Karampatakis Nikolaos, Karampatakis Theodoros, Galli-Tsinopoulou Assimina, Kotanidou Eleni P, Tsergouli Katerina, Eboriadou-Petikopoulou Maria, Haidopoulou Katerina
4th Department of Pediatrics, Medical School, Papageorgiou General Hospital of Thessaloniki, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Department of Clinical Microbiology, Hippokration General Hospital of Thessaloniki, Thessaloniki, Greece.
Pediatr Pulmonol. 2017 Feb;52(2):160-166. doi: 10.1002/ppul.23516. Epub 2016 Jun 30.
The prevalence of asthma and obesity has risen in parallel over the last decades, but the exact mechanisms linking these two diseases still remain unclear. The aim of the present study was to investigate the associations between bronchial hyperresponsiveness (BHR), impaired glucose metabolism, obesity, and asthma in prepubertal children.
A total of 71 prepubertal children were included in the study and divided in four groups according to the presence of asthma and their Body Mass Index (BMI): Group 1-Healthy Controls (HC), Group 2-Non Obese Asthmatics (NOA), Group 3-Obese Non Asthmatics (ONA), Group 4-Obese Asthmatics (OA) Αll children underwent spirometry and bronchial hyperresponsiveness testing by using the cumulative Provoking Dose of mannitol (PD primary study variable); homeostasis model assessment-estimated insulin resistance (HOMA-IR) index was calculated in order to evaluate insulin resistance. Obese children also underwent an oral glucose tolerance testing (OGTT).
A statistically significant difference in bronchial hyperreactivity (mean ± SD) was detected in the group of obese asthmatic children who had lower values of PD , (174.16 ± 126.42) as compared to normal weight asthmatic children (453.93 ± 110.27), (P < 0.001). Moreover, obese asthmatic children with confirmed insulin resistance (HOMA-IR ≥2.5), had significantly lower PD values (89.05 ± 42.75) as compared to those with HOMA-IR <2.5 (259.27 ± 125.75), (P = 0.006). Finally, obese asthmatic children with impaired OGTT had likewise significantly lower PD (81.02 ± 42.16) measurements as compared to children with normal OGTT (267.3 ± 112.62), (P = 0.001).
Our findings suggest that obesity per se does not correlate to airway hyperreactivity unless it is accompanied by glucose intolerance and insulin resistance. Pediatr Pulmonol. 2017;52:160-166. © 2016 Wiley Periodicals, Inc.
在过去几十年中,哮喘和肥胖的患病率呈平行上升趋势,但将这两种疾病联系起来的确切机制仍不清楚。本研究的目的是调查青春期前儿童支气管高反应性(BHR)、糖代谢受损、肥胖和哮喘之间的关联。
本研究共纳入71名青春期前儿童,并根据哮喘的存在情况及其体重指数(BMI)分为四组:第1组-健康对照(HC),第2组-非肥胖哮喘患者(NOA),第3组-肥胖非哮喘患者(ONA),第4组-肥胖哮喘患者(OA)。所有儿童均接受肺活量测定,并使用甘露醇累积激发剂量(PD,主要研究变量)进行支气管高反应性测试;计算稳态模型评估估计的胰岛素抵抗(HOMA-IR)指数以评估胰岛素抵抗。肥胖儿童还接受了口服葡萄糖耐量测试(OGTT)。
在肥胖哮喘儿童组中检测到支气管高反应性(平均值±标准差)存在统计学显著差异,其PD值(174.16±126.42)低于正常体重哮喘儿童(453.93±110.27),(P<0.001)。此外,确诊为胰岛素抵抗(HOMA-IR≥2.5)的肥胖哮喘儿童的PD值(89.05±42.75)显著低于HOMA-IR<2.5的儿童(259.27±125.75),(P=0.006)。最后,OGTT受损的肥胖哮喘儿童的PD测量值(81.02±42.16)同样显著低于OGTT正常的儿童(267.3±112.62),(P=0.001)。
我们的研究结果表明,肥胖本身与气道高反应性无关,除非伴有葡萄糖不耐受和胰岛素抵抗。《儿科肺科杂志》。2017年;52:160 - 166。©2016威利期刊公司。