Abstract

Role of Allergy, Respiratory Infection, and Passive Smoking in Early Onset Adenotonsillar Hypertrophy

Highlights

  • Adenoids and palatine tonsils and the tubal and lingual tonsils compose Waldeyer’s ring [1], which produces antigens to environmental allergens [2]

  • We investigated whether there is any relationship between upper respiratory tract infections (URTI) or exposure to parental smoking and Adenotonsillar hypertrophy (ATH)

  • Our results show 64.1% of the early onset group subjects reported a parental history of allergy and 64.7% of the late onset group subjects had a parental history of allergy (p=0.920)

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Summary

Introduction

Adenoids and palatine tonsils and the tubal and lingual tonsils compose Waldeyer’s ring [1], which produces antigens to environmental allergens [2]. Adenotonsillar hypertrophy (ATH) has burdened families for decades; it is the most common cause of airway obstruction and obstructive sleep apnea in the pediatric age group [3,4]. Infections remain the most common cause of enlargement of adenoids and/or tonsils. The role of allergies has not been examined as a cause of adenotonsillar hypertrophy. Sadeghi-Shabestari et al [10] evaluated 217 children with ATH and allergy and found 70.3% of the study group had positive skin prick test results. Only 10% of the control group had positive skin prick test results. Similar results were found among Polish children in three studies by Modrzyński et al [12,13,14] who concluded that allergy

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