Comparison between curettage adenoidectomy and endoscopic-assisted microdebrider adenoidectomy in terms of Eustachian tube dysfunction.

INTRODUCTION: Adenoidectomy can be performed with many ways, including curettage and microdebrider endoscopic-assisted adenoidectomy. Those two techniques have advantages and disadvantages. OBJECTIVE: The objective of this study is to research the effects of curettage adenoidectomy and endoscopic-assisted microdebrider adenoidectomy on the tympanum pressures in pediatric patients with adenoid hypertrophy without otitis media with effusion. METHODS: This prospective descriptive study was performed with 65 patients who had a normal tympanic membrane and normal tympanogram and then underwent adenoidectomy or adenotonsillectomy for adenoid and tonsil hypertrophy. The subjects were randomly divided into two groups: curettage adenoidectomy group and endoscopic microdebrider-assisted adenoidectomy group. They underwent tympanometry, and the preoperative as well as 1st and 7th day postoperative values of the tympanum pressures were compared within and among the groups. RESULTS: There were 32 patients in the curettage adenoidectomy group and 33 patients in the microdebrider adenoidectomy group. Statistically significant differences were observed in the median tympanum pressure on the preoperative and 1st and 7th postoperative days for both the left and right ears with curettage adenoidectomy (p<0.001, p<0.001). This difference occurred on the 1st postoperative day, and the value returned to normal on the 7th day. There was no significant difference in the median tympanum pressure on the preoperative and 1st and 7th postoperative days for both the left and right ears in the microdebrider adenoidectomy group (p=0.376, p=0.128). CONCLUSION: Postoperative Eustachian tube dysfunction is seen less often with the endoscopic-assisted microdebrider adenoidectomy technique than with the conventional adenoidectomy technique.

Association of Ugrp2 gene polymorphisms with adenoid hypertrophy in the pediatric population.

INTRODUCTION: Adenoid hypertrophy is a condition that presents itself as the chronic enlargement of adenoid tissues; it is frequently observed in the pediatric population. The Ugrp2 gene, a member of the secretoglobin superfamily, encodes a low-molecular weight protein that functions in the differentiation of upper airway epithelial cells. However, little is known about the association of Ugrp2 genetic variations with adenoid hypertrophy. OBJECTIVE: The aim of this study is to investigate the association of single nucleotide polymorphisms in the Ugrp2 gene with adenoid hypertrophy and its related phenotypes. METHODS: A total of 219 children, comprising 114 patients suffering from adenoid hypertrophy and 105 healthy patients without adenoid hypertrophy, were enrolled in this study. Genotypes of the Ugrp2 gene were determined by DNA sequencing. RESULTS: We identified four single nucleotide polymorphisms (IVS1-189G>A, IVS1-89T>G, c.201delC, and IVS2-15G>A) in the Ugrp2 gene. Our genotype analysis showed that the Ugrp2 (IVS1-89T>G) TG and (c.201delC) CdelC genotypes and their minor alleles were associated with a considerable increase in the risk of adenoid hypertrophy compared with the controls (p=0.012, p=0.009, p=0.013, and p=0.037, respectively). Furthermore, Ugrp2 (GTdelCG, GTdelCA) haplotypes were significantly associated with adenoid hypertrophy (four single nucleotide polymorphisms ordered from 5' to 3'; p=0.0001). Polymorfism-Polymorfism interaction analysis indicated a strong interaction between combined genotypes of the Ugrp2 gene contributing to adenoid hypertrophy, as well as an increased chance of its diagnosis (p<0.0001). In addition, diplotypes carrying the mutant Ugrp2 (c.201delC) allele were strongly associated with an increased risk of adenoid hypertrophy with asthma and with allergies (p=0.003 and p=0.0007, respectively). CONCLUSION: Some single nucleotide polymorphisms and their combinations in the Ugrp2 gene are associated with an increased risk of developing adenoid hypertrophy. Therefore, we tried to underline the importance of genetic factors associated with adenoid hypertrophy and its related clinical phenotypes.