Bevacizumab may lead to vitreoretinal fibrosis in patients with Coats’ disease

This small retrospective analysis indicates that Coats' disease patients treated with intravitreal bevacizumab in addition to standard therapy can develop vitreoretinal fibrosis and potentially traction retinal detachment, which are not often found in Coats' disease treated with standard measures without bevacizumab. The authors advise caution in the use of bevacizumab for Coats' disease and have suspended their own use of anti-VEGF agents in these patients, due to this unfavorable outcome and the absence of obvious benefits from the therapy.

They report on eight cases of Coats' disease patients manifesting total or partial exudative retinal detachment in which retinal telangiectasia was treated with standard laser photocoagulation and/or cryotherapy plus intravitreal bevacizumab (1.25 mg/0.05 ml). This is the largest published series of patients with Coats' disease treated, in part, with bevacizumab.

The mean patient age was 88 (range 7 to 240) months. Sixty-three percent were male. Coats' disease was classified as stage 2 in one patient, 3a in three patients and 3b in four patients. Common features included retinal detachment, telangiectasia and peripheral retinal ischemia. There was no evidence of neovascularization.

All patients were treated with cryotherapy and bevacizumab intravitreal injection, and half also underwent laser photocoagulation. They received a median of one injection per eye (mean 1.75, range 1 to 4 injections).

After a mean follow-up of 8.5 months, retinopathy resolved in all patients. Coats'-related subretinal fluid was found in all patients and retinal exudation in six patients. Vitreous fibrosis developed in four patients at a mean of five months, with three cases evolving into traction retinal detachment. The authors write that vitreoretinal fibrosis following bevacizumab injection has not been previously noted in historical cases treated with standard measures.

They note that the fibrosis and traction seen in the current study's patients were similar to reported vitreoretinal fibrosis found with retinopathy of prematurity (ROP) and familial exudative vitreoretinopathy (FEVR) following anti-VEGF therapy. But unlike with ROP and FEVR, their Coats' disease patients did not have clinically evident neovascularization prior to therapy. In addition, traction retinal detachment is observed in the natural course of ROP and FEVR but rarely encountered with Coats' disease.

They speculate that the pathogenesis of vitreoretinal fibrosis following anti-VEGF therapy for Coats' disease could be related to dysregulation of angiogenic factors.