首页> 外文OA文献 >Acute Liver Failure In A Term Neonate After Repeated Paracetamol Administration [falência Hepática Aguda Em Neonato De Termo Após Ingestão De Doses Repetidas De Paracetamol]
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Acute Liver Failure In A Term Neonate After Repeated Paracetamol Administration [falência Hepática Aguda Em Neonato De Termo Após Ingestão De Doses Repetidas De Paracetamol]

机译:重复服用扑热息痛后足月新生儿的急性肝衰竭[摄入重复剂量的扑热息痛后足月新生儿的急性肝衰竭]

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摘要

Objective: Severe hepatotoxicity caused by paracetamol is rare in neonates. We report a case of paracetamol-induced acute liver failure in a term neonate. Case description: A 26-day-old boy was admitted with intestinal bleeding, shock signs, slight liver enlargement, coagulopathy, metabolic acidosis (pH=7.21; bicarbonate: 7.1mEq/L), hypoglycemia (18mg/dL), increased serum aminotransferase activity (AST=4,039IU/L; ALT=1,087IU/L) and hyperbilirubinemia (total: 9.57mg/dL; direct: 6.18mg/dL) after receiving oral paracetamol (10mg/kg/dose every 4 hours) for three consecutive days (total dose around 180mg/kg; serum concentration 36-48 hours after the last dose of 77μg/ mL). Apart from supportive measures, the patient was successfully treated with intravenous N-acetylcysteine infusion during 11 consecutive days, and was discharged on day 34. The follow-up revealed full recovery of clinical and of laboratory findings of hepatic function. Comments: The paracetamol pharmacokinetics and pharmacodynamics in neonates and infants differ substantially from those in older children and adults. Despite the reduced rates of metabolism by the P-450 CYP2E1 enzyme system and the increased ability to synthesize glutathione - which provides greater resistance after overdoses -, it is possible to produce hepatotoxic metabolites (N-acetyl-p-benzoquinone) that cause hepatocellular damage, if glutathione sources are depleted. Paracetamol clearance is reduced and the half-life of elimination is prolonged. Therefore, a particular dosing regimen should be followed due to the toxicity risk of cumulative doses. This report highlights the risk for severe hepatotoxicity in neonates after paracetamol multiple doses for more than two to three days.
机译:目的:对乙酰氨基酚引起的严重肝毒性在新生儿中很少见。我们在足月新生儿中报告了一例扑热息痛引起的急性肝衰竭。病例描述:一名26岁男孩入院,其肠道出血,休克迹象,轻微肝肿大,凝血病,代谢性酸中毒(pH = 7.21;碳酸氢盐:7.1mEq / L),低血糖(18mg / dL),血清转氨酶升高连续3次口服对乙酰氨基酚(每4小时10mg / kg /剂量)后,其活动(AST = 4,039IU / L; ALT = 1,087IU / L)和高胆红素血症(总计:9.57mg / dL;直接:6.18mg / dL)天(总剂量约180mg / kg;最后一次剂量后77-g / mL后36-48小时的血清浓度)。除支持措施外,该患者已连续11天成功接受静脉内N-乙酰半胱氨酸静脉滴注治疗,并于第34天出院。随访结果显示临床和实验室检查发现肝功能完全恢复。注释:新生儿和婴儿中对乙酰氨基酚的药代动力学和药效学与年龄较大的儿童和成人的显着不同。尽管P-450 CYP2E1酶系统降低了新陈代谢的速度,增强了合成谷胱甘肽的能力-服用过量后提供了更大的抵抗力-但仍可能产生引起肝细胞损伤的肝毒性代谢产物(N-乙酰基-对-苯醌) ,如果耗尽了谷胱甘肽来源。扑热息痛的清除率降低,消除的半衰期延长。因此,由于累积剂量的毒性风险,应遵循特定的给药方案。该报告强调了对乙酰氨基酚多次给药超过两到三天后,新生儿发生严重肝毒性的风险。

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