Hughes Bradley, Feiz Vahid, Flynn Steven B, Brodsky Michael C
Cornea Service, Jones Eye Institute, and Department of Ophthalmology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Cornea. 2004 Nov;23(8):823-4. doi: 10.1097/01.ico.0000130417.91438.7e.
To document reversible corneal edema caused by amantadine in a pediatric patient.
A 14-year-old boy with a neurologic tremor was referred for bilateral visual loss. Our examination disclosed bilateral corneal edema without ocular inflammation. Pachymetry confirmed significantly increased corneal thickness above 900 microm.
Review of the patient's medical information revealed recent institution of amantadine as a means to control the patient's tremor. On cessation of this agent, rapid resolution of corneal edema and recovery of visual acuity occurred. Repeat pachymetry measurement revealed normal corneal thickness.
In cases of corneal edema and in the absence of any identifiable ocular causes, a review of toxic effects of systemic medication should be undertaken. Amantadine can cause corneal decompensation and needs to be considered as part of the differential diagnosis of corneal edema.
记录金刚烷胺在一名儿科患者中引起的可逆性角膜水肿。
一名患有神经性震颤的14岁男孩因双眼视力丧失前来就诊。我们的检查发现双眼角膜水肿但无眼部炎症。角膜测厚证实角膜厚度显著增加至900微米以上。
回顾患者的医疗信息发现最近开始使用金刚烷胺来控制患者的震颤。停用该药物后,角膜水肿迅速消退且视力恢复。重复角膜测厚测量显示角膜厚度正常。
在角膜水肿且无任何可识别的眼部病因的情况下,应审查全身用药的毒性作用。金刚烷胺可导致角膜失代偿,需要作为角膜水肿鉴别诊断的一部分加以考虑。