Choriocapillaris degeneration in human diabetes

Purpose. We have recently reported increased numbers of polymorphonuclear leukocytes (PMNs) in the human diabetic choroidal vasculature compared to nondiabetics (Cao et al, IOVS 36:5480, 1995). We also showed that loss of alkaline phosphatase (APase) activity in choriocapillaris (CC) indicated loss of endothelial cells and, therefore, CC degeneration and presumed nonperfusion (McLeod and Lutty, IOVS 35:3799, 1994). Kohner and Henkind demonstrated that an endothelial cell lining is essential for perfusion of retinal capillaries (A.J.O. 69:403, 1970), and the same is probably true for choroid. The goal of the present study was to evaluate CC degeneration (nonperfusion) in diatetic choroids and its association with PMNs and with pathological changes in Bruch's membrane. Methods. Human choroids from 10 subjects (5 diabetic, 5 nondiabetic) were incubated for histochemical demonstration of APase and nonspecific esterase (NSE) for analysis of the choroidal vasculature and PMNs respectively, and then the tissue was flat-embedded and sectioned for structural analysis. Areas of CC degeneration were measured in the flat perspective by digital image analysis and verified in cross sections. The number, size, distribution of PMNs were also determined. Results. CC degeneration in diabetics appeared diffuse and was more prominent in posterior pole than peripheral choroid. Area of CC degeneration in the diabetic group was 4.87±1.3% of the total choroidal area versus 1.15 ±0.34% in the nondiabetic group (P<0.001). An increased number of PMNs within the diabetic CC was positively correlated with area of degeneration (r= 0.65, P<0.05), but there was no such a correlation in nondiabetic choroids. Pathologic changes in Bruch's membrane were often associated with CC degeneration. Conclusion. We conclude from this study that area of CC degeneration is more than four fold greater in diabetic choroids than in nondiabetic choroids. The CC degeneration or presumed nonperfusion was associated with an increased number of PMNs, suggesting that they may be involved in the pathogenesis of diabetic choroidopathy.