Recurrence Of Retinopathy Of Prematurity Research Articles

Reactivation of Retinopathy of Prematurity After Bevacizumab Injection

To report late reactivation and progression of retinopathy of prematurity (ROP) after intravitreal bevacizumab monotherapy. Retrospective review of 9 patients (17 eyes) with recurrence of ROP after initial treatment with intravitreal bevacizumab monotherapy. Data collected included (1) location and stage of ROP activity, (2) number and timing of treatments, and (3) structural outcomes. Mean age at treatment-requiring recurrence was 49.3 weeks (SD, 9.1 weeks; minimum, 37 weeks; maximum, 69 weeks) postmenstrual age (PMA). The mean time between initial treatment and treatment-requiring recurrence was 14.4 weeks, with a minimum of 4 and maximum of 35 weeks. Fives eyes progressed to retinal detachment (4 eyes stage 5, 1 eye stage 4a). Age at retinal detachment ranged from 49 to 69 weeks PMA with a median of 55 weeks PMA and mean of 58.4 weeks PMA. No eye that received laser treatment for recurrence progressed to retinal detachment. Although intravitreal bevacizumab treatment is effective in inducing regression of ROP, the effect may be transient. Recurrence can occur later in the course than with conventional laser therapy. Late retinal detachment can occur despite early regression. Longterm favorable structural outcome may require extended observation and retreatment. Laser may be a useful treatment for recurrences.

Antivascular endothelial growth factor for retinopathy of prematurity

This review will discuss a potentially more effective treatment for retinopathy of prematurity (ROP) with fewer acute and long-term complications. Avastin (bevacizumab) therapy is a promising anti-vascular endothelial growth factor (anti-VEGF) administered directly into the vitreous. Recent reports detail the use of Avastin alone, and in combination with light amplification by stimulated emission of radiation (LASER) therapy and vitrectomy, for ROP stages 3, 4, and 5. Currently, one clinical trial is studying Avastin alone for acute vision-threatening ROP stage 3 in zone I and posterior zone II without LASER therapy. Another clinical trial is investigating Avastin following LASER therapy for recurrent ROP stages 4 and 5. Treatment for ROP has evolved from later, more destructive (cryotherapy) to earlier, less destructive (LASER therapy) peripheral retinal ablation. If evidence-based data supports early findings, the use of Avastin may be recommended without the need for ablative LASER therapy and before retinal detachment develops. Avastin will be especially useful for ROP stage 3 cases with hemorrhage decreasing retinal visualization, rigid pupils, intravitreal neovascularization with early or developing (minimal) fibrous membranes, or aggressive posterior retinopathy of prematurity (AP-ROP). These cases all continue to have poor outcomes with LASER therapy.

Histopathology and vascular endothelial growth factor in untreated and diode laser-treated retinopathy of prematurity

Objectives: We had the unique opportunity to compare the eyes of a premature infant with stage 3 retinopathy of prematurity (ROP) in both eyes after the condition was treated by diode laser photocoagulation in one eye only. After the infant's death, we investigated the extent of structural damage incurred with the diode laser and examined the effect of treatment on vascular endothelial growth factor (VEGF) expression. Methods: The eyes were fixed and embedded in paraffin. Adjacent 6 μm sections were either stained for histopathologic analysis or used for in situ hybridization. VEGF messenger RNA (mRNA) was detected by using radiolabeled antisense riboprobes. Results: In the treated eye, histopathologic results demonstrated the clinically evident dose-response effect, with sparing of inner retinal elements with mild laser burns and full-thickness retinal cell disruption with severe burns. Scleral and ciliary nerve effects were absent. VEGF mRNA was localized primarily in the ganglion cell layer but was also found in the inner nuclear layer. In the untreated eye, an increase in VEGF mRNA was detected at the peripheral edge of the vascularized retina anterior to the ridge. In the laser-treated eye, VEGF mRNA expression was dramatically upregulated in the ganglion cell layer in areas adjacent to laser burns. Conclusions: VEGF mRNA was found to be elevated in the peripheral, avascular retina of the untreated eye, consistent with the hypothesis that retinal hypoxia stimulates VEGF expression. In the treated eye with recurrent ROP, VEGF mRNA was not detected in the photocoagulated areas of retina but was increased between laser scars. This finding confirms the results of prior animal studies and validates the use of these models.