Qiu Caixia, Ai Si, Zhuang Xiangli, Huang Suping, Zheng Jian
Department of Pediatrics, Fujian Provincial People's Hospital, Fuzhou, Fujian, China; College of Integrated Chinese and Western Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China.
Department of Pediatrics, Fujian Provincial People's Hospital, Fuzhou, Fujian, China.
Int J Pediatr Otorhinolaryngol. 2019 Feb;117:105-109. doi: 10.1016/j.ijporl.2018.11.022. Epub 2018 Nov 22.
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.
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.
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).
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.
变应性鼻炎(AR)的发病机制可能涉及自主神经系统(ANS)失调。唾液分泌量和唾液α淀粉酶(sAA)分泌分别能够反映副交感神经系统(PNS)和交感神经系统(SNS)的活动。本研究旨在通过测量唾液分泌模式来探讨新诊断AR患儿的ANS特征。
我们招募了33例新诊断的AR患儿和31例年龄及性别匹配的健康儿童作为对照。于上午采集唾液样本,并相应测定唾液参数,包括唾液流速(SFR,ml/分钟)和sAA分泌率(μg/分钟)。我们还测定了每个个体sAA基因AMY1的基因拷贝数。
我们检测到AR患儿的SFR显著高于健康对照(2.20±0.55对1.63±0.61;p = 0.0002)。两组间观察到相似的sAA分泌率(健康组312.8±124.8对AR组347.9±114.0 μg/分钟;p = 0.2444)。此外,两组在AMY1基因拷贝数上无差异(健康组7.2±2.3对AR组7.7±2.2;p = 0.3493)。
我们的结果提示新诊断AR患儿的PNS活动亢进,而SNS活动正常。这些发现支持了ANS功能障碍在AR发病机制中的作用。