Myasthenic syndromes are typically characterized by muscle weakness and increased fatigability due to an impaired transmission at the neuromuscular junction (NMJ). Most cases are caused by acquired autoimmune conditions such as myasthenia gravis (MG), typically with antibodies against the acetylcholine receptor (AChR). Different drugs are among the major factors that may complicate pre-existing autoimmune myasthenic conditions by further impairing transmission at the NMJ. Some clinical observations are substantiated by experimental data, indicating that presynaptic, postsynaptic or more complex pathomechanisms at the NMJ may be involved, depending on the individual compound. Most robust data exist for the risks associated with some antibiotics (e.g., aminoglycosides, ketolides, fluoroquinolones) and cardiovascular medications (e.g., class Ia antiarrhythmics, beta blockers). Apart from primarily autoimmune-mediated disorders of the NMJ, de novo myasthenic manifestations may also be triggered by medical treatments that induce an autoimmune reaction. Most notably, there is growing evidence that the immune checkpoint inhibitors (ICI), a modern class of drugs to treat various malignancies, represent a relevant risk factor to develop severe and progressive medication-induced myasthenia via an immune-mediated mechanism. From a clinical perspective, it is of utmost importance for the treating physicians to be aware of such adverse treatment effects and their consequences. In this article, we aim to summarize existing evidence regarding the key molecular and immunological mechanisms as well as the clinical implications of medication-aggravated and medication-induced myasthenic syndromes.

由于神经肌肉接头 (NMJ) 的传输受损，肌无力综合征的典型特征是肌肉无力和易疲劳性增加。大多数病例是由获得性自身免疫性疾病引起的，例如重症肌无力 (MG)，通常具有针对乙酰胆碱受体 (AChR) 的抗体。不同的药物是可能通过进一步削弱 NMJ 的传播而使预先存在的自身免疫性肌无力病症复杂化的主要因素。一些临床观察得到了实验数据的证实，表明可能涉及 NMJ 的突触前、突触后或更复杂的病理机制，具体取决于单个化合物。与某些抗生素（例如氨基糖苷类、酮内酯类、氟喹诺酮类）和心血管药物（例如，Ia 类抗心律失常药、β 受体阻滞剂）。除了主要由自身免疫介导的 NMJ 疾病外，从头开始引起自身免疫反应的药物治疗也可能引发肌无力表现。最值得注意的是，越来越多的证据表明免疫检查点抑制剂 (ICI)，一种用于治疗各种恶性肿瘤的现代药物，是通过免疫介导机制发展为严重和进行性药物诱导的肌无力的相关风险因素。从临床角度来看，治疗医师了解此类不良治疗效果及其后果至关重要。在本文中，我们旨在总结关于关键分子和免疫学机制以及药物加重和药物诱导的肌无力综合征的临床意义的现有证据。