Schrör Karsten
Institut für Pharmakologie und Klinische Pharmakologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany.
Paediatr Drugs. 2007;9(3):195-204. doi: 10.2165/00148581-200709030-00008.
Reye syndrome is an extremely rare but severe and often fatal disease. Death occurs in about 30-40% of cases from brainstem dysfunction. The disease typically is preceded by a viral infection with an intermediate disease-free interval of 3-5 days. The biochemical explanation for Reye-like symptoms is a generalized disturbance in mitochondrial metabolism, eventually resulting in metabolic failure in the liver and other tissues. The etiology of 'classical' Reye syndrome is unknown. Hypothetically, the syndrome may result from an unusual response to the preceding viral infection, which is determined by host genetic factors but can be modified by a variety of exogenous agents. Thus, several infections and diseases might present clinically with Reye-like symptoms. Exogenous agents involve a number of toxins, drugs (including aspirin [acetylsalicylic acid]), and other chemicals. The 'rise and fall' in the incidence of Reye syndrome is still poorly understood and unexplained. With a few exceptions, there were probably no new Reye-like diseases reported during the last 10 years that could not be explained by an inherited disorder of metabolism or a misdiagnosis. This may reflect scientific progress in the better understanding of cellular and molecular dysfunctions as disease-determining factors. Alternatively, the immune response to and the virulence of a virus might have changed by alteration of its genetic code. The suggestion of a defined cause-effect relationship between aspirin intake and Reye syndrome in children is not supported by sufficient facts. Clearly, no drug treatment is without side effects. Thus, a balanced view of whether treatment with a certain drug is justified in terms of the benefit/risk ratio is always necessary. Aspirin is no exception.
瑞氏综合征是一种极其罕见但严重且往往致命的疾病。约30%-40%的病例因脑干功能障碍而死亡。该疾病通常由病毒感染引发,中间有3至5天的无病间隔期。瑞氏综合征样症状的生化解释是线粒体代谢的普遍紊乱,最终导致肝脏和其他组织的代谢衰竭。“经典”瑞氏综合征的病因尚不清楚。据推测,该综合征可能是对先前病毒感染的异常反应所致,这种反应由宿主遗传因素决定,但可被多种外源性因素改变。因此,一些感染和疾病在临床上可能表现出瑞氏综合征样症状。外源性因素包括多种毒素、药物(包括阿司匹林[乙酰水杨酸])和其他化学物质。瑞氏综合征发病率的“起起落落”仍未得到充分理解和解释。除了少数例外,在过去10年中可能没有报告过无法用遗传性代谢紊乱或误诊来解释的新的瑞氏综合征样疾病。这可能反映了在更好地理解细胞和分子功能障碍作为疾病决定因素方面的科学进展。或者,病毒的免疫反应和毒力可能因其遗传密码的改变而发生了变化。阿司匹林摄入与儿童瑞氏综合征之间存在明确因果关系的说法没有得到充分事实的支持。显然,没有一种药物治疗是没有副作用的。因此,始终有必要从获益/风险比的角度对某种药物治疗是否合理持平衡的观点。阿司匹林也不例外。