首页> 外文期刊>American Journal of Ophthalmology Case Reports >Is it melanoma-associated retinopathy or drug toxicity? Bilateral cystoid macular edema posing a diagnostic and therapeutic dilemma
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Is it melanoma-associated retinopathy or drug toxicity? Bilateral cystoid macular edema posing a diagnostic and therapeutic dilemma

机译:是黑素瘤相关性视网膜病还是药物毒性?双侧囊样黄斑水肿引起诊断和治疗困境

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Purpose To report the clinical presentation, multimodal imaging, and management of a patient with metastatic melanoma who presented with cystoid macular edema (CME). Observations We report a case of a 71-year-old Caucasian male with metastatic melanoma who presented with bilateral cystoid macular edema after being on treatment with a programmed T cell death ligand 1 inhibitor, MPDL3280, for 1 year. Multimodal imaging techniques, including color fundus photographs, autofluorescence, spectral domain optical coherence tomography (OCT), fluorescein angiography (Spectralis, Heidelberg, Germany), and spectral-domain OCT angiography (Zeiss; California, USA) were performed to evaluate the etiology of his CME and to monitor his response to treatment. Clinical examination and multimodal imaging revealed 1?+?chronic vitreous cells, an epiretinal membrane, and mild macular edema in both eyes. Fundus autofluorescence showed paravenous hypoautofluorescence in the right eye and scattered hypoautofluorescent spots in the left eye. Optical coherence tomography angiography (OCTA) revealed mild drop out of superficial vessels in the peri-foveal region bilaterally. These findings were concerning for melanoma-associated retinopathy, drug-related uveitis, or activation of a previous chronic autoimmune process. The patient was started on prednisone 30 mg oral daily and ketorolac tromethamine 0.5% 1 drop four times daily. He was then treated with bilateral sustained-release dexamethasone intravitreal implants (Ozurdex). He had complete resolution of CME, and was tapered off of oral steroids within 6 weeks. Conclusions and Importance Melanoma-associated retinopathy can be accompanied by CME, which presents a diagnostic and therapeutic dilemma in cases where a new drug has been recently initiated. By treating the condition locally, the ophthalmologist may be able to taper systemic immunosuppression more quickly.
机译:目的报告患有囊性黄斑水肿(CME)的转移性黑色素瘤患者的临床表现,多模态成像和管理。观察结果我们报告了一例71岁的白人男性,患有转移性黑色素瘤,在接受程序化T细胞死亡配体1抑制剂MPDL3280治疗1年后,出现双侧囊样黄斑水肿。进行多模态成像技术,包括彩色眼底照片,自发荧光,光谱域光学相干断层扫描(OCT),荧光素血管造影术(Spectralis,海德堡,德国)和光谱域OCT血管造影术(Zeiss;加利福尼亚,美国),以评估病因。他的CME并监视他对治疗的反应。临床检查和多模态成像显示双眼出现1 + +慢性玻璃体细胞,视网膜前膜和轻度黄斑水肿。眼底自发荧光在右眼显示静脉自发性自发荧光,在左眼显示散在的自发荧光。光学相干断层扫描血管造影(OCTA)显示双侧中央凹区双侧浅表血管轻度脱落。这些发现与黑色素瘤相关的视网膜病变,药物相关的葡萄膜炎或先前慢性自身免疫过程的激活有关。病人开始每天口服泼尼松30 mg,酮咯酸氨丁三醇0.5%1滴,每天四次。然后,他接受了双侧缓释地塞米松玻璃体内植入物(Ozurdex)的治疗。他具有完全的CME缓解能力,并且在6周内逐渐停用口服类固醇。结论和重要性黑色素瘤相关性视网膜病变可伴有CME,如果最近开始使用新药,则将带来诊断和治疗的难题。通过局部治疗该病症,眼科医生可能能够更快地逐渐减少全身性免疫抑制。

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