Coronary spastic angina after the administration of intravenous immunoglobulin in myasthenia gravis: a case report
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CASE REPORT
Open Access
Coronary spastic angina after the administration of intravenous immunoglobulin in myasthenia gravis: a case report Masaru Yanagihashi1*, Ryuichi Okamoto1, Harumi Morioka1, Masahiro Sawada1, Shingo Matsumoto2, Takanori Ikeda2 and Osamu Kano1
Abstract Background: Myasthenia gravis (MG) is an autoimmune disease caused by antibodies that block or destroy nicotinic acetylcholine receptors at the neuromuscular junction. Most of MG patients need immunosuppression agents in addition to treatments that alleviate the symptoms. Intravenous immunoglobulin (IVIg) and plasma exchange are specific treatments given to patients with severe MG and myasthenia gravis crisis. IVIg therapy can cause an increase in serum viscosity; therefore, the risk for thromboembolic events, such as stroke, myocardial infarction, and pulmonary embolism, are reported after IVIg therapy. Case presentation: An MG patient was treated with pyridostigmine bromide and prednisolone. The patient’s symptoms worsened 26 days after the commencement of treatment and was presented with head drop and dyspnea. The patient was diagnosed with MG crisis and IVIg was initiated. However, the patient reported chest pain and dyspnea 3 days after IVIg had started. An electrocardiogram (ECG) revealed ST elevations in leads II, III, and aVF. A cardiac catheterization was performed and stenosis, obstruction, and sclerosis were ruled out. Glyceryl trinitrate relieved the patient’s symptoms, suggesting coronary spastic angina (CSA). Conclusions: We report the first case of CSA after IVIg. Practitioners should be aware of the potential risks of CSA when administering IVIg for MG patients, in particular in old patients with vascular risk factors. Keywords: Coronary spastic angina (CSA), Intravenous immunoglobulin (IVIG), Myasthenia gravis (MG)
Background Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction (NMJ), manifesting as skeletal muscle fatigable weakness. In most cases of MG, the number of available acetylcholine receptors is decreased due to the autoimmune attack. However, the musclespecific kinase, lipoprotein receptor-related protein 4, * Correspondence: [email protected] 1 Division of Neurology, Toho University Omori Faculty of Medicine, 6-11-1, Omorinishi, Ota-ku, Tokyo 143-8541, Japan Full list of author information is available at the end of the article
agrin, titin, and ryanodine receptors are targeted in some cases of MG [1, 2]. Acetylcholinesterase inhibitors and immunosuppressive agents such as prednisolone and azathioprine are effective in treating MG. However, patients with MG crisis that require intubation or noninvasive ventilation should receive immunosuppressive agents and intensive care [2]. In MG exacerbation and crisis, intravenous immunoglobulin (IVIg) and plasma exchange are recognized as effective therapies, providing benefits within 2 weeks of treatment commencement [3, 4]. IVIg is often regarded as convenient and safe for
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