January 2, 2018
HIV infection increased the risk of airway obstruction within a 1,053-person study of cigarette smokers in France, according to findings published online in the journal AIDS. The study also found that chronic obstructive pulmonary disease (COPD) was nearly twice as common among participants living with HIV.
Small airway obstruction and COPD are highly prevalent among people living with HIV, partly because of high-frequency risk factors such as smoking and lung infection. Previous research has found higher COPD rates among people with HIV than among the general population, according to the authors of the French study. But those studies are limited by reliance on ICD codes for COPD diagnosis and from incomplete smoking data, the authors said. They also noted that HIV did not always remain an independent predictor of COPD after adjustment for confounders.
To get a better understanding of airway obstruction in the context of HIV infection, researchers working on the ANRS CHEST study conducted this matched comparison of people with and without HIV.
HIV-positive participants were enrolled in CHEST, a pilot study exploring the feasibility of early lung cancer diagnosis with low-dose chest tomography. Participants were at least 40 years old, had smoked at least 20 pack-years (i.e., smoked a pack of cigarettes a day for 20 years), and were either active smokers or had quit within the past three years. All had a nadir CD4 count above 350 cells/µL, and their most recent CD4 count was above 100 cells/µL. The study excluded people with active cancer, an AIDS-defining disease, or lung infection in the past two months.
HIV-negative participants came from the CONSTANCES cohort, a randomly selected, nationally representative sample of 200,000 adults between 18 and 69 years old. For this analysis, researchers selected CONSTANCES members who were current or recent 20 pack-year smokers at least 40 years old and matched them 2:1 to the HIV-positive group by age and gender.
The investigators systematically offered spirometry to volunteers in the HIV-positive and negative groups. The primary outcome was prebronchodilator forced expiratory volume in one second to forced vital capacity (FEV1/FVC) ratio. The secondary outcome was FEV1/FVC
The analysis included 351 people with HIV and 702 HIV-uninfected people, 17% of them women, with a median age of 50 years. Most people with HIV, 89%, had a plasma viral load below 50 copies/mL, and their median CD4 count stood at 573 cells/µL.
Mean FEV1/FVC ratio was significantly lower (worse) in the HIV-positive group than in HIV-negative controls (0.72 versus 0.77, P < .0001). COPD, determined by the proxy calculation explained above, affected 68 people with HIV and 60 without HIV (19% versus 9%, P < .0001). Multivariate linear regression analysis identified four variables associated with lower FEV1/FVC: HIV infection (β -2.19, 95% confidence interval [CI] -3.52 to -0.87), every 10 years of age (β -2.81, 95% CI -3.72 to -1.90), every five pack-years of tobacco use (β -0.34, 95% CI -0.58 to -0.09), and hepatitis C infection (HCV; β -2.50, 95% CI -4.33 to -0.67). Two factors were associated with higher FEV1/FVC ratio: being a woman (β 1.57, 95% CI 0.17 to 2.98) and every 1-point greater body mass index (β 0.29, 95% CI 0.16 to 0.43).
Multivariate analysis identified three independent predictors of study-defined airway obstruction: HIV (odds ratio [OR] 1.72, 95% CI 1.08 to 2.73), every 10 years of age (OR 1.77, 95% CI 1.28 to 2.43), and every five pack-years of tobacco use (OR 1.11, 95% CI 1.03 to 1.20). This analysis found no association between airway obstruction and any the following: gender, body mass index, smoking cessation in the past three years, cannabis smoking, or HCV status.
The study authors believe this is the first matched-control study of HIV and airway obstruction in an all-smoking population 40 years old or older. In such a population, the authors note, COPD screening is recommended by the Global Initiative for Chronic Obstructive Lung Disease. Higher odds of airway obstruction with HIV could be explained, the researchers hypothesize, by "an interaction between HIV, increased lung immune activation despite antiretroviral therapy[,] and smoking," leading to oxidative stress, local inflammation, and parenchyma destruction.
Mark Mascolini writes about HIV infection.
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