Study of antiphospholipid antibodies in type 2 diabetes mellitus with and without diabetic retinopathy

Antiphospholipid antibodies (aPL) are considered to be contributory factors in the development of thrombotic events. The objective of the study was to determine if aPL are involved in the pathogenesis of diabetic retinopathy (DR) in patients with type 2 diabetes mellitus. IgG anticardiolipin antibodies (IgG aCL), lupus anticoagulant (LA), and anti-IgG beta2-glycoprotein I antibodies (anti-beta2-GPI) were prospectively tested in 34 patients with DR (group 1), 20 males and 14 females, range of age 52-79 years, mean age 57 +/- 4.6 years, duration of diabetes 8-15 years, as compared to 29 type 2 diabetic patients without DR (group 2), 19 males and 10 females, range of age 54-77 years, mean age 58 +/- 4.8 years, duration of diabetes 10-13 years, and to 31 controls matched for age and sex (group 3). IgG aCL and anti-beta2-GPI were detected by enzyme-linked immunosorbent assay (ELISA) and LA was detected by activated partial thromboplastin time, kaolin clotting time, dilute Russell's viper venom time, dilute prothrombin time. Comparison between patients and controls and patients group were expressed as relative risk with its 95% confidence interval (RR [95%/CI], where a lower limit > 1.0 was considered significant. All values were determined by Fischer's exact test. A value of p < 0.05 was considered statistically significant. The incidence of IgG aCL positive (low 4-15 GPL U IgG aCL titers) in group 1 was 21/34 (62%) vs. 12/29 (41%) in group 2 (RR 1.460 95% CI [0.9052 to 2.382]), p = 0.1330. The incidence of LA positive in group 1 was 27/34 (79%) vs. 8/29 (28%) in group 2 (RR 3.086 95% CI [1.584 to 6.010]), p < 0.0001. The incidence of anti-IgG beta2-GPI positive in group 1 was 29/34 (85%) vs. 6/29 (21%) in group 2 (RR 4.640 95% CI [2.067-10.418]), p < 0.0001. The results suggest the possible participation of anti-beta2-GPI and LA in the pathogenesis of DR, shifting the hemostatic balance toward a pro-thrombotic state increasing the risk of developing thrombosis.