Golomb Beatrice Alexandra, Koslik Hayley Jean, Redd Alan J
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Department of Anthropology, University of Kansas, Lawrence, Kansas, USA.
BMJ Case Rep. 2015 Oct 5;2015:bcr2015209821. doi: 10.1136/bcr-2015-209821.
We present a case series of four previously healthy, employed adults without significant prior medical history in each of whom symptoms developed while on fluoroquinolones (FQs), with progression that continued following discontinuation evolving to a severe, disabling multisymptom profile variably involving tendinopathy, muscle weakness, peripheral neuropathy, autonomic dysfunction, sleep disorder, cognitive dysfunction and psychiatric disturbance. Physicians and patients should be alert to the potential for FQ-induced severe disabling multisymptom pathology that may persist and progress following FQ use. Known induction by FQs of delayed mitochondrial toxicity provides a compatible mechanism, with symptom profiles (and documented mechanisms of FQ toxicity) compatible with the hypothesis of an exposure-induced mitochondrial neurogastrointestinal encephalomyopathy.
我们报告了一个病例系列，其中4名既往健康的在职成年人，每人既往均无重大病史，他们在使用氟喹诺酮类药物（FQ）时出现症状，停药后症状仍持续进展，发展为严重的、致残的多症状表现，不同程度地累及肌腱病、肌肉无力、周围神经病变、自主神经功能障碍、睡眠障碍、认知功能障碍和精神障碍。医生和患者应警惕FQ诱发的严重致残性多症状病理状况的可能性，这种状况在使用FQ后可能持续并进展。已知FQ可诱发迟发性线粒体毒性，这提供了一种与之相符的机制，其症状表现（以及已记录的FQ毒性机制）与暴露诱发的线粒体神经胃肠脑肌病假说相符。
