Leppert D, Waespe W
Neurologische Klinik, Universitätsspital, Zürich.
Ital J Neurol Sci. 1988 Feb;9(1):31-4. doi: 10.1007/BF02334404.
A 56-year old patient presented 3 months after initiation of an antituberculous regimen with Isoniacid (INH, 5 mg/kg daily), Ethambutol (20 mg/kg daily) and Rifampicin (675 mg daily) a mild sensory polyneuropathy and a bilateral retrobulbar neuritis which progressed to a severe optic atrophy. Multiple hyperintense foci were detected with NMR-imaging in the cerebral white matter suggestive of demyelination. INH and Ethambutol are known for their neurotoxic effects but suggestion was made that neurologic signs may not be due to drug neurotoxicity but could be induced by immunological processes initiated by the tubercle bacillus. In the reported patient the suspected tuberculosis of the urogenital tract was never proved histologically. Most likely his neurological symptoms were therefore cause by the administration of INH and Ethambutol. Patients with a low serum zinc level and a slow acetylation of INH are reported to be at special risk; both factors were present in our patient.
一名56岁患者在开始使用异烟肼（INH，每日5mg/kg）、乙胺丁醇（每日20mg/kg）和利福平（每日675mg）的抗结核治疗方案3个月后，出现轻度感觉性多发性神经病和双侧球后视神经炎，并进展为严重的视神经萎缩。核磁共振成像在脑白质中检测到多个高信号灶，提示脱髓鞘。已知INH和乙胺丁醇具有神经毒性作用，但有人认为神经体征可能并非药物神经毒性所致，而是由结核杆菌引发的免疫过程所诱发。在该报告患者中，泌尿生殖道疑似结核病从未经组织学证实。因此，很可能他的神经症状是由INH和乙胺丁醇的使用引起的。据报道，血清锌水平低且INH乙酰化缓慢的患者处于特殊风险中；这两个因素在我们的患者中都存在。
