Evidence map›Paper›PMID 22731637›Full record

ArticleGenetic testing and molecular biomarkers2012

N-acetyltransferase-2 genotypes among patients with rheumatoid arthritis attending Jordan University Hospital.

Muna K Oqal, Khader N Mustafa, Yacoub M Irshaid

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Article in Genetic testing and molecular biomarkers, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.1field-weighted citation impact, top 48% of its field
1 · What the graph read from it

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2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Haplotype-specific PCR forHuman genome variation · 2020
    Article
  4. BioMed research international · 2018
    Article
4 · The record

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5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Muna K OqalDepartment of Pharmacology, Faculty of Medicine, The University of Jordan, Amman, Jordan.
Khader N Mustafa
Yacoub M Irshaid
University of Jordan · JO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo determine the frequency of major N-acetyltransferase (NAT2) alleles and genotypes among Jordanian patients with rheumatoid arthritis (RA).

methodsThe study was approved by the IRB of the Jordan University Hospital. An informed consent was signed by every patient. DNA samples from 150 healthy volunteers and 108 patients with RA were analyzed by polymerase chain reaction followed by a restriction fragment length polymorphism assay (PCR-RFLP) to determine the frequency of four major alleles: NAT2*4, NAT2*5, NAT2*6, and NAT2*7.

resultsThe most prevalent genotypes are those that encode the slow acetylation phenotype. About 59.3% of the patients with RA carried the slow, 33.3% the intermediate, and 7.4% the fast-encoding genotypes. The frequency of NAT2 alleles was 0.241 (95% confidence interval [CI] 0.184-0.298) for NAT2*4, 0.449 (95% CI 0.383-0.515) for NAT2*5, 0.273 (95% CI 0.214-0.332) for NAT2*6, and 0.037 (95% CI 0.012-0.062) for NAT2*7 allele. The overall frequency of the slow acetylation genotype in patients with RA is similar to that in healthy Jordanian volunteers. However, the NAT2*5/7 genotype was found in seven patients (6.5%) with RA and was absent in Jordanian volunteers, and the z test revealed that the difference was statistically significant. This genotype constituted 10.9% of the genotypes encoding slow acetylation.

conclusionThe overall acetylator genotype in RA is similar to that in healthy volunteers. The overall slow acetylator genotypes do not seem to be a genetic risk factor for RA among Jordanians. However, the NAT2*5/7 genotype seems to be related to RA. The nature of this relationship needs further clarification.

Indexed as

AcetylationArthritis, RheumatoidArylamine N-AcetyltransferaseAsian PeopleFemaleGene FrequencyGenotypeHospitals, UniversityHumansJordanMalePolymerase Chain ReactionPolymorphism, Restriction Fragment LengthArylamine N-AcetyltransferaseNAT2 protein, human

Identifiers

PMID22731637
PMCPMC3438808
OpenAlexW2026198621

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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.