Adiposity influences airway wall thickness and the asthma phenotype of HIV-associated obstructive lung disease: a cross-sectional study
Adiposity influences airway wall thickness and the asthma phenotype of HIV-associated obstructive lung disease: a cross-sectional study
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DOI：
10.1186/s12890-016-0274-5
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发表时间：
2016-08-04
影响因子：
3.1
通讯作者：
Gingo, Matthew R.
中科院分区：
文献类型：
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作者：
Barton, Julia H.;Ireland, Alex;Gingo, Matthew R.
背景：气流阻塞在 HIV 感染者中很常见，其中包括多种表型。在未感染艾滋病毒的人中，肥胖和脂肪相关炎症与慢性阻塞性肺病（固定气流阻塞）和哮喘（可逆性气流阻塞）有关，但与艾滋病毒感染者的气道炎症和气流阻塞的关系尚不清楚。本研究的目的是确定肥胖和脂肪相关炎症是否与 HIV 感染者的气道阻塞表型相关。方法：我们对 121 名 HIV 感染者进行了横断面分析，通过肺功能测试、胸部 CT 扫描来测量气道壁厚度（壁面积百分比 [WA%]）和脂肪组织体积（纵隔和脂肪组织体积）。 皮下），以及艾滋病毒和脂肪相关的炎症标志物。参与者被定义为 COPD 表型（支气管扩张剂后 FEV1/FVC < 正常下限）或哮喘表型（医生诊断的哮喘或支气管扩张剂反应）。计算脂肪测量值、WA% 和肺功能之间的皮尔逊相关系数。使用多变量逻辑和线性回归模型来确定气流阻塞和气道重塑 (WA%) 与脂肪测量和参与者特征的关联。结果：23 名 (19%) 参与者被分类为 COPD 表型，33 名 (27%) 参与者被分类为哮喘表型。患有和不患有 COPD 的人的体重指数 (BMI) 相似，但患有哮喘的人比不患有哮喘的人更高（平均 [SD] 30.7 kg/m(2) [8.1] vs. 26.5 kg/m(2) [5.3]，p = 0.008）。 WA% 与较大的 BMI（r = 0.55，p < 0.001）和脂肪组织体积（皮下，r = 0.40；p < 0.001；纵隔，r = 0.25；p = 0.005）相关。多变量回归发现 COPD 表型与较大年龄和吸烟年数相关。哮喘表型年龄较小、女性、有吸烟史、脂联素水平较低； BMI 越大、年龄越小、可溶性 CD163 和 CD4 计数越高，WA% 越大。 结论：肥胖和脂肪相关炎症与 HIV 感染者阻塞性肺病的哮喘表型相关，但与 COPD 表型无关。气道壁厚度与肥胖和炎症有关。脂肪相关炎症可能在艾滋病毒相关哮喘中发挥作用。
Background: Airflow obstruction, which encompasses several phenotypes, is common among HIV-infected individuals. Obesity and adipose-related inflammation are associated with both COPD (fixed airflow obstruction) and asthma (reversible airflow obstruction) in HIV-uninfected persons, but the relationship to airway inflammation and airflow obstruction in HIV-infected persons is unknown. The objective of this study was to determine if adiposity and adipose-associated inflammation are associated with airway obstruction phenotypes in HIV-infected persons.Methods: We performed a cross-sectional analysis of 121 HIV-infected individuals assessed with pulmonary function testing, chest CT scans for measures of airway wall thickness (wall area percent [WA%]) and adipose tissue volumes (mediastinal and subcutaneous), as well as HIV- and adipose-related inflammatory markers. Participants were defined as COPD phenotype (post-bronchodilator FEV1/FVC < lower limit of normal) or asthma phenotype (doctor-diagnosed asthma or bronchodilator response). Pearson correlation coefficients were calculated between adipose measurements, WA%, and pulmonary function. Multivariable logistic and linear regression models were used to determine associations of airflow obstruction and airway remodeling (WA%) with adipose measurements and participant characteristics.Results: Twenty-three (19 %) participants were classified as the COPD phenotype and 33 (27 %) were classified as the asthma phenotype. Body mass index (BMI) was similar between those with and without COPD, but higher in those with asthma compared to those without (mean [SD] 30.7 kg/m(2) [8.1] vs. 26.5 kg/m(2) [5.3], p = 0.008). WA% correlated with greater BMI (r = 0.55, p < 0.001) and volume of adipose tissue (subcutaneous, r = 0.40; p < 0.001; mediastinal, r = 0.25; p = 0.005). Multivariable regression found the COPD phenotype associated with greater age and pack-years smoking; the asthma phenotype with younger age, female gender, smoking history, and lower adiponectin levels; and greater WA% with greater BMI, younger age, higher soluble CD163, and higher CD4 counts.Conclusions: Adiposity and adipose-related inflammation are associated with an asthma phenotype, but not a COPD phenotype, of obstructive lung disease in HIV-infected persons. Airway wall thickness is associated with adiposity and inflammation. Adipose-related inflammation may play a role in HIV-associated asthma.