Ranibizumab is a potential prophylaxis for proliferative vitreoretinopathy, a nonangiogenic blinding disease.

Proliferative vitreoretinopathy (PVR) exemplifies a disease that is difficult to predict, lacks effective treatment options, and substantially reduces the quality of life of an individual. Surgery to correct a rhegmatogenous retinal detachment fails primarily because of PVR. Likely mediators of PVR are growth factors in vitreous, which stimulate cells within and behind the retina as an inevitable consequence of a breached retina. Three classes of growth factors [vascular endothelial growth factor A (VEGF-A), platelet-derived growth factors (PDGFs), and non-PDGFs (growth factors outside of the PDGF family)] are relevant to PVR pathogenesis because they act on PDGF receptor α, which is required for experimental PVR and is associated with this disease in humans. We discovered that ranibizumab (a clinically approved agent that neutralizes VEGF-A) reduced the bioactivity of vitreous from patients and experimental animals with PVR, and protected rabbits from developing disease. The apparent mechanism of ranibizumab action involved derepressing PDGFs, which, at the concentrations present in PVR vitreous, inhibited non-PDGF-mediated activation of PDGF receptor α. These preclinical findings suggest that available approaches to neutralize VEGF-A are prophylactic for PVR, and that anti-VEGF-based therapies may be effective for managing more than angiogenesis- and edema-driven pathological conditions.

Oral gabapentin for photorefractive keratectomy pain.

PURPOSE: To compare the efficacy of oral gabapentin versus placebo for the control of severe pain after photorefractive keratectomy (PRK). SETTING: Center for Refractive Surgery, Walter Reed Army Medical Center, Washington, DC, USA. DESIGN: Randomized masked clinical trial. METHODS: This single-center clinical trial comprised active-duty United States Army soldiers aged 21 years or older having bilateral PRK for myopia with or without astigmatism. Patients received gabapentin 300 mg or placebo 3 times daily for 7 days beginning 2 days before and continuing for 4 days after surgery. Current and maximum pain levels were assessed using the Visual Analog Pain scale 2 hours after surgery and then daily on days 1 through 4. Repeated-measures analysis of variance (ANOVA) was used to compare the current and maximum pain scores over time between the gabapentin group and the placebo group. The Fisher exact test was used to determine whether there was a difference in severe pain (>7/10) between the 2 groups. RESULTS: Forty-two patients received gabapentin and 41 patients, placebo. The repeated-measures ANOVA showed no significant difference between the 2 groups in current pain (P = .84) or in maximum pain over time (P = .35). Oxycodone-acetaminophen use in the gabapentin group was significantly higher than in the placebo group 1 day postoperatively (P = .034). CONCLUSION: When added to a standardized postoperative pain regimen, gabapentin use led to no additional improvement in PRK pain control compared with a placebo at the dose and the time intervals tested.