PURPOSE: Cystoid macular edema (CME) is a rarely reported side effect of nanoparticle albumin bound (nab)-paclitaxel therapy-an antimitotic agent used for breast cancer. We describe a patient with bilateral CME secondary to Abraxane that was minimally responsive to intravitreal bevacizumab. To our knowledge, this is the first reported case of the use of intravitreal bevacizumab for this condition. A previous report has described the ineffectiveness of concurrent intravenous bevacizumab with Abraxane. This lack of efficacy and knowledge of the mechanism of paclitaxel may provide insights into the mechanisms of CME without angiographic leakage. METHODS: Retrospective, interventional case report of a patient with bilateral CME after starting Abraxane therapy for recurrent breast cancer treated with intravitreal bevacizumab (1.25 mg/0.05 mL) every 4 weeks. Records were reviewed for visual acuity and macular edema as assessed by spectral-domain optical coherence tomography (SD-OCT). RESULTS: A 73-year-old patient with recurrent, metastatic breast cancer presented with bilateral visual loss 3 months after nab-paclitaxel was initiated. Baseline visual acuities (VA) were 20/50 in the right eye (OD) and 20/80 in the left eye (OS). Fundus exam showed marked CME in both eyes (OU). Fluorescein angiography was notable for the marked absence of petalloid late-phase leakage characteristic of vascular, ischemic, and inflammatory causes of CME. SD-OCT showed marked cystoid spaces predominantly involving the outer and inner nuclear layers with central subfield thicknesses (CST) of 398 μm OD and 441 μm OS. Serial intravitreal bevacizumab injections (OD, 2 injections; OS, 3 injections) were administered on a 4-week basis with an improvement and stabilization of VA at 20/50 OD and 20/70 OS. However, CME on SD-OCT persisted with CST of 492 μm OD and 478 μm OS. CONCLUSIONS: The pathogenesis of CME without leakage is poorly understood; however, fluid accumulation in Muller cells due to toxicity has been proposed. The persistence of CME suggests that additional nonvascular endothelial growth factor-mediated mechanisms are involved. Improved understanding of the mechanisms underlying paclitaxel-associated CME is needed, especially in patients with limited systemic options for metastatic carcinoma.
PURPOSE:Cystoid macular edema (CME) is a rarely reported side effect of nanoparticle albumin bound (nab)-paclitaxel therapy-an antimitotic agent used for breast cancer. We describe a patient with bilateral CME secondary to Abraxane that was minimally responsive to intravitreal bevacizumab. To our knowledge, this is the first reported case of the use of intravitreal bevacizumab for this condition. A previous report has described the ineffectiveness of concurrent intravenous bevacizumab with Abraxane. This lack of efficacy and knowledge of the mechanism of paclitaxel may provide insights into the mechanisms of CME without angiographic leakage. METHODS: Retrospective, interventional case report of a patient with bilateral CME after starting Abraxane therapy for recurrent breast cancer treated with intravitreal bevacizumab (1.25 mg/0.05 mL) every 4 weeks. Records were reviewed for visual acuity and macular edema as assessed by spectral-domain optical coherence tomography (SD-OCT). RESULTS: A 73-year-old patient with recurrent, metastatic breast cancer presented with bilateral visual loss 3 months after nab-paclitaxel was initiated. Baseline visual acuities (VA) were 20/50 in the right eye (OD) and 20/80 in the left eye (OS). Fundus exam showed marked CME in both eyes (OU). Fluorescein angiography was notable for the marked absence of petalloid late-phase leakage characteristic of vascular, ischemic, and inflammatory causes of CME. SD-OCT showed marked cystoid spaces predominantly involving the outer and inner nuclear layers with central subfield thicknesses (CST) of 398 μm OD and 441 μm OS. Serial intravitreal bevacizumab injections (OD, 2 injections; OS, 3 injections) were administered on a 4-week basis with an improvement and stabilization of VA at 20/50 OD and 20/70 OS. However, CME on SD-OCT persisted with CST of 492 μm OD and 478 μm OS. CONCLUSIONS: The pathogenesis of CME without leakage is poorly understood; however, fluid accumulation in Muller cells due to toxicity has been proposed. The persistence of CME suggests that additional nonvascular endothelial growth factor-mediated mechanisms are involved. Improved understanding of the mechanisms underlying paclitaxel-associated CME is needed, especially in patients with limited systemic options for metastatic carcinoma.