Dear Editor,

Recently we reviewed the paper entitled: “Does adenoid hypertrophy affect disease severity in children with allergic rhinitis?” by Dogru et al. [1]. This is an excellent work and constitutes an interesting study. The authors evaluated the presence of adenoid hypertrophy (AH) in children with allergic rhinitis (AR) and the associations between AH severity and clinical laboratory findings, concluding that AH increased disease severity and prolonged disease duration. A negative relationship was evident between AH and asthma in children with AR. AH was more common among children who were sensitive to molds. AH should be considered particularly in non-asthmatic children with pronounced nasal congestion who are sensitive to A. alternata. However, we believe that a more detailed study is required.

The authors considered that AH increased AR severity and prolonged disease duration [1]. However, we earlier found that adenoidectomy did not significantly improve AR symptoms. Although AH may cause allergen (e.g., dust, pollen) accumulation in the nasal cavity and nasopharynx, thereby, aggravating AR symptoms and duration, any causal relationship between AH and AR remains unclear. Most scholars suggest that AR triggers AH [2]. Colavita et al. [3] found that adenoidectomy did not notably benefit 80% of children with AR and AH. It is important to prescribe medical anti-allergic therapy to eliminate local inflammation; this improves the nasal symptoms and prevents adenoid regrowth. Eren et al. [4] believed that AH and AR were significantly (negatively) correlated. Ameli et al. [5] posited that AH was frequently associated with tonsillar hypertrophy, but inversely associated with AR. Ameli et al. [6] later suggested that AH might in fact be associated with the absence of allergy. However, some authors have speculated that children with both AR and AH may be sensitive to specific allergens [7, 8]. Allergens that induced AR did not trigger allergic asthma, and vice versa. Huang et al. suggested that children with both AR and AH were more likely to be hypersensitive to pollen and mold allergens. Sensitivity to the latter type of allergen is an important risk factor for AH in children with AR. The risk of AH was positively correlated with the extent of skin test reactivity to mold spores. Positive skin tests to animal danders or seasonal allergens did not predict the risk of AH [8]. Thus, large multicenter studies of the causal relationship between AH and AR are required. In addition, the effects of specific allergens should be explored in children with both AH and AR.

Recent studies found that children were more likely to have gastroesophageal reflux (GER). Argon et al. [9] found that the prevalence of GER was 37% in 108 infants and children. Miura et al. [10] reported that the mean rate of laryngopharyngeal reflux was 48.6% in children with AH. However, some authors have suggested that AR is more likely to cause GER in children [11, 12]. Somerville [12] believed that GER status should be evaluated even in the absence of suggestive signs or symptoms in many patients with moderate or severe AR. However, GER is easily missed because children often do not report symptoms. Thus, careful assessment of GER status is important in children with both AR and AH. In addition, it is essential to determine if AR signs and symptoms improve after adenoidectomy alone, to assess whether AH increases the severity of AR. Therefore, a randomized controlled trial of adenoidectomy to treat children with AR and AH is required.