The relationship between soluble L-selectin and the development of diabetic retinopathy.

Diabetic retinopathy is a leading cause of adult vision loss and blindness. Earlier studies have shown that polymorphonuclear neutrophils play an important role in the pathogenesis of diabetic vascular complications. Stimulation of these cells is associated with the desquamation of L-selectin. The aim of the study was to evaluate the relationship between the serum concentration of L-selectin and the development of retinopathy in Type 2 diabetic patients. The study comprised 51 Type 2 diabetic patients, aged 65.2 +/- 7.5 years, with a diabetes duration of 10.1 +/- 8.9 years and HbA1c of 8.2 +/- 1.4. The study subjects were divided into two groups: Group A diabetic patients with retinopathy (n = 28) and Group B diabetic patients without retinopathy (n = 23). Twenty age- and sex-matched nondiabetic healthy subjects were enrolled as the control group. Patients with any inflammatory disease were excluded. Retinopathy was assessed by centrally graded retinal photographs. The serum concentration of sL-selectin was estimated using an ELISA test. We observed significantly higher serum concentrations of sL-selectin in Type 2 diabetic patients with retinopathy than in healthy subjects (36.5 +/- 18.1 vs. 11.4 +/- 7.5 ng/ml, p < 0.001). There was also a significant difference between Group A and Group B (36.5 +/- 18.1 vs. 24.2 +/- 13.5 ng/ml, p < 0.05) as well as between Group B and the controls (24.2 +/- 13.5 vs. 11.4 +/- 7.5 ng/ml, p < 0.01) with regard to sL-selectin levels. sL-selectin was significantly correlated with HbA1c (r = 0.93, p < 0.001) and with diabetes duration (r = 0.44, p < 0.001). These results suggest that there was a strong relationship between sL-selectin and diabetic retinopathy. The strong correlation between sL-selectin and HbA1c levels supports the concept that the sL-selectin level is increased with poor glycemic control, which may affect endothelial cell activity and cause subsequent microvascular complications.