Alteration of plasma von Willebrand factor in the treatment of retinal vein occlusion with cystoid macular edema

Retinal vein occlusion (RVO) is a major retinal disease caused by venous thrombosis. Although several studies have proposed an association between venous thrombosis and von Willebrand factor (VWF), the association between RVO and VWF remains unclear. We aimed to investigate the association between RVO and VWF and the alteration of VWF levels under anti-vascular endothelial growth factor (VEGF) treatment. We enrolled 55 patients with RVO involved cystoid macular edema. They received intravitreal injection of anti-VEGF drugs, either ranibizumab or aflibercept. We examined the clinical data and measured plasma VWF antigen and a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) activity to identify variabilities during treatment. At baseline, there was no significant difference between the RVO group and age-matched controls in both VWF antigen and ADAMTS13 activity levels, but ADAMTS13 activity was significantly lower in central RVO than in branch RVO (P = 0.015). In branch RVO, VWF antigen was negatively correlated with central choroidal thickness (r = −0.51, P < 0.001). In branch RVO after anti-VEGF treatment, VWF antigen levels decreased significantly from 134% at baseline to 109% at 1 day (P = 0.002) and 107% at 1 month (P = 0.030) after treatment. In contrast, ADAMTS13 activity showed no significant difference during this period. In branch RVO at 1 month after treatment, VWF antigen was negatively correlated with central choroidal thickness (r = −0.47, P = 0.001). Our findings suggest an association between VWF and central choroidal thickness in patients with branch RVO, thus the measurement of VWF may be useful for evaluating disease activity and prognosis.