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Low rates of hepatotoxicity among Asian patients with paracetamol overdose: a review of 1024 casesKeywords: Paracetamol, Acetaminophen, Hepatotoxicity, Acute liver failure, N-acetyl cysteine, Asian Abstract: A retrospective review of adult cases with paracetamol overdose over a five-year duration was performed in two of the largest public institutions in this country. Prevalence and predictive factors for hepatotoxicity were determined.Data on 1024 patients (median age 23 years, 82.0% female, ethnic groups: Malays 40.8%, Chinese 20.9% , Indian 33.2%) were obtained from January 2005 to December 2009. The median amount of paracetamol ingestion was 10.0 (IQR 5.0 - 15.0) g and the median serum paracetamol level was 274.80 (IQR 70.0 - 640.0) μmol/L at presentation. 75 (7.3%) patients developed hepatotoxicity. 23/ 55 (41.8%) patients who had ingested?>?10 g of paracetamol and had a delayed (> 24 hour) administration of N-acetyl cystine (NAC) developed hepatotoxicity. No patients developed acute liver failure nor suffered any mortality (0%). Independent predictors for hepatotoxicity were identified as Malay (OR 2.22, 95% CI?=?1.13-4.37) and Chinese (OR 3.26, 95% CI?=?1.55-6.84) ethnicity, paracetamol dose?>?10 g (OR 2.61, 95% CI?=?1.53-4.46), prolonged duration of time from paracetamol ingestion to hospital presentation (> 24 hours OR 10.71, 95% CI?=?3.46-33.15) and prolonged duration of time from paracetamol ingestion to NAC administration (> 24 hours OR 9.02, 95% CI?=?2.97-27.45).Paracetamol-induced hepatotoxicity rates in a multi-ethnic Asian population was low at 7.3%. Mortality and morbidity were non-existent despite high doses of paracetamol ingestion and delayed presentations to hospital.Paracetamol, or acetaminophen, overdose is a common means of self-poisoning worldwide due its wide availability and accessibility. It has been reported as the most common drug overdose either accidentally or unintentionally in the United Kingdom (UK), Europe, United States (US), and Australasia [1-3]. Paracetamol overdose is recognised to cause a range of hepatic damage from mild to severe hepatotoxicity, leading to acute liver failure (ALF) and death, despite the availability of antido
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