Serum Albumin and Glycemic Variability Could Contribute to Diabetic Retinopathy Progression by Regulating Chronic Inflammatory Pathways
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Le résumé fourni par la source
Purpose Despite managing glycemic levels and other risk factors, individuals with type 2 diabetes (T2DM) may still experience diabetic retinopathy (DR) progression. This study investigated clinical predictors of DR progression in T2DM patients following bariatric surgery. Methods This study was a retrospective post hoc analysis of participants from a clinical randomized controlled trial of bariatric surgery patients with T2DM (ACTRN12611000751976) who had complete DR screening and blood data at baseline and 5 years post‐bariatric surgery. Plasma cytokine concentrations were also examined. Results DR progression was strongly associated with a postoperative decrease in serum albumin (OR = 0.461, 95% CI: 0.221–0.962, p = 0.039). This decrease also predicted postoperative increases in IL‐6 (OR = infinity, sensitivity = 100.00%, p = 0.0162) and IL‐1β (OR = 11.250, sensitivity = 81.82%, p = 0.0154), known to be linked to NLRP3 inflammasome activation. In addition, individuals who progressed in DR severity showed greater month‐to‐month HbA1c variability compared to stable individuals (mean difference: 0.6583%, 95% CI: 0.1821–1.134%, p = 0.0115). Conclusions Decreases in serum albumin and increased glycemic variability may influence DR progression through the NLRP3 inflammasome and inflammatory pathways. Further research is needed to clarify the role and mechanism of albumin loss in DR progression.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Serum Albumin and Glycemic Variability Could Contribute to Diabetic Retinopathy Progression by Regulating Chronic Inflammatory Pathways
- Date Crossref
- 01/01/2025
- Éditeur
- Wiley
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
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