Qiu Hui, Li Hong-Wei, Zhang Shu-Hong, Zhou Xiao-Ge, Li Wei-Ping
Department of Cardiology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.
Department of Pathology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.
World J Clin Cases. 2021 Apr 26;9(12):2899-2907. doi: 10.12998/wjcc.v9.i12.2899.
QT interval prolongation can induce torsades de pointes (TdP), a potentially fatal ventricular arrhythmia. Recently, an increasing number of non-cardiac drugs have been found to cause QT prolongation and/or TdP onset. Moreover, recent findings have demonstrated the key roles of systemic inflammatory activation and fever in promoting long-QT syndrome (LQTS) and TdP development.
A 30-year-old woman was admitted with a moderate to high-grade episodic fever for two weeks. The patient was administered with multiple antibiotics after hospitalization but still had repeating fever and markedly elevated C-reactive protein. Once after a high fever, the patient suddenly lost consciousness, and electrocardiogram (ECG) showed transient TdP onset after frequent premature ventricular contraction. The patient recovered sinus rhythm and consciousness spontaneously, and post-TdP ECG revealed a prolonged QTc interval of 560 ms. The patient's clinical manifestations and unresponsiveness to the antibiotics led to the final diagnosis of adult-onset Still's disease (AOSD). There was no evidence of cardiac involvement. After the AOSD diagnosis, discontinuation of antibiotics and immediate initiation of intravenous dexamethasone administration resulted in the normal temperature and QTc interval. The genetic analysis identified that the patient and her father had heterozygous mutations in (c.1370C>T) and (c.7725A>C). During the 2-year follow-up period, the patient had no recurrence of any arrhythmia and maintained normal QTc interval.
This case study highlights the risk of systemic inflammatory activation and antibiotic-induced TdP/LQTS onset. Genetic analysis should be considered to identify individuals at high risk of developing TdP.
QT间期延长可诱发尖端扭转型室速（TdP），这是一种潜在致命的室性心律失常。最近，越来越多的非心脏药物被发现可导致QT间期延长和/或TdP发作。此外，最近的研究结果表明全身炎症激活和发热在促进长QT综合征（LQTS）和TdP发生发展中起关键作用。
一名30岁女性因中度至高度间歇性发热两周入院。患者住院后接受了多种抗生素治疗，但仍反复发热且C反应蛋白显著升高。一次高热后，患者突然失去意识，心电图（ECG）显示频发室性早搏后出现短暂的TdP发作。患者自发恢复窦性心律和意识，TdP发作后的心电图显示QTc间期延长至560毫秒。患者的临床表现及对抗生素无反应最终诊断为成人斯蒂尔病（AOSD）。无心脏受累证据。AOSD诊断后，停用抗生素并立即开始静脉注射地塞米松，体温和QTc间期恢复正常。基因分析确定患者及其父亲在（c.1370C>T）和（c.7725A>C）存在杂合突变。在2年的随访期内，患者未再发生任何心律失常，QTc间期维持正常。
本病例研究强调了全身炎症激活和抗生素诱发TdP/LQTS发作的风险。应考虑进行基因分析以识别发生TdP的高危个体。
