Cited by 373Pharmacogenetics and Drug MetabolismDrug-Induced Adverse ReactionsDrug-Induced Hepatotoxicity and Protection

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Differences in Metabolism of Sulfonamides Predisposing to Idiosyncratic Toxicity

SHEAR, NEIL H., SPIELBERG, STEPHEN P., GRANT, DENIS M., TANG, BING K., KALOW, WERNER·1986·Annals of Internal Medicine

DOI 10.7326/0003-4819-105-2-179

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Abstract

Individual differences in metabolism of the sulfonamides may predispose patients to idiosyncratic reactions. Sulfonamides are metabolized by N-acetylation (mediated by a genetically polymorphic enzyme) and oxidation to potentially toxic metabolites. We examined 6 patients who had severe reactions to sulfonamides and compared them with 20 controls. Acetylator phenotype was determined with caffeine, a safe in-vivo probe of enzyme activity. All 6 patients were slow acetylators (expected, 55%; p less than 0.05). Detoxification of oxidative metabolites was studied in vitro with a lymphocyte assay evaluating cell death from metabolites generated by a murine hepatic microsomal system. Cells from each patient showed increased toxicity from sulfonamide metabolites but not from the drugs themselves. Cells from parents of 3 patients had intermediate toxicity from sulfonamide metabolites, whereas cells from a sibling of 1 patient had a normal response. Susceptibility to sulfonamide reactions may be due to interaction of metabolic pathways, possibly under genetic control, regulating N-acetylation and specific detoxification of toxic metabolites of the drugs.

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Authors: SHEAR, N. H., SPIELBERG, S. P., GRANT, D. M., TANG, B. K., & KALOW, W.
Affiliations: Toronto, Ontario Canada
Corresponding author: SHEAR, NEIL H.
ORCID: SHEAR, NEIL H.
Venue: Annals of Internal Medicine
Publisher: American College of Physicians
Published: 1986-08-01
Volume: 105
Issue: 2
Pages: 179-184
ISSN: 0003-4819 (ISSN-L)
1539-3704
DOI: 10.7326/0003-4819-105-2-179
OpenAlex: W2058391540
Cited by: 373
References: 16
Citations by year: 2026: 4 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 5 · 2021: 6 · 2020: 4 · 2019: 5 · 2018: 6 · 2017: 4 · 2016: 7 · 2015: 8 · 2014: 6 · 2013: 3 · 2012: 15
FWCI: 9.43
Type: journal article
Language: en
Open access: closed
Licence: www.acpjournals.org/journal/aim/text-and-data-mining (tdm)
Locations: Annals of Internal Medicine (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
Health Sciences › Medicine › Pharmacology (medical) › Drug-Induced Adverse Reactions
Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Keywords: sulfonamides, idiosyncratic drug toxicity, N-acetylation, acetylator phenotype, slow acetylators, detoxification, genetic polymorphism, hepatic microsomal enzymes, lymphocyte cytotoxicity, familial predisposition
MeSH terms: Acetylation, Adult, Animals, Cell Survival, Child, Child, Preschool, Female, Humans, Infant, Lymphocytes, Male, Microsomes, Liver, Phenotype, Sulfonamides, Mice, In Vitro Techniques

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Differences in Metabolism of Sulfonamides Predisposing to Idiosyncratic Toxicity

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