Effect of lipopolysaccharide (LPS)-evoked host defense activation on hepatic microsomal formation and reduction of sulfamethoxazole hydroxylamine in the rat12Abbreviations: ADR, adverse drug reaction; CYP, cytochrome P450; LPS, lipopolysaccharide; NMHR, NADH-dependent microsomal hydroxylamine reductase; SMX, sulfamethoxazole; SMX-HA, sulfamethoxazole hydroxylamine; and SMX-TMP, sulfamethoxazole-trimethoprim.

Drug-induced hepatotoxicity is a serious problem and has repeatedly led to the withdrawal of a drug after successful launching. Although reactive metabolites (which are predictable) are often involved, genetic or acquired host factors (which are unpredictable) can increase the penetrance and expressivity of the potential hepatotoxicity in a small subset of patients. The molecular mechanisms underlying liver injury are largely unknown. Evidence suggests, however, that there are four major modes of action: covalent modification of target proteins and oxidoreductive stress; immune-mediated reactions; interference with hepatobiliary export; and mitochondrial injury. A better prediction will include new animal models, new biomarkers, and genomics/transcriptomics analysis.

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Mechanistic perspectives on sulfonamide-induced cutaneous drug reactions

Reilly

2002

Current Opinion in Allergy and Clinical Immunology

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Cited by 5 publications

References 7 publications

Effect of pro-inflammatory cytokines on the toxicity of the arylhydroxylamine metabolites of sulphamethoxazole and dapsone in normal human keratinocytes

Effect of pro-inflammatory cytokines on the toxicity of the arylhydroxylamine metabolites of sulphamethoxazole and dapsone in normal human keratinocytes

Idiosyncratic Drug Hepatotoxicity Revisited: New Insights from Mechanistic Toxicology

Mechanistic perspectives on sulfonamide-induced cutaneous drug reactions

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