Trial reportJournal of medical genetics1997
A simplified assay for the arylamine N-acetyltransferase 2 polymorphism validated by phenotyping with isoniazid.
Trial report in Journal of medical genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 88 citations in OpenAlex.
- Acetylator status-guided rapid reintroduction of isoniazid in tuberculosis patients with drug-induced hepatotoxicity.Journal of clinical tuberculosis and other mycobacterial diseases · 2026Article
- Population Pharmacokinetics and Pharmacodynamics of Isoniazid and its Metabolite Acetylisoniazid in Chinese Population.Frontiers in pharmacology · 2022Article
- Arylamine N-acetyltransferase acetylation polymorphisms: paradigm for pharmacogenomic-guided therapy- a focused review.Expert opinion on drug metabolism & toxicology · 2021Review
- Article
- Genotype-Guided Hydralazine Therapy.American journal of nephrology · 2020Review
- Genetic heterogeneity among slow acetylator N-acetyltransferase 2 phenotypes in cryopreserved human hepatocytes.Archives of toxicology · 2017Article
- ArylamineActa pharmaceutica Sinica. B · 2017Article
- Cornerstones of Toxicology.Toxicologic pathology · 2017Article
- Prevention of isoniazid toxicity by NAT2 genotyping in Senegalese tuberculosis patients.Toxicology reports · 2016Article
- Genetic polymorphisms of phase I and phase II metabolic enzymes as modulators of lung cancer susceptibility.Journal of cancer research and clinical oncology · 2015Article
- Pharmacokinetics of isoniazid, rifampicin, pyrazinamide and ethambutol in Indian children.BMC infectious diseases · 2015Article
- Pharmacogenetically driven patient selection for a first-in-human phase I trial of batracylin in patients with advanced solid tumors and lymphomas.Cancer chemotherapy and pharmacology · 2013Article
- Genetic polymorphism of NAT2 metabolizing enzymes on phenytoin pharmacokinetics in Indian epileptic patients developing toxicity.CNS neuroscience & therapeutics · 2012Article
- Accuracy of various human NAT2 SNP genotyping panels to infer rapid, intermediate and slow acetylator phenotypes.Pharmacogenomics · 2012Article
- A prospective study of antituberculous drug-induced hepatotoxicity in an area endemic for liver diseases.Hepatology international · 2008Article
- CYP2E1 genotype and isoniazid-induced hepatotoxicity in patients treated for latent tuberculosis.European journal of clinical pharmacology · 2006Article
- The influence of various genotypes on the metabolic activity of NAT2 in a Chinese population.European journal of clinical pharmacology · 2006Article
- N-acetyltransferase 2 genetic polymorphism: effects of carcinogen and haplotype on urinary bladder cancer risk.Oncogene · 2006Review
- Phenotyping of N-acetyltransferase type 2 by caffeine from uncontrolled dietary exposure.European journal of clinical pharmacology · 2004Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human arylamine N-acetyltransferase (NAT) activity is determined by two distinct genes, NAT1 and NAT2, and the classical acetylation polymorphism in NAT2 has been associated with a variety of disorders, including lupus erythematosus and arylamine induced cancers. Over 50% of the white population exhibit a slow acetylator phenotype. The genetic basis of the defect has been identified and several DNA based assays are available for genotyping studies. We present here a simplified, rapid PCR based assay for the identification of the major slow acetylator genotypes and validate it using isoniazid as probe drug. This assay was 100% predictive of phenotype. The three genotypes (homozygous mutated, heterozygous, and homozygous rapid) corresponded to a trimodal distribution of Ac-INH/INH metabolic ratios (slow, intermediate, and rapid) without overlapping.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.