{"title":"Nab-Paclitaxel Induced Cystoid Macular Oedema: Case Report and Literature Review.","authors":"Tejas Shivarthi, Sujithra Haridas, Keechilat Pavithran","doi":"10.22336/rjo.2025.76","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Nab-paclitaxel, a nanoparticle formulation of paclitaxel, is commonly used to treat solid tumors but is associated with rare adverse effects, including cystoid macular oedema (CMO). This case highlights the CMO in a patient undergoing nab-paclitaxel treatment for metastatic pancreatic cancer.</p><p><strong>Methods: </strong>A 72-year-old male receiving nab-paclitaxel and gemcitabine presented with progressive bilateral vision loss. Ophthalmological evaluation, including spectral-domain optical coherence tomography (SD-OCT), confirmed bilateral CMO. Nab-paclitaxel was discontinued, and the chemotherapy regimen was adjusted accordingly.</p><p><strong>Results: </strong>Visual symptoms improved significantly within 1 month of nab-paclitaxel cessation. Follow-up OCT and best-corrected visual acuity (BCVA) assessments showed significant improvement.</p><p><strong>Discussion: </strong>In this case, nab-paclitaxel-induced cystoid macular oedema (CMO) was confirmed by OCT and resolved rapidly after drug cessation. Review of 32 cases revealed predominantly bilateral involvement with highly variable onset and recovery times. In pancreatic cancer patients (n=8), cessation was the main management, with symptom onset ranging from 1-6 months and recovery typically within weeks to months. The variability in presentation may reflect acute toxic effects on Müller cells, disrupting retinal fluid homeostasis. Cases treated with carbonic anhydrase inhibitors showed faster resolution, supporting their role in modulating subretinal fluid dynamics. Alternative therapies such as NSAIDs or anti-VEGF agents demonstrated limited benefit, highlighting a non-inflammatory pathogenesis.</p><p><strong>Conclusions: </strong>Nab-paclitaxel-induced CMO is a rare but reversible condition that requires prompt cessation. Carbonic anhydrase inhibitors or anti-VEGF agents may expedite recovery in refractory cases. This report underscores the importance of early recognition and management of ocular toxicity in patients receiving nab-paclitaxel.</p>","PeriodicalId":94355,"journal":{"name":"Romanian journal of ophthalmology","volume":"69 4","pages":"482-487"},"PeriodicalIF":0.0000,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13065110/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Romanian journal of ophthalmology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22336/rjo.2025.76","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction: Nab-paclitaxel, a nanoparticle formulation of paclitaxel, is commonly used to treat solid tumors but is associated with rare adverse effects, including cystoid macular oedema (CMO). This case highlights the CMO in a patient undergoing nab-paclitaxel treatment for metastatic pancreatic cancer.
Methods: A 72-year-old male receiving nab-paclitaxel and gemcitabine presented with progressive bilateral vision loss. Ophthalmological evaluation, including spectral-domain optical coherence tomography (SD-OCT), confirmed bilateral CMO. Nab-paclitaxel was discontinued, and the chemotherapy regimen was adjusted accordingly.
Results: Visual symptoms improved significantly within 1 month of nab-paclitaxel cessation. Follow-up OCT and best-corrected visual acuity (BCVA) assessments showed significant improvement.
Discussion: In this case, nab-paclitaxel-induced cystoid macular oedema (CMO) was confirmed by OCT and resolved rapidly after drug cessation. Review of 32 cases revealed predominantly bilateral involvement with highly variable onset and recovery times. In pancreatic cancer patients (n=8), cessation was the main management, with symptom onset ranging from 1-6 months and recovery typically within weeks to months. The variability in presentation may reflect acute toxic effects on Müller cells, disrupting retinal fluid homeostasis. Cases treated with carbonic anhydrase inhibitors showed faster resolution, supporting their role in modulating subretinal fluid dynamics. Alternative therapies such as NSAIDs or anti-VEGF agents demonstrated limited benefit, highlighting a non-inflammatory pathogenesis.
Conclusions: Nab-paclitaxel-induced CMO is a rare but reversible condition that requires prompt cessation. Carbonic anhydrase inhibitors or anti-VEGF agents may expedite recovery in refractory cases. This report underscores the importance of early recognition and management of ocular toxicity in patients receiving nab-paclitaxel.