{'fraction_non_alphanumeric': 0.02309782608695652, 'fraction_numerical': 0.009510869565217392, 'mean_word_length': 5.635135135135135, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Idiosyncratic drug-induced liver injury: an update on the 2007 overview

Introduction: Idiosyncratic drug induced liver injury (DILI) is rare, with an incidence of approximately 19 per 100,000 treated individuals. Areas covered: An update on the epidemiology, pathogenic mechanisms, diagnosis, outcome, risk factors for idiosyncratic drug-induced hepatotoxicity, specific classes of drug hepatotoxicity and biomarkers to predict DILI are covered. Cumulative drug exposure and HLA phenotypes play an important role in the pathogenesis of DILI. Patients who present with suspected DILI and jaundice should have biliary obstruction and acute viral hepatitis, including hepatitis E excluded. Immune-mediated DILI will respond to steroid therapy. Patients with an elevated bilirubin and a hepatocellular pattern of liver function tests have severe liver injury with a mortality of greater than 10% and a risk of acute liver failure. Women have an increased risk of hepatocellular DILI. Antibiotics, anticonvulsants, and antidepressant therapy remain the commonest causes of DILI in the Western Hemisphere. Statin therapy rarely causes severe liver injury. Expert opinion: The establishment of prospective registries for DILI has provided valuable data on the pathogenesis and outcome of DILI. Drug-specific computerised causality assessment tools should improve the diagnosis of DILI. The clinical utility of genetic polymorphisms associated with drug-specific DILI is limited.