AIA levels were lower in the DR study group, which suggests that AIA may not cause DR.
RESUMEN
Background and Aim: Adipocytes secrete a peptide hormone called leptin, which plays a crucial role in controlling appetite and energy expenditure. Alterations in leptin concentrations are associated with CKD-related cardiovascular problems such as hypertensive heart disease (HHD). Despite the link, data on the precise function of leptin in people with CKD and HHD is scant. Methods: An observational cross-sectional study involving a total of 108 participants (72 CKD patients with HHD and 36 healthy controls). Their demographic and anthropometric information was collected using a standardized questionnaire. Certain clinical measures such as blood pressure and body mass index (BMI) were assessed. Fasting blood samples were analyzed for levels of plasma glucose (FPG), lipids, creatinine, and leptin. Data were analyzed with SPSS v23. Results: Leptin, FPG, creatinine and triglyceride levels were all significantly higher in CKD patients with HHD compared to controls (p < 0.01 for all). Furthermore, advanced CKD status (being in stage 5), having a 6-year diagnosis of HHD, being female, having a higher BMI, and elevation in levels of HDL and FPG contributed significantly to the variance in serum leptin levels in the case group (ß = 0.37, 0.22, 0.19, 0.18, 0.27, 0.28; p < 0.05 for all). In the control group, the female gender had the biggest unique effect on circulating leptin levels, followed by BMI and eGFR (ß = 0.71, 0.34, -0.22; p < 0.01 for all). Conclusion: Patients with CKD who also had HHD reported considerably higher circulating leptin levels. Significantly higher blood leptin levels were shown to be associated with CKD stage 5 in the case group. These results are consistent with the role of leptin in the metabolic complexity seen in CKD patients. There needs to be more research into treatments that aim to lower leptin levels in CKD patients with HHD.