Narcolepsy with cataplexy and hyperthyroidism sudden appeared after H1N1 vaccination
Narcolepsy with cataplexy and hyperthyroidism sudden appeared after H1N1 vaccination
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DOI：
10.5935/1984-0063.20180008
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发表时间：
2018-01-01
期刊：
影响因子：
1.6
通讯作者：
Podesta, Claudio
中科院分区：
文献类型：
--
作者：
Leiva, Silvia;Madrazo, Jimena;Podesta, Claudio
1型发作性睡病（NT1）是一种慢性睡眠障碍，其特征是白天过度嗜睡、发作和夜间睡眠碎片化。它是由于产生下丘脑分泌素的神经元显著减少而引起的下丘脑分泌素缺乏。在过去的几年里，人们一直假设自身免疫机制会对那些遗传易感患者的这些神经元的破坏负责。众所周知，在2009-2010年H1N1流感大流行性疫苗接种运动之后，发作性睡病的发病率有所增加。我们在下面报告一个成年患者的病例，他在接种H1N1疫苗10天后，在入睡后发生交通事故。随后的研究显示甲状腺功能亢进是由格雷夫斯病引起的。尽管进行了治疗，患者仍持续出现每日和致残的日间嗜睡、睡眠发作和全身性肌肉张力发作，但意识保持。经夜间多导睡眠图和多次睡眠潜伏期试验（MSLT）诊断为NT1。本病例的特殊之处在于无佐剂H1N1疫苗引发的两种自身免疫性疾病，迄今为止只有NT1与有佐剂和病毒感染的疫苗相关的证据。这两种实体的关联使我们对自身免疫机制进行了反思，加强了其在疾病发病中的作用理论。
Narcolepsy type 1 (NT1) is a chronic sleep disorder, characterized by excessive daytime sleepiness, cataplexy and fragmented nocturnal sleep. It is caused by a hypocretin deficiency due to a significant reduction of the neurons producing it. In the last years, it has been postulated that an autoimmune mechanism would be responsible for the destruction of these neurons in those genetically predisposed patients. The increased incidence of narcolepsy after the pandemic H1N1 influenza vaccination campaign in 2009-2010 is known. We present below the case of an adult patient who, 10 days after receiving H1N1 vaccination, suffers a traffic accident after falling asleep. Subsequent studies revealed hyperthyroidism due to Graves disease. In spite of the treatment, the patient persisted with daily and disabling daytime sleepiness, sleep attacks and episodes of generalized muscle atony with preservation of consciousness. A nocturnal polysomnography and multiple sleep latency test (MSLT) were performed with a diagnosis of NT1. The particularity of this case is the presentation of 2 autoimmune diseases triggered by an H1N1 vaccine without adjuvant, so far there is only evidence of NT1 associated with vaccines with adjuvant and viral infection. The association of both entities has made us reflect on the autoimmune mechanism, reinforcing the theory of its role in the onset of the disease.