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三氧化二砷治疗急性早幼粒细胞白血病后发生的严重急性轴索性神经病:一例报告

Severe Acute Axonal Neuropathy following Treatment with Arsenic Trioxide for Acute Promyelocytic Leukemia: a Case Report.

作者信息

Kühn Marcus, Sammartin Kety, Nabergoj Mitja, Vianello Fabrizio

机构信息

Hematology and Immunology Unit, Padua University School of Medicine, via Giustiniani 1, 35128, Padua, Italy.

出版信息

Mediterr J Hematol Infect Dis. 2016 Apr 1;8(1):e2016023. doi: 10.4084/MJHID.2016.023. eCollection 2016.

Abstract

Peripheral neuropathy is a common complication of arsenic toxicity. Symptoms are usually mild and reversible following discontinuation of treatment. A more severe chronic sensorimotor polyneuropathy characterized by distal axonal-loss neuropathy can be seen in chronic arsenic exposure. The clinical course of arsenic neurotoxicity in patients with coexistence of thiamine deficiency is only anecdotally known but this association may potentially lead to severe consequences. We describe a case of acute irreversible axonal neuropathy in a patient with hidden thiamine deficiency who was treated with a short course of arsenic trioxide for acute promyelocytic leukemia. Thiamine replacement therapy and arsenic trioxide discontinuation were not followed by neurological recovery and severe polyneuropathy persisted at 12-month follow-up. Thiamine plasma levels should be measured in patients who are candidate to arsenic trioxide therapy. Prophylactic administration of vitamin B1 may be advisable. The appearance of polyneuropathy signs early during the administration of arsenic trioxide should prompt electrodiagnostic testing to rule out a pattern of axonal neuropathy which would need immediate discontinuation of arsenic trioxide.

摘要

周围神经病变是砷中毒的常见并发症。停药后症状通常较轻且可逆转。在慢性砷暴露中可出现一种更严重的以远端轴突丢失性神经病变为特征的慢性感觉运动性多发性神经病变。硫胺素缺乏并存患者的砷神经毒性临床过程仅为个案报道,但这种关联可能会导致严重后果。我们描述了一例隐匿性硫胺素缺乏患者的急性不可逆性轴索性神经病变,该患者因急性早幼粒细胞白血病接受了短疗程的三氧化二砷治疗。补充硫胺素并停用三氧化二砷后神经功能未恢复,在12个月的随访中严重的多发性神经病变持续存在。对于接受三氧化二砷治疗的患者,应检测其血浆硫胺素水平。预防性给予维生素B1可能是可取的。在三氧化二砷给药早期出现多发性神经病变体征应促使进行电诊断测试,以排除轴索性神经病变模式,这种情况需要立即停用三氧化二砷。

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