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"Lung Age" 3 Years Older in Middle-Aged HIV+ Versus HIV- IDU Group
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3rd International Workshop on HIV and Aging, November 5-6, 2012, Baltimore
Mark Mascolini
HIV-positive injection drug users (IDUs) had a 3-year older lung-function age than HIV-negative IDUs in the same Baltimore cohort, despite similar chronologic age in the two groups [1]. But a history of pneumonia may largely explain that association. Higher viral load was linked to lower forced expiratory volume in 1 second (FEV1).
A prior cross-sectional analysis involving this Baltimore-based AIDS Linked to the IntraVenous Experience (ALIVE) cohort found an association between high viral load (but not CD4 count) and a higher prevalence of spirometry-defined obstructive lung disease [2]. To shed more light on longitudinal changes in HIV variables, inflammation, and obstructive lung disease in ALIVE, the same Johns Hopkins University team conducted this study. They hypothesized that both HIV infection and inflammatory markers would propel a faster decline in lung function.
HIV-positive and negative ALIVE cohort members make twice-yearly visits for clinical, laboratory, and spirometric evaluation. The researchers used repeated-measure random-effects models to estimate independent effects of HIV infection, viral load, CD4 count, and two inflammatory markers--interleukin 6 (IL-6) and C-reactive protein--on annual drop in FEV1. They used a standard formula to estimate "lung age" from FEV1 data.
The analysis involved 1064 current or former IDUs who had 4555 spirometry readings during a median 2.75 years of follow-up (range 0.5 to 3.9). Nearly one third of the cohort (30%) had HIV infection, and 55% of those with HIV were taking antiretrovirals. The vast majority of cohort members, 94%, were current or former smokers. Two thirds of the study group (65%) were men, and 91% were African American. Age averaged 49 years and did not differ significantly between the HIV-positive group and the HIV-negative group. There were 711 respiratory infections during follow-up, including 617 bacterial infections and 25 cases of Pneumocystis pneumonia.
HIV infection was associated with a steeper annual decline in lung function over 3 years. In an analysis adjusted for age, sex, race, pack-years of smoking, current smoking, body mass index, and pneumonia, HIV-negative cohort members had a 23.6 mL/year drop in FEV1. For HIV-positive people the FEV1 decline stood at 35.7 mL/year, a difference that approached statistical significance (P = 0.06).
When the ALIVE investigators divided HIV-positive people into those with a viral load below or above 75,000 copies, FEV1 dropped 29.2 mL/year in the under-75,000 group and 99.1 mL/year in the over-75,000 group. The rate of FEV1 decline in the high viral load group differed significantly from the low viral load group and the HIV-negative group (P < 0.01).
Higher levels of IL-6 were associated with reduced lung function at cohort entry but did not affect annual decline in lung function. C-reactive protein had no impact on lung function.
Although HIV-positive and negative cohort members were similar in age, the ALIVE team estimated that "lung age" was 3.1 years older in the HIV group, after statistical adjustment for age, sex, race, and pack-years of smoking (P = 0.018). In an analysis that adjusted for the same variables, a pneumonia diagnosis boosted lung age 8.5 years (P < 0.001). When the researchers included both HIV and pneumonia in the model, HIV added 1.7 years to lung age, and that association lost statistical significance (P = 0.183). But in this analysis pneumonia still added 8.0 years to lung age (P < 0.001). These findings indicate pulmonary infection at least partly explains the impact of HIV on lung age.
The researchers noted that the FEV1 decline seen with a viral load above 75,000 copies is greater than the 50- to 70-mL/year drop recorded in smokers. They figured that the impact of uncontrolled HIV on lung age approximates the impact of smoking an additional 25 pack-years.
The ALIVE investigators believe their findings "suggest that optimal antiretroviral therapy with HIV virological suppression may diminish the accelerated decline in lung function." They suggested that further work is needed to understand the behavioral and biological mechanisms of lung function decline in this population.
References
1. Kirk G, Merlo C, Astemborski J, et al. The effect of HIV and inflammation on lung function decline. 3rd International Workshop on HIV and Aging. November 5-6, 2012, Baltimore. Abstract O_10.
2. Drummond MB, Kirk GD, Astemborski J, et al. Association between obstructive lung disease and markers of HIV infection in a high-risk cohort. Thorax. 2012;67:309-314.
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