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Nicardipine-Induced Acute Hepatitis in an Intensive Care Unit Patient

机译:重症监护病房患者尼卡地平诱导的急性肝炎

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Drug-related hepatotoxicity is now the leading cause of acute liver failure in the United States, especially among patients who have no prior liver disease. Nicardipine is the only IV calcium channel blocker available for the short-term treatment of hypertension with a considerably good safety profile. We report a case of nicardipine-induced hepatitis. A patient with history of hypertension was admitted because of right middle cerebral artery infarction. Computed tomography of the brain showed evolving stroke. The patient went for cerebral angiography and stent placement, and during the procedure he had cerebral hemorrhage. He was transferred to neurosurgery. After surgery, he was started on hypertonic saline, mannitol for cerebral edema, and nicardipine drip for blood pressure control. On the fourth day after operation, he started to have fever with progressive elevation of liver enzymes [Aspartate amino transferase (AST) 450, Alanine amino transferase (ALT) 356, and alkaline phosphatase 299]. Serum bilirubin was 0.6. He did not receive blood transfusion. No medical history of hepatitis or liver disease was reported. Other medications included metoprolol and heparin. White blood cell count was 13,000. Chest x-ray did not show evidence of consolidation. Urine analysis was unremarkable. Cultures were negative. Acute hepatitis panel was negative. Cerebrospinal fluid examination was normal. Liver enzymes were trending up gradually with normal protein and bilirubin. Computed tomography of the abdomen was unremarkable. The patient's medications were reviewed. It was noticed that the patient started to have fever and elevated liver enzymes after administration of nicardipine drip. It was postulated that nicardipine may be the culprit of acute hepatitis. Nicardipine drip was stopped, and the patient was started on labetalol. Fever started to resolve, and liver enzymes started trending down toward normal. The patient remained afebrile after that.
机译:在美国,与药物相关的肝毒性现已成为急性肝衰竭的主要原因,尤其是在以前没有肝病的患者中。尼卡地平是唯一可用于短期高血压治疗的静脉内钙通道阻滞剂,具有相当好的安全性。我们报告了一例尼卡地平诱发的肝炎。患有高血压病史的患者因右中脑动脉梗塞而入院。脑部计算机断层扫描显示中风正在发展。该患者进行了脑血管造影和支架置入,并且在手术过程中发生了脑出血。他被转到神经外科。手术后,他开始使用高渗盐水,甘露醇治疗脑水肿,并使用尼卡地平进行血压控制。手术后第四天,他开始发烧,肝脏酶逐渐升高[天冬氨酸氨基转移酶(AST)450,丙氨酸氨基转移酶(ALT)356和碱性磷酸酶299]。血清胆红素为0.6。他没有接受输血。没有肝炎或肝病的病史报道。其他药物包括美托洛尔和肝素。白细胞计数为13,000。胸部X光片未显示巩固的证据。尿液分析无异常。文化是消极的。急性肝炎阴性。脑脊液检查正常。肝酶与正常蛋白和胆红素逐渐升高。腹部计算机体层摄影术并不明显。审查了患者的药物。注意到患者在服用尼卡地平滴注后开始发烧和肝酶升高。据推测,尼卡地平可能是急性肝炎的元凶。停止尼卡地平滴注,开始使用拉贝洛尔治疗。发烧开始消退,肝酶开始趋向正常。此后,患者保持发热。

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