TITLE

Association Between Achalasia and Nitric Oxide Synthase Gene Polymorphisms

AUTHOR(S)
Mearin, Fermín; García-González, María-Asunción; Strunk, Michael; Zárate, Natalia; Malagelada, Juán-Ramón; Lanas, Angel
PUB. DATE
September 2006
SOURCE
American Journal of Gastroenterology;Sep2006, Vol. 101 Issue 9, p1979
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
BACKGROUND: Our group previously reported the absence of nitric oxide synthase (NOS) in the gastroesophageal junction of patients with achalasia. NOS exists in three distinct isoforms: neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible isoform (iNOS). Some studies have shown that NO production is regulated by NOS polymorphisms. AIM: To assess whether some functional polymorphisms in the nNOS, iNOS, or eNOS genes are involved in susceptibility to suffer from achalasia. METHODS: Genomic DNA from 80 unrelated Spanish Caucasian patients with sporadic achalasia and 144 healthy subjects matched for age (±5 yr) and gender was typed by PCR and RFLP methods for the 27-bp variable number of tandem repeat (VNTR) polymorphism in intron 4 of the eNOS gene, a CA microsatellite repeat and a Nla III (C→T) restriction fragment length polymorphism (RFLP) in exon 29 of the nNOS gene, and two nucleotide substitutions located in exon 16 (C→T) and exon 22 (G→A) of the iNOS gene. RESULTS: No significant differences in carriage, genotype, and allele frequencies of the nNOS, iNOS, or eNOS gene polymorphisms were found between patients with achalasia and controls. Individuals homozygous for genotype iNOS22*A/A tended to be more frequent in achalasia (20% vs 11%, odds ratio [OR] 1.79, 95% confidence interval [CI] 0.89–3.59, p= 0.09) as were those homozygous for the rare eNOS*4a allele (6.2% vs 1.4%, OR 4.5, 95% CI 0.89–22.67, p= 0.1) although the difference did not reach statistical significance. No differences in genotype and allele distribution were found with respect to epidemiological and clinical characteristics of patients with achalasia. CONCLUSION: Our data suggest that NOS gene polymorphisms are not involved in the susceptibility to and nature of the clinical course of sporadic achalasia. However, studies in a greater number of patients are required to analyze the tendency toward a higher prevalence of genotypes iNOS22*A/A and eNOS*4a4a.
ACCESSION #
22208108

 

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