Acute neurologic decompensation in an infant with cobalamin deficiency exposed to nitrous oxide
Acute neurologic decompensation in an infant with cobalamin deficiency exposed to nitrous oxide
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DOI：
10.1067/mpd.2000.107387
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发表时间：
2000-09-01
影响因子：
5.1
通讯作者：
Hayflick, SJ
中科院分区：
文献类型：
--
作者：
Felmet, K;Robins, B;Hayflick, SJ
暴露于一氧化二氮后，一名患有未被识别的钴胺素缺乏症的婴儿出现神经功能恶化和全血细胞减少。维生素补充后，血液学恢复，神经系统变化部分消退。一氧化二氮消耗生物可利用的钴胺素，可能是钴胺素缺乏症患者的危险麻醉剂。
After exposure to nitrous oxide, an infant with unrecognized cobalamin deficiency developed neurologic deterioration and pancytopenia. Hematologic recovery and partial resolution of his neurologic changes followed repletion of the vitamin. Nitrous oxide depletes bioavailable cobalamin and may be a dangerous anesthetic in patients with cobalamin deficiency.