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左氧氟沙星相关性低血糖症并发脑桥髓鞘溶解症和四肢瘫痪。

Levofloxacin-associated hypoglycaemia complicated by pontine myelinolysis and quadriplegia.

作者信息

Vallurupalli S, Huesmann G, Gregory J, Jakoby M G

机构信息

Department of Internal Medicine, University of Illinois College of Medicine at Urbana-Champaign, IL, USA.

出版信息

Diabet Med. 2008 Jul;25(7):856-9. doi: 10.1111/j.1464-5491.2008.02465.x.

DOI:10.1111/j.1464-5491.2008.02465.x
PMID:18644072
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2613252/
Abstract

BACKGROUND

Central pontine myelinolysis (CPM) usually presents in chronic alcoholics and in patients in whom hyponatraemia has been corrected rapidly. However, CPM may occur in other clinical circumstances, including patients with severe hypoglycaemia. We describe the occurrence of CPM and quadriplegia in a patient who experienced fluoroquinolone-associated severe hypoglycaemia.

CASE REPORT

A 63-year-old man with Type 2 diabetes mellitus was admitted to hospital for resection of a large liposarcoma. Renal-dose levofloxacin was utilized as part of an antimicrobial regimen to treat post-operative peritonitis. On days 6-8 of levofloxacin therapy, the patient experienced recurrent hypoglycaemia despite total parenteral nutrition, 10% dextrose containing fluids and cessation of insulin therapy 3 days prior to the first hypoglycaemic episode. Hypoglycaemia resolved within 24 h of stopping levofloxacin. After a final and severe hypoglycaemic event, the patient developed quadriplegia and tonic left deviation of gaze. Magnetic resonance imaging revealed a high-intensity lesion in the central pons consistent with CPM.

CONCLUSIONS

Fluoroquinolones should be considered as a potential cause of hypoglycaemia. Severe hypoglycaemia has the potential to cause white matter lesions in the pons. Putative mechanisms include failure of membrane ion channels, oligodendrocyte apoptosis and oxidative stress of glucose reperfusion. Fluoroquinolone-associated hypoglycaemia and hypoglycaemia-induced quadriplegia are both rare and we believe this is the first case report linking the two events.

摘要

背景

中央桥脑髓鞘溶解症(CPM)通常见于慢性酒精中毒患者以及低钠血症迅速纠正的患者。然而,CPM也可能发生在其他临床情况下,包括严重低血糖患者。我们描述了一例发生氟喹诺酮相关严重低血糖后出现CPM和四肢瘫痪的病例。

病例报告

一名63岁2型糖尿病男性因切除巨大脂肪肉瘤入院。肾剂量左氧氟沙星作为抗菌方案的一部分用于治疗术后腹膜炎。在左氧氟沙星治疗的第6至8天,尽管给予了全胃肠外营养、含10%葡萄糖的液体并在首次低血糖发作前3天停止了胰岛素治疗,患者仍反复出现低血糖。停用左氧氟沙星后24小时内低血糖症状缓解。在最后一次严重低血糖事件后,患者出现四肢瘫痪和凝视向左强直性偏斜。磁共振成像显示脑桥中央有一个高强度病变,符合CPM表现。

结论

应考虑氟喹诺酮类药物为低血糖的潜在病因。严重低血糖有可能导致脑桥白质病变。推测的机制包括膜离子通道功能障碍、少突胶质细胞凋亡和葡萄糖再灌注氧化应激。氟喹诺酮相关低血糖和低血糖诱导的四肢瘫痪均很罕见,我们认为这是首例将这两个事件联系起来的病例报告。

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