Sabaté M, Ibáñez L, Pérez E et al.
Universitat Autònoma de Barcelona, Barcelona, Spain.
Aliment Pharmacol Ther 2007;25:1401–9.
[2] Long-term follow-up of patients with mild to moderate drug-induced liver injury.
Björnsson E, Kalaitzakis E, Av Klinteberg V et al.
Sahlgrenska University Hospital, Gothenburg, Sweden.
Aliment Pharmacol Ther 2007;26:79–85.
[3] The impact of eosinophilia and hepatic necrosis on prognosis in patients with drug-induced liver injury.
Björnsson E, Kalaitzakis E, Olsson R.
Sahlgrenska University Hospital, Gothenburg, Sweden.
Aliment Pharmacol Ther 2007;25:1411–21.
Editor’s note: Drug-induced acute liver injury (ALI) is often a diagnosis of exclusion, even when a hepatototoxic drug is recognized early on as being the potential cause. The authors of the first article presented an interesting multicenter, prospective study involving hospital populations in Barcelona, Spain[1]. Over a 6-year period, data on all patients aged >15 years with ALI and jaundice were collected. The most frequent acute drug-induced ALIs were a result of isoniazid, pyrazinamide, rifampicin, amoxicillin with clavulanic acid, erythromycin, chlorpromazine, nimesulide, and ticlopidine. Drug exposures were considered to be causative if the agent had been taken within 15days (hepatic pattern) or 30 days (cholestatic/mixed pattern) of the onset of symptoms. The prevalence of drug-induced ALI within the Spanish population was estimated using drug consumption (as recorded in the country’s National Health System statistics) as the denominator. Consumption was transformed into a defined daily dose so that the mean number of individuals treated with the drug of interest could be determined. The relative risk for each drug was calculated using 99% confidence intervals.