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Acetaminophen-induced, Not Desflurane-induced, Hepatotoxicity

机译:对乙酰氨基酚诱导的而非地氟烷诱导的肝毒性

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摘要

I believe that the case of hepatotoxicity after desfluraneanesthesia in a 15-month-old child with Mobius syndrome after previous exposure to isoflurane, reported by Drs. Cote and Bouchard, is not a case of desflurane-induced but acetaminophen-induced hepatotoxicity. Drs. Cote and Bouchard ignored that liver enzyme levels were too high for desflurane-induced hepatotoxicity, that the serum level of acetaminophen on the second postoperative day after multiple doses was high enough to induce hepatotoxicity, and that omeprazole is an inducer of the cytochrome P-450 enzymes (CYPs) CYP 1A2 and CYP 3A4, which increase oxidative metabolism of acetaminophen. They also ignored that cisapride increases the bioavailability of acetaminophen by inhibiting its glucuronidation in humans.
机译:我认为,以前曾接触过异氟烷的15个月大Mobius综合征患儿在去氟醚麻醉后发生了肝毒性病例。 Cote和Bouchard不是由地氟醚引起的,而是由对乙酰氨基酚引起的肝毒性。博士Cote和Bouchard忽略了肝酶水平对于地氟醚引起的肝毒性而言过高,对乙酰氨基酚在多次给药后第二天的血清水平过高而足以引起肝毒性,而奥美拉唑是细胞色素P-450的诱导剂。酵素(CYPs)CYP 1A2和CYP 3A4,增加对乙酰氨基酚的氧化代谢。他们还忽略了西沙必利通过抑制人体内的葡糖醛酸糖苷化来增加对乙酰氨基酚的生物利用度。

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