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• W2056178485 abstract "Editor—The safety profile of acetaminophen (N-acetyl-para-aminophenol) makes it one of the most widely prescribed analgesics.1Benson GD Koff RS Tolman KG The therapeutic use of acetaminophen in patients with liver disease.Am J Ther. 2005; 12: 133-141Crossref PubMed Scopus (114) Google Scholar Acute liver failure due to therapeutic doses of acetaminophen is controversial.1Benson GD Koff RS Tolman KG The therapeutic use of acetaminophen in patients with liver disease.Am J Ther. 2005; 12: 133-141Crossref PubMed Scopus (114) Google Scholar 2Krähenbühl S Brauchli Y Kummer O et al.Acute liver failure in two patients with regular alcohol consumption ingesting paracetamol at therapeutic dosage.Digestion. 2007; 75: 232-237Crossref PubMed Scopus (25) Google Scholar Some clinicians encourage regular postoperative administration of acetaminophen 4–5 g day−1.3Myles PS Power I Clinical update: postoperative analgesia.Lancet. 2007; 369: 810-812Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar However, liver injury with therapeutic doses cannot be excluded.4Jalan R Williams R Bernau J Paracetamol: are therapeutic doses entirely safe?.Lancet. 2006; 368: 2195-2196Abstract Full Text Full Text PDF PubMed Scopus (46) Google Scholar We report two cases of postoperative acute liver failure attributed to therapeutic doses of acetaminophen. Case 1: A 43-yr-old female (70 kg, 166 cm, BMI 25) was re-operated on for laparoscopic readjustment of her gastric band. Anaesthesia was induced with propofol followed by desflurane, sufentanil, and rocuronium. The surgery was uncomplicated. She received a dose of ketorolac i.v. (30 mg) and acetaminophen 1 g four times a day. On the third day, after a total intake of acetaminophen 11 g, she presented with acute liver failure associated with multiple organ failure (factor V level 5% of normal, prothrombin time: 71 s, INR 12.9, liver cytolysis: ASAT: 5321 U litre−1, ALAT: 3401 U litre−1) (Table 1). Serum concentration of acetaminophen was 31.8 mg litre−1 (17 h after the last dose). She was treated with N-acetylcysteine (NAC) and supported by a Molecular Adsorbed Recirculation System (MARS). Two days later, an orthotopic liver transplantation (OLT) was successfully performed under desflurane-based anaesthesia. Histopathology of the liver showed generalized steatosis in the viable hepatocytes and major centrolobular necrosis (zone 3) highly suggestive of a toxic origin. The patient was discharged after 6 weeks at home.Table 1Pre- and postoperative laboratory values in two cases of fulminant hepatitis due to acetaminophen. Day 1, day of admission to the ICU. For case 1, MARS started on D2 and OLT performed on D3Preop.D1D2D3D4D5D6D7D14Case 1 ALAT (U litre−1)83401311032801451829513345120 ASAT (U litre−1)205321419025329162611248161 INR (s)1.112.93.142.852.371.090.970.891.11 LDH (U litre−1)4945481377010901018230219194189 Bilirubin (mg dl−1)0.54.55.77.53.91.71.91.41.4 γGT (U litre−1)10243445221976150110Case 2 ALAT (U litre−1)2750112535918502———51 ASAT (U litre−1)19930155401816493———30 INR (s)1.02.01.331.231.17———1.1 LDH (U litre−1)36193764000606351———493 Bilirubin (mg dl−1)0.50.91.52.41.9———0.9 γGT (U litre−1)217712571568551———362 Open table in a new tab Case 2: A 60-yr-old female (90 kg, 160 cm, BMI 35) with a chronic elevation of γ-glutamyl transpeptidase (γGT) (preoperative value: 217 U litre−1) and seizures controlled with valproic acid and carbamazepine presented in acute liver failure 2 days after a re-intervention for a post-lumbar laminectomy dural leak. Anaesthesia, at that time, was induced with propofol followed by sevoflurane, sufentanil, and rocuronium. Analgesia included diclofenac and morphine (48 h). Acetaminophen 1 g four times daily had been given for 10 days before the intensive care unit (ICU) admission. The acute liver failure was associated with a severe coagulopathy and encephalopathy (prothrombin time: 41 s, INR: 2.0, cephalin activated time: 48.5 s, severe thrombocytopenia: 9000 plat µl−1, liver cytolysis: ASAT: 9301 U litre−1, ALAT: 5011 U litre−1, renal insufficiency: serum creatinine 2.7 mg dl−1) (Table 1). Serum concentration of acetaminophen was 10 mg litre−1 (48 h after the last dose). She was treated with NAC. Improvement of all parameters permitted discharge from the ICU after 48 h. In the two cases, CT scan and abdominal ultrasound showed a highly hypodense and hyperechogenic, homogeneous and enlarged liver, clearly suggestive of chronic liver steatosis. In the two patients, serological investigations did not show evidence of viral hepatitis (A, B, or C). Acetaminophen toxicity proposed in these cases because of well-known risk factors (antiepileptic drugs and liver steatosis), highly suggestive histopathology, classical clinical course,2Krähenbühl S Brauchli Y Kummer O et al.Acute liver failure in two patients with regular alcohol consumption ingesting paracetamol at therapeutic dosage.Digestion. 2007; 75: 232-237Crossref PubMed Scopus (25) Google Scholar and exclusion of other causes. Non-steroidal anti-inflammatory drugs (NSAIDs) may cause idiosyncratic liver damage but typically, the onset of the NSAIDs-induced hepatic injury is delayed and follows long-term administration.5Boelsterli UA Diclofenac-induced liver injury: a paradigm of idiosyncratic drug toxicity.Toxicol Appl Pharmacol. 2003; 192: 307-322Crossref PubMed Scopus (354) Google Scholar The clinical course did not suggest inhaled anaesthetic-induced liver failure. Obesity and liver steatosis risk factors may be associated with depletion of glutathione (GSH) stores due to impaired hepatocellular function. The first patient was not overweight, but inter-individual variations of acetaminophen glucuronidation have been also suggested.2Krähenbühl S Brauchli Y Kummer O et al.Acute liver failure in two patients with regular alcohol consumption ingesting paracetamol at therapeutic dosage.Digestion. 2007; 75: 232-237Crossref PubMed Scopus (25) Google Scholar Acetaminophen is conjugated in the liver by the UDP-glucuronosyl-transferase and by sulphotransferase.6Wills EJ Walton B A morphologic study of unexplained hepatitis following halothane anesthesia.Am J Pathol. 1978; 91: 11-32PubMed Google Scholar Other metabolic enzyme system is cytochrome P450 (mainly CYP2E1 but also 1A2 and 3A4) resulting in production of NAPQI. NAPQI-mediated mitochondrial injury may be the source of the superoxide leading to hepatotoxicity.6Wills EJ Walton B A morphologic study of unexplained hepatitis following halothane anesthesia.Am J Pathol. 1978; 91: 11-32PubMed Google Scholar Conditions leading to depletion of GSH stores (obesity, liver steatosis, starvation, and malnutrition) could be considered as risk factors for acetaminophen-induced hepatotoxicity along with CYP inducers (alcohol, antiepileptic drugs).3Myles PS Power I Clinical update: postoperative analgesia.Lancet. 2007; 369: 810-812Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar 7Van der Rijt CC Schalm SW De Groot GH De Vlieger M Objective measurement of hepatic encephalopathy by means of automated EEG analysis.Electroencephalogr Clin Neurophysiol. 1984; 57: 423-426Abstract Full Text PDF PubMed Scopus (135) Google Scholar 8Barnett CR Abbott RA Bailey CJ Flatt PR Ionnides C Cytochrome P-45 0-dependent mixed-function oxidase and glutathione S-transferase activities in spontaneous obesity-diabetes.Biochem Pharmacol. 1992; 43: 1868-1871Crossref PubMed Scopus (44) Google Scholar We conclude that when prescribing acetaminophen after operation, particular attention must be paid to patients who are at risk of hepatotoxicity due to pre-existing liver steatosis or other risk factors of hepatotoxicity." @default.
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• W2056178485 title "Therapeutic dose of acetaminophen may induce fulminant hepatitis in the presence of risk factors: a report of two cases" @default.
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