International journal of pediatric otorhinolaryngology · 2012
Manganese-superoxide dismutase and glutathione peroxidase 1 polymorphisms in recurrent tonsillitis and tonsillar hypertrophy.
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Gurbuzler Levent, Sogut Erkan, Koc Sema, Eyibilen Ahmet, Yelken Kursat, Senkal Hilmi A, Aksakal Ceyhun
Аннотация
OBJECTIVES: To investigate the association of manganese-superoxide dismutase and glutathione peroxidase 1 polymorphisms with susceptibility to recurrent tonsillitis and tonsillar hypertrophy.
METHODS: The study consisted of 103 patients with recurrent tonsillitis, 105 patients with tonsillar hypertrophy and 106 control subjects with similar age and sex. Genomic DNA was extracted from peripheral leukocytes of whole blood which were obtained from all patients and control subjects. Genotyping was performed to identify MnSOD Ala-9Val and GPx1 Pro198Leu polymorphisms by a method based on PCR amplification and detection of polymorphisms with hybridization probes labeled with fluorescent dyes. Genotype and allele frequencies were compared between patients with recurrent tonsillitis and tonsillar hypertrophy and 106 healthy control subjects.
RESULTS: The genotype distribution of the MnSOD Ala-9Val single nucleotide polymorphism was significantly different for the controls and the recurrent tonsillitis patients (P=0.009). Whereas, no significant difference was found between the patients with tonsillar hypertrophy and the control group (P=0.369). The frequency of the MnSOD CC genotype was lower, and that of the T allele was significantly higher, in recurrent tonsillitis patients than in control subjects. In addition, the frequency of tonsillitis was significantly higher in recurrent tonsillitis patients with the MnSOD Ala-9Val polymorphism than the patients with wild-type (P=0.008). Also, no significant difference was found between patient groups and control subjects in the distribution of the genotype and allele frequency of the GPx1 Pro198Leu single nucleotide polymorphism.
CONCLUSIONS: The MnSOD Ala-9Val polymorphism causes susceptibility to recurrent tonsillitis in Turkish children. And we suggest that there may be a possible relation between local and recurrent infections or inflammation of the tonsillar tissue and the MnSOD Ala-9Val single nucleotide polymorphism in pediatric patients with RT.
METHODS: The study consisted of 103 patients with recurrent tonsillitis, 105 patients with tonsillar hypertrophy and 106 control subjects with similar age and sex. Genomic DNA was extracted from peripheral leukocytes of whole blood which were obtained from all patients and control subjects. Genotyping was performed to identify MnSOD Ala-9Val and GPx1 Pro198Leu polymorphisms by a method based on PCR amplification and detection of polymorphisms with hybridization probes labeled with fluorescent dyes. Genotype and allele frequencies were compared between patients with recurrent tonsillitis and tonsillar hypertrophy and 106 healthy control subjects.
RESULTS: The genotype distribution of the MnSOD Ala-9Val single nucleotide polymorphism was significantly different for the controls and the recurrent tonsillitis patients (P=0.009). Whereas, no significant difference was found between the patients with tonsillar hypertrophy and the control group (P=0.369). The frequency of the MnSOD CC genotype was lower, and that of the T allele was significantly higher, in recurrent tonsillitis patients than in control subjects. In addition, the frequency of tonsillitis was significantly higher in recurrent tonsillitis patients with the MnSOD Ala-9Val polymorphism than the patients with wild-type (P=0.008). Also, no significant difference was found between patient groups and control subjects in the distribution of the genotype and allele frequency of the GPx1 Pro198Leu single nucleotide polymorphism.
CONCLUSIONS: The MnSOD Ala-9Val polymorphism causes susceptibility to recurrent tonsillitis in Turkish children. And we suggest that there may be a possible relation between local and recurrent infections or inflammation of the tonsillar tissue and the MnSOD Ala-9Val single nucleotide polymorphism in pediatric patients with RT.