• diabetic retinopathy
• ICAM-1
• immunohistochemistry

There has been considerable interest in the past few years in the early pathological events that lead to vascular occlusion in diabetic retinopathy. The finding of increased leucostasis (leucocytes attached to the endothelial wall) is a common pathological event in both human disease^1,2 and in experimental models.^3,4 The heightened leucocyte/endothelial interaction induced by hyperglycaemia occurs very early in the diabetic process and, as a result, endothelial dysfunction and subsequent apoptosis occur. Although there is some reserve in terms of endothelial division and proliferation, this becomes exhausted with time, leading to the appearance of acellular capillary tubes, the pathological hallmark of disease.⁵ These tubes do not support blood flow and retinal ischaemia supervenes. Presumably there is pre-capillary arteriolar thrombosis due to the loss of the anti-thrombogenic endothelial lining, but pathological evidence for this is scant.⁶ The question arises as to whether this process is mediated by changes in leucocytes (sticky blood), changes in the endothelial surface (sticky …