Singh Paramveer, Idowu Olakunle, Malik Imrana, Nates Joseph L
Tex Heart Inst J. 2015 Oct 1;42(5):495-7. doi: 10.14503/THIJ-14-4584. eCollection 2015 Oct.
Magnesium is known to act at the neuromuscular junction by inhibiting the presynaptic release of acetylcholine and desensitizing the postsynaptic membrane. Because of these effects, magnesium has been postulated to potentiate neuromuscular weakness. We describe the case of a 62-year-old woman with myasthenia gravis and a metastatic thymoma who was admitted to our intensive care unit for management of a myasthenic crisis. The patient's neuromuscular weakness worsened in association with standard intravenous magnesium replacement, and the exacerbated respiratory failure necessitated intubation, mechanical ventilation, and an extended stay in the intensive care unit. The effect of magnesium replacement on myasthenia gravis patients has not been well documented, and we present this case to increase awareness and stimulate research. In addition, we discuss the relevant medical literature.
已知镁通过抑制乙酰胆碱的突触前释放和使突触后膜脱敏而作用于神经肌肉接头。由于这些作用，有人推测镁会增强神经肌肉无力。我们描述了一名62岁重症肌无力合并转移性胸腺瘤的女性病例，她因重症肌无力危象入住我们的重症监护病房。在进行标准静脉镁补充治疗过程中，患者的神经肌肉无力加重，呼吸衰竭加剧，需要进行插管、机械通气，并在重症监护病房延长住院时间。镁补充对重症肌无力患者的影响尚未得到充分记录，我们呈现此病例以提高认识并激发研究。此外，我们还讨论了相关医学文献。
