Gnanashanmugam G, Balakrishnan R, Somasundaram S P, Parimalam N, Rajmohan P, Pranesh M B
Department of Neurology, PSGIMSR, Coimbatore, Tamil Nadu, India.
Ann Indian Acad Neurol. 2018 Jan-Mar;21(1):49-56. doi: 10.4103/aian.AIAN_274_17.
Mercury is used extensively in the preparation of Siddha medicines, after purification. In this study, we present 32 patients of mercury toxicity following unauthorized Siddha medicine intake who mimicked neuromyotonia clinically. We analyzed the clinical features of these patients, the role of autoimmunity in etiopathology, and compared it with acquired neuromyotonia.
This is a retrospective study to analyze inpatients in a tertiary care center, admitted with mercury toxicity following Siddha medicine intake from August 2012 to October 2016. We analyzed the clinical features, laboratory data including mercury, arsenic and lead levels in blood, and serum voltage-gated potassium channels (VGKC)-CASPR2 Ab in selected patients.
Thirty-two patients who had high blood mercury levels following Siddha medicine intake were included in the study. All patients (100%) had severe intractable neuropathic pain predominantly involving lower limbs. Twenty-six (81.25%) patients had fasciculations and myokymia. Fifteen patients (46.86%) had autonomic dysfunction (postural hypotension and resting tachycardia). Nine (28.12%) patients had encephalopathic features such as dullness, apathy, drowsiness, or delirium. Anti-VGKC Ab was positive in 12 patients with myokymia. All the patients in the study consumed Siddha medicines obtained from unauthorized dealers.
Mercury toxicity following Siddha medicine intake closely mimics acquired neuromyotonia; severe intolerable neuropathic pain is the hallmark feature; Positive VGKC-CASPR2 antibody in some patients must be due to triggered autoimmunity secondary to mercury toxicity due to Siddha medicine intake. The government should establish licensing system to prevent distribution of unauthorized Siddha medicines.
汞在经过提纯后被广泛用于悉达医学药物的制备。在本研究中,我们报告了32例因私自服用悉达医学药物而导致汞中毒的患者,这些患者临床上表现为拟似神经性肌强直。我们分析了这些患者的临床特征、自身免疫在病因病理中的作用,并将其与获得性神经性肌强直进行了比较。
这是一项回顾性研究,分析了2012年8月至2016年10月期间在一家三级医疗中心因服用悉达医学药物后出现汞中毒而入院的患者。我们分析了临床特征、实验室数据,包括血液中的汞、砷和铅水平,以及部分患者的血清电压门控钾通道(VGKC)-接触蛋白相关蛋白2抗体(CASPR2 Ab)。
本研究纳入了32例因服用悉达医学药物后血汞水平升高的患者。所有患者(100%)均有严重的顽固性神经性疼痛,主要累及下肢。26例(81.25%)患者有肌束震颤和肌纤维颤搐。15例(46.86%)患者有自主神经功能障碍(体位性低血压和静息性心动过速)。9例(28.12%)患者有脑病特征,如精神迟钝、淡漠、嗜睡或谵妄。12例有肌纤维颤搐的患者抗VGKC抗体呈阳性。本研究中的所有患者均服用了从非法经销商处获得的悉达医学药物。
服用悉达医学药物后的汞中毒与获得性神经性肌强直极为相似;严重的难以忍受的神经性疼痛是其标志性特征;部分患者中VGKC-CASPR2抗体呈阳性必定是由于服用悉达医学药物导致汞中毒引发的自身免疫反应。政府应建立许可制度,以防止非法悉达医学药物的流通。