International journal of pediatric otorhinolaryngology · 2018
Increased salivary fluid flow in children with newly diagnosed allergic rhinitis.
СтатьяНазвание и аннотация: Перевод в очереди
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Qiu Caixia, Ai Si, Zhuang Xiangli, Huang Suping, Zheng Jian
Аннотация
OBJECTIVES: The pathogenesis of allergic rhinitis (AR) may involve dysregulation of the autonomic nervous system (ANS). Salivary fluid flow and salivary alpha-amylase (sAA) secretion are able to reflect the activity of parasympathetic (PNS) and sympathetic nervous system (SNS), respectively. The study aims to address the ANS profile in children with newly diagnosed AR by measuring the salivary secretion pattern.
METHODS: We recruited thirty-three children with newly diagnosed AR and thirty-one age- and sex-matched healthy children as control. Saliva samples were collected in the morning and the salivary parameters, including salivary flow rate (SFR, ml/min) and sAA secretion rate (μg/min), were determined accordingly. We also measured the gene copy number of the sAA gene, AMY1, for each individual.
RESULTS: We detected a significantly higher SFR in AR children compared with healthy control (2.20 ± 0.55 vs. 1.63 ± 0.61; p = 0.0002). Similar sAA secretion rate was observed between the two groups (312.8 ± 124.8 (Healthy) vs. 347.9 ± 114.0 (AR) μg/min; p = 0.2444). Besides, the two groups did not differ in AMY1 gene copy number (7.2 ± 2.3 (Healthy) vs. 7.7 ± 2.2 (AR); p = 0.3493).
CONCLUSIONS: Our results implicate an overactivity of the PNS while normal SNS activity in children with newly diagnosed AR. The findings support a contributing role of the ANS dysfunction in the pathogenesis of AR.
METHODS: We recruited thirty-three children with newly diagnosed AR and thirty-one age- and sex-matched healthy children as control. Saliva samples were collected in the morning and the salivary parameters, including salivary flow rate (SFR, ml/min) and sAA secretion rate (μg/min), were determined accordingly. We also measured the gene copy number of the sAA gene, AMY1, for each individual.
RESULTS: We detected a significantly higher SFR in AR children compared with healthy control (2.20 ± 0.55 vs. 1.63 ± 0.61; p = 0.0002). Similar sAA secretion rate was observed between the two groups (312.8 ± 124.8 (Healthy) vs. 347.9 ± 114.0 (AR) μg/min; p = 0.2444). Besides, the two groups did not differ in AMY1 gene copy number (7.2 ± 2.3 (Healthy) vs. 7.7 ± 2.2 (AR); p = 0.3493).
CONCLUSIONS: Our results implicate an overactivity of the PNS while normal SNS activity in children with newly diagnosed AR. The findings support a contributing role of the ANS dysfunction in the pathogenesis of AR.