Trial reportPharmaceutical research2004
N-acetyltransferase 2 genotype-related efficacy of sulfasalazine in patients with rheumatoid arthritis.
Trial report in Pharmaceutical research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- The association between NAT2 acetylator status and adverse drug reactions of sulfasalazine: a systematic review and meta-analysis.Scientific reports · 2020Pooled it
- Unified pharmacogenetics-based parent-metabolite pharmacokinetic model incorporating acetylation polymorphism for talampanel in humans.Journal of pharmacokinetics and pharmacodynamics · 2005Trial
- Significance of 5-Aminosalicylic Acid Intolerance in the Clinical Management of Ulcerative Colitis.Digestion · 2023Review
- Arylamine N-acetyltransferase acetylation polymorphisms: paradigm for pharmacogenomic-guided therapy- a focused review.Expert opinion on drug metabolism & toxicology · 2021Review
- Sepiapterin Reductase Inhibition Leading to Selective Reduction of Inflammatory Joint Pain in Mice and Increased Urinary Sepiapterin Levels in Humans and Mice.Arthritis & rheumatology (Hoboken, N.J.) · 2020Article
- Arylamine N-acetyltransferase polymorphisms in Han Chinese patients with ankylosing spondylitis and their correlation to the adverse drug reactions to sulfasalazine.BMC pharmacology & toxicology · 2014Article
- Pharmacogenetics and pharmacogenomics in rheumatology.Immunologic research · 2013Review
- N-acetyltransferase-2 genotypes among patients with rheumatoid arthritis attending Jordan University Hospital.Genetic testing and molecular biomarkers · 2012Article
- Causes of DMARD withdrawal following ADR within 6 months of initiation among Indian rheumatoid arthritis patients.Rheumatology international · 2012Article
- The role of N-acetyltransferase 2 polymorphism in the etiopathogenesis of inflammatory bowel disease.Digestive diseases and sciences · 2011Article
- Pharmacogenetics of rheumatoid arthritis: Potential targets from susceptibility genes and present therapies.Pharmacogenomics and personalized medicine · 2010Article
- N-acetyltransferase 2 slow acetylator genotype associated with adverse effects of sulphasalazine in the treatment of inflammatory bowel disease.Canadian journal of gastroenterology = Journal canadien de gastroenterologie · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeFor the individual optimization of drug therapy with sulfasalazine (SASP), we studied the influence of the N-acetyltransferase 2 (NAT2) genotype on the pharmacokinetics, efficacy, and incidence of adverse reactions of SASP in patients.
methodsNinety-six rheumatoid arthritis (RA) patients were treated or had been treated with 0.5 and/or 1.0 g/day of SASP. The wild-type allele (NAT2*4) and three variant alleles (NAT2*5B, *6A, and *7B) of NAT2 were determined by the polymerase chain reaction-restriction fragment length polymorphism method. Plasma concentrations of SASP and its two metabolites, sulfapyridine (SP) and N-acetylsulfapyridine (AcSP), were estimated by HPLC. Therapeutic efficacy and incidence of adverse reactions were also monitored as recommended by the American College of Rheumatology.
resultsPatients were classified into three groups by NAT2 genotyping: Rapid Type (homozygote for NAT2*4), Intermediate Type (heterozygote for NAT2*4 and variant alleles), and Slow Type (homozygote for variant alleles). There was no clear difference in the genotype frequencies between RA patients and healthy subjects. NAT2 genotypes significantly affected both the plasma concentration ratios of SP to AcSP (SP/AcSP) and the efficacy of SASP (p < 0.05). Adverse reactions to SASP were found in 26 (27.1%) out of 96 patients, and there was no difference among the three genotype groups.
conclusionsNAT2 gene polymorphism is related to the plasma SP/AcSP ratio and the efficacy of SASP.
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