Correlation of Serum Intercellular Adhesion Molecule 1 and Transforming Growth Factor Beta 1 With Diabetic Retinopathy in North Indian Patients With Type 2 Diabetes Mellitus

Background: Diabetic retinopathy is a major microvascular complication of diabetes mellitus. Inflammatory and fibrotic pathways, mediated by intercellular adhesion molecule 1 and transforming growth factor beta 1, play crucial roles in its pathogenesis. Objective: This study aims to investigate the correlation of serum intercellular adhesion molecule 1 and transforming growth factor beta 1 levels with diabetic retinopathy in patients with type 2 diabetes mellitus. Methods: A hospital-based case-control study was conducted comprising 60 participants, divided into 30 cases with diabetic retinopathy and 30 controls without retinopathy. Fasting blood sugar, postprandial blood sugar, glycated hemoglobin, lipid profile, and renal function parameters were evaluated. Serum intercellular adhesion molecule 1 and transforming growth factor beta 1 levels were measured using enzyme-linked immunosorbent assay. Diabetic retinopathy was graded using the Early Treatment Diabetic Retinopathy Study (ETDRS) classification. Results: Patients with diabetic retinopathy exhibited significantly higher levels of serum intercellular adhesion molecule 1 (1638.8 ± 839.7 ng/L) and transforming growth factor beta 1 (755.45 ± 237.86 ng/L) compared to controls (315.73 ± 385.80 ng/L and 342.26 ± 138.42 ng/L, respectively) (p < 0.001). Both biomarkers showed significant positive correlations with glycated hemoglobin, fasting blood sugar, postprandial blood sugar, blood urea nitrogen, and serum creatinine. Furthermore, levels of both biomarkers increased progressively with advancing severity of diabetic retinopathy. Conclusions: Elevated serum intercellular adhesion molecule 1 and transforming growth factor beta 1 levels are significantly associated with the presence and severity of diabetic retinopathy. These biomarkers may serve as valuable noninvasive indicators of endothelial dysfunction, inflammation, and fibrosis in disease progression.