Department of Pediatric Allergy and Clinical Immunology, Ankara Health Research and Application Center, University of Health Sciences, Ankara, Turkey,
Department of Pediatric Allergy and Clinical Immunology, Ankara Children's Hematology Oncology Training and Research Hospital, University of Health Sciences, Ankara, Turkey.
Int Arch Allergy Immunol. 2021;182(8):679-689. doi: 10.1159/000513809. Epub 2021 Mar 22.
Obese asthma is a complex syndrome with certain phenotypes that differ in children and adults. There is no clear evidence regarding the presence of additive or synergistic pathological interaction between obesity and asthma in children.
Our aim was to demonstrate the interaction of obesity and asthma in children in terms of airway and systemic inflammation by a controlled observational study.
Four groups were formed: asthma obese (AO), asthma nonobese (ANO), non-AO (NAO), nonasthma nonobese (NANO). Spirometry test, fractional exhaled nitric oxide (FeNO) test, skin prick test, serum inflammatory biomarkers (C-reactive protein, C3, C4, adiponectin, leptin, resistin, periostin, YKL-40, Type 1, and Type 2 cytokines) were conducted and evaluated in all participants. Sputum inflammatory cells (sputum eosinophils and neutrophils) were evaluated in patients who could produce induced sputum and obesity-asthma interactions were determined.
A total of 153 participants aged 6-18 years were included in the study, including the AO group (n = 46), the ANO group (n = 45), the NAO group (n = 30), and the NANO group (n = 32). IL-4 (p < 0.001), IL-5 (p < 0.001), IL-13 (p < 0.001), resistin (p < 0.001), and YKL-40 (p < 0.001) levels were higher in patients with asthma independent of obesity. The lowest adiponectin level was found in the AO group and obesity-asthma interaction was detected (p < 0.001). Sputum eosinophilia (p < 0.01), sputum neutrophilia (p < 0.01), and FeNO levels (p = 0.07) were higher in asthmatic patients independent of obesity. In the group with paucigranulocytic inflammation, resistin and YKL-40 levels were significantly lower than in the group without paucigranulocytic inflammation (p < 0.01).
No interaction was found between obesity and asthma in terms of airway inflammation. Interaction between obesity and asthma was shown in terms of adiponectin level and resistin/adiponectin and leptin/adiponectin ratios. It was found that serum YKL-40 and resistin levels could be associated with airway inflammation.
肥胖型哮喘是一种具有特定表型的复杂综合征，在儿童和成人中存在差异。目前尚缺乏肥胖和哮喘在儿童中存在累加或协同病理性相互作用的明确证据。
通过对照观察性研究，旨在证明肥胖与哮喘在儿童气道和全身炎症方面的相互作用。
共形成 4 组：哮喘肥胖组（AO）、哮喘非肥胖组（ANO）、非哮喘非肥胖组（NAO）、非哮喘肥胖组（NANO）。对所有参与者进行肺量测定、呼出气一氧化氮（FeNO）测试、皮肤点刺试验、血清炎症生物标志物（C 反应蛋白、C3、C4、脂联素、瘦素、抵抗素、骨膜蛋白、YKL-40、1 型和 2 型细胞因子）检测和评估。能够产生诱导痰的患者评估痰中炎症细胞（痰嗜酸性粒细胞和中性粒细胞），并确定肥胖与哮喘的相互作用。
本研究共纳入 153 名 6-18 岁的参与者，包括 AO 组（n=46）、ANO 组（n=45）、NAO 组（n=30）和 NANO 组（n=32）。无论肥胖与否，哮喘患者的 IL-4（p<0.001）、IL-5（p<0.001）、IL-13（p<0.001）、抵抗素（p<0.001）和 YKL-40（p<0.001）水平均较高。AO 组的脂联素水平最低，且检测到肥胖与哮喘的相互作用（p<0.001）。无论肥胖与否，哮喘患者的痰嗜酸性粒细胞（p<0.01）、痰中性粒细胞（p<0.01）和 FeNO 水平（p=0.07）均较高。在少粒细胞性炎症组中，抵抗素和 YKL-40 水平明显低于非少粒细胞性炎症组（p<0.01）。
在气道炎症方面，肥胖与哮喘之间未发现相互作用。在脂联素水平以及抵抗素/脂联素和瘦素/脂联素比值方面，发现肥胖与哮喘之间存在相互作用。发现血清 YKL-40 和抵抗素水平可能与气道炎症有关。
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