Early treatment with N-acetylcysteine in children with acute liver failure secondary to hepatitis A
Early treatment with N-acetylcysteine in children with acute liver failure secondary to hepatitis A
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DOI：
10.1016/s1665-2681(19)31749-1
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发表时间：
2009-10-01
影响因子：
3.8
通讯作者：
Dhanakotti, Nagasharmila
中科院分区：
文献类型：
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作者：
Sotelo, Norberto;de los Angeles Durazo, Maria;Dhanakotti, Nagasharmila
介绍。如果不逆转，甲型肝炎病毒可能会演变成急性肝功能衰竭，并导致致命的后果。客观的。我们描述了 12 名患有甲型肝炎急性肝衰竭并接受口服 N-乙酰半胱氨酸 (NAC) 治疗的儿童的临床病程。材料和方法。 72 名甲型病毒性肝炎患者中，12 名患有急性肝功能衰竭。评估的变量包括年龄、性别、住院前临床特征的持续时间、体征和症状、实验室参数[丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、凝血酶原时间（PT）、部分凝血活酶时间（PTT）、内部标准化比和氨、治疗（口服NAC 100 mg/kg/天， 乳果糖、新霉素和一般措施）以及住院期间的临床病程。结果。其中包括六名男性和六名女性。学龄儿童和青春期儿童占多数。所有患者均出现黄疸、恶心、呕吐和肝肿大。根据 West-Haven 量表，其中两人出现 2 期神经系统体征。所有这些都改变了实验室参数。所有患者均接受 NAC，其中 6 名患者接受一周，其余 6 名患者接受 9-36 天。直到患者出现临床和实验室改善后才停止治疗。所有数据均使用学生 t 检验和 Wilcoxon 符号等级进行分析，α = 0.05，ALT P = 0.0003 和 0.005，AST P = 0.0001 和 0.0005，PT P = 0.0237 和 0.0005，PTT P = 0.0515 和 0.0039，氨 P = 0.0197 和 0.0015 以及直接胆红素，P = 0.0190 和0.068。对药物有良好的耐受性，临床病程令人满意。讨论。如果提供得当，口服 NAC 似乎是治疗甲型肝炎引起的肝衰竭的有效替代方案。它可以将临床病程改变为有利的，并预防肝性脑病的致命结果。
Introduction. Hepatitis A virus can evolve to acute liver failure with a fatal outcome if it is not reversed. Objective. We describe the clinical course of 12 children who presented with hepatitis A acute liver failure and received treatment with oral N-acetylcysteine (NAC). Materials and methods. Of the seventy-two patients with viral hepatitis A, 12 patients who had acute hepatic failure were included. The variables evaluated were age, sex, duration of clinical features prior to hospitalization, signs and symptoms, laboratory parameters [alanine aminotransferase (ALT), aspartate aminotransferase (AST), prothrombin time (PT), partial thromboptastin time (PTT), internal normalization ratio and ammonial, treatment (oral NAC 100 mg/kg/day, lactulose, neomycin and general measures) and clinical course during hospitalization. Results. Six males and six females were included. School-aged and adolescent children predominated. All presented with jaundice, nausea, vomiting and hepatomegaly. Two had stage 2 neurological signs as per the West-Haven scale. All had altered laboratory parameters. All received NAC, six patients for a week and the remaining six for 9-36 days. Treatment was not ceased until patients showed clinical and laboratory improvement. All data were analyzed using both student's t test and Wilcoxon signed rank with alpha = 0.05, the ALT with P = 0.0003 and 0.005, AST with P = 0.0001 and 0.0005, PT with P = 0.0237 and 0.0005, PTT with P = 0.0515 and 0.0039, ammonia with P = 0.0197 and 0.0015 and direct bilirubin with P = 0.0190 and 0.068. There was good tolerance to medications and a satisfactory clinical course. Discussion. The use of oral NAC appears to be an effective therapeutic alternative for hepatitis A-induced liver failure if it is offered appropriately. It can modify the clinical course to a favorable one and prevent the fatal outcome of hepatic encephalopathy.