Inhibition of experimental proliferative vitreoretinopathy by retroviral vector-mediated transfer of suicide gene. Can proliferative vitreoretinopathy be a target of gene therapy?
Severity of experimental PVR clearly was reduced by transfer of the HStk gene and administration of GCV. This inhibitory effect also was produced by a combination of 10% HStk fibroblasts and 90% normal fibroblasts, indicating a significant bystander effect. These data suggest the potential of somatic gene therapy for the treatment of PVR.
We found marked radiographic evidence of incomplete correction of deformity in patients with residual symptoms compared with patients with successful results with residual deformity present in the large majority of patients (45 of 50 [90%]) undergoing residual FAI surgery. We recommend careful attention to full 3-D resection of impinging structures.