We read with great interest the article by Wroblewski and associates regarding the effect of intravitreal pegaptanib (IVP) in treating macular edema secondary to branch retinal vein occlusion (BRVO). The aim of the study was to investigate the role of IVP for macular edema from BRVO. The study showed that IVP was effective in terms of reducing foveal thickness and improving vision.
In the article, an observation window was not defined before treatment was initiated. As the authors pointed out in the article, the natural course of BRVO can vary. With good perfusion, macular edema may subside with time, and the natural disease course may be favorable even without treatment. The authors stated that all cases recruited had macular edema secondary to BRVO of more than 1 month’s and fewer than 6 months’ duration. This meant that there were cases that had IVP as early as 1 month after onset of BRVO. In the classic Branch Retinal Vein Occlusion Study, 3 months was given to allow spontaneous resolution before treatment with grid laser was initiated. Similarly, in the study by Prager and associates, intravitreal bevacizumab (IVB) was given for cases where edema persisted for at least 3 months without signs of resolution, and in the study by Jaissle and associates, a mean observation period of 6 months was given between onset of BRVO and first IVB treatment. Although the current study was not meant to compare the effect of IVP with that of laser or bevacizumab treatment, this simply explains the fact that if IVP is given without allowing an opportunity for spontaneous recovery, we may expose the patient to added risks. In the current study, there was a case of retinal detachment in which the contribution from intravitreal injections cannot be ruled out entirely.
Furthermore, after 18 weeks from the first dose of pegaptanib, a portion of subjects underwent grid laser for residual macular edema. Hence, during result analysis, the effect of laser cannot be excluded completely. In this sense, the study looked at a combined effect of pegaptanib plus grid laser rather than that of pegaptanib monotherapy. To eliminate this confounding factor, the authors need to exclude all subjects who underwent grid laser treatment, either before or after treatment with pegaptanib. If these subjects could not be excluded, the authors could consider highlighting specific patients, for instance, in Table 1, who underwent grid laser treatment, such that readers can have a better interpretation of the results.
Third, the authors pointed out that pegaptanib has a theoretical advantage over other nonselective anti–vascular endothelial growth factor agents in being vascular endothelial growth factor 165 selective. It would be necessary for the authors to include other treatment arms of subjects being given ranibizumab or bevacizumab. Otherwise, it may be difficult for the current study to impact difference in clinical practice.