1995
DOI: 10.1080/09595239500185071
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A review of the hepatotoxicity of paracetamol at therapeutic or near‐therapeutic dose levels, with particular reference to alcohol abusers

Abstract: The number of published reports associating hepatotoxicity with paracetamol ingestion at therapeutic or near-therapeutic dose levels is small but is, nevertheless, suggestive of a relationship. There is however, mounting evidence that certain groups of patients, such as alcohol-dependent people, patients receiving enzyme-inducing drugs (particularly anti-convulsant and anti-tuberculosis medications) as well as those with certain infectious diseases, are rendered more susceptible to paracetamol-induced hepatoto… Show more

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Cited by 10 publications
(11 citation statements)
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References 92 publications
(104 reference statements)
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“…This is some 175 μg/ml lower than that typically associated with a risk of hepatotoxicity (Bunchorntavakul and Reddy, 2013 ) and 275 μg/ml lower than the established thresholds for liver damage (Prescott, 1983 ). Liver damage in response to therapeutic ACT doses have only been seen in very specific populations—those who are alcohol dependent, patients receiving enzyme-inducing drugs and those with specific infectious diseases such as measles and infectious mononucleosis (Collins and Starmer, 1995 ; Zimmerman and Maddrey, 1995 ; Prescott, 2000 ; Aminoshariae and Khan, 2015 ). Indeed, doses in the range of 1–1.5 g (when a 20 mg.kg LBM dose is employed) in exercise performance research (Mauger et al, 2010 , 2014 ; Mauger and Hopker, 2012 ; Foster et al, 2014 ) and 20 mg.kg LBM (up to a maximum of 1.5 g) in thermophysiology literature (Foster et al, 2016 , 2017 ) have been used, without reported side-effects; not unexpected given the previous comments regarding plasma ACT concentrations and liver damage.…”
Section: Acetaminophen Dose and Pharmacokineticsmentioning
confidence: 99%
“…This is some 175 μg/ml lower than that typically associated with a risk of hepatotoxicity (Bunchorntavakul and Reddy, 2013 ) and 275 μg/ml lower than the established thresholds for liver damage (Prescott, 1983 ). Liver damage in response to therapeutic ACT doses have only been seen in very specific populations—those who are alcohol dependent, patients receiving enzyme-inducing drugs and those with specific infectious diseases such as measles and infectious mononucleosis (Collins and Starmer, 1995 ; Zimmerman and Maddrey, 1995 ; Prescott, 2000 ; Aminoshariae and Khan, 2015 ). Indeed, doses in the range of 1–1.5 g (when a 20 mg.kg LBM dose is employed) in exercise performance research (Mauger et al, 2010 , 2014 ; Mauger and Hopker, 2012 ; Foster et al, 2014 ) and 20 mg.kg LBM (up to a maximum of 1.5 g) in thermophysiology literature (Foster et al, 2016 , 2017 ) have been used, without reported side-effects; not unexpected given the previous comments regarding plasma ACT concentrations and liver damage.…”
Section: Acetaminophen Dose and Pharmacokineticsmentioning
confidence: 99%
“…In this connection, it would be useful to note other examples of interactive toxicity of drugs. For examples, acetaminophen 37,38 and anticonvulsants 39 have been reported to be associated with hepatotoxicity when used alongside antituberculosis drugs, particularly in those regimens including isoniazid.…”
Section: Risk Factors Of Antituberculosis Drug‐induced Hepatotoxicitymentioning
confidence: 99%
“…In the absence of control data these anecdotal case reports in themselves cannot ‘prove’ that therapeutic doses of paracetamol cause liver injury in chronic alcoholics. The fact that there are similar (but sometimes equally suspect) reports of patients who were not chronic alcoholics [7, 18, 40, 41, 58, 103, 123–127] is conveniently overlooked. Indeed, if paracetamol in normal doses is as dangerous in chronic alcoholics as it is claimed, liver damage should be commonplace considering the enormous scale on which the drug is used and the prevalence of alcoholism.…”
Section: Clinical Studiesmentioning
confidence: 99%
“…There have been many reports claiming that the hepatotoxicity of paracetamol (acetaminophen) is increased in chronic alcoholics, and that such individuals not only carry an increased risk of severe and fatal liver damage after acute overdosage [1–20], but that similar serious liver damage may also occur with ‘therapeutic’ use [5, 9, 10, 17, 18, 21–64]. In the original studies of the mechanisms of toxicity, paracetamol was found to cause liver damage through conversion by hepatic cytochrome P450 enzymes to a minor but toxic intermediate metabolite [65–68] and this was subsequently identified as N ‐acetyl‐ p ‐benzoquinoneimine [69, 70].…”
Section: Introductionmentioning
confidence: 99%