HIV Infection and Lung Function Decline in IDUs
HIV Infection and Lung Function Decline in IDUs
Objective: As survival with HIV infection improves, HIV-infected individuals appear to be susceptible to development of chronic diseases, including restrictive and obstructive lung diseases. We sought to determine the independent association of HIV infection on lung function decline.
Design: Longitudinal analysis of the AIDS Linked to the Intravenous Experience study, an observational cohort of current and former IDUs.
Methods: Generalized estimating equations were used to determine the effects of markers of HIV infection on adjusted annual change in forced expiratory volume in one second (FEV1) and forced vital capacity (FVC).
Results: A total of 1064 participants contributed 4555 spirometry measurements over a median follow-up time of 2.75 years. The mean age of the cohort was 48 years; nearly, two-thirds were men and 85% current smokers. After adjustment, the overall annual decline of FEV1 and FVC between HIV-infected and uninfected persons did not differ. However, there was a 76 ml/year greater rate of decline in FEV1 and 86 ml/year greater rate of decline in FVC among HIV-infected participants with viral load more than 75 000 copies/ml compared with HIV-uninfected individuals (P < 0.01). Similarly, HIV-infected individuals with CD4 cell count less than 100 cells/μl had a 57 ml/year more rapid decline in FEV1 and 86 ml/year more rapid decline in FVC than HIV-uninfected participants (P = 0.018 and P = 0.001, respectively).
Conclusion: Markers of poorly controlled HIV disease are independently associated with accelerated annual lung function decline, with decrements in both FEV1 and FVC. These findings highlight the need for optimized HIV antiretroviral therapy in addition to smoking cessation among HIV-infected individuals with tobacco dependence.
The advancement of antiretroviral therapy (ART) has led to improved survival and longer life expectancy for persons living with HIV infection. Subsequently, there is an increased recognition of development of age-associated chronic diseases (e.g. cardiovascular, metabolic, renal, neurological) and non-AIDS-defining malignancies occurring in these individuals. Emerging data suggest an increased prevalence of chronic lung disease in HIV-infected individuals, the spectrum of which includes both chronic airflow obstruction and restrictive lung disease. HIV infection has been shown to increase the diagnosis of self-reported and administratively diagnosed COPD. We have previously shown that the odds of airflow obstruction were increased more than three-fold among HIV-infected individuals with the highest plasma viral load independent of smoking compared with epidemiologically similar HIV-negative individuals. Respiratory infections, increased in HIV-infected individuals, are associated with restrictive lung disease. Beyond these cross-sectional reports, few studies have evaluated longitudinal lung function decline among HIV-infected persons. Because earlier studies were prior to widespread ART availability and recent studies were limited by small numbers of persons, short duration of follow-up and lack of HIV-negative comparator groups, the independent effect of HIV disease markers on lung function decline remains unanswered.
The AIDS Linked to the Intravenous Experience (ALIVE) study is a longitudinal cohort of persons with a history of injecting drugs with or at-risk for HIV infection followed in Baltimore, Maryland, since 1988. The ALIVE study collects behavioural, clinical and laboratory data at regular 6-month intervals and recently instituted serial spirometric measures into the data collection protocol. With nearly ubiquitous cigarette smoking and substantial prevalence of respiratory symptoms and obstructive lung disease (OLD), ALIVE represents an appropriate population to examine the effect of HIV infection on changes in lung function. In the current study, we used longitudinal data from ALIVE to determine the independent association of HIV infection on lung function decline over almost 3 years of observations. We hypothesized that HIV infection, particularly more advanced HIV disease, would be associated with accelerated lung function decline. Some of these results have been previously presented at the 19th Conference on Retroviruses and Opportunistic Infections and published in an abstract form.
Abstract and Introduction
Abstract
Objective: As survival with HIV infection improves, HIV-infected individuals appear to be susceptible to development of chronic diseases, including restrictive and obstructive lung diseases. We sought to determine the independent association of HIV infection on lung function decline.
Design: Longitudinal analysis of the AIDS Linked to the Intravenous Experience study, an observational cohort of current and former IDUs.
Methods: Generalized estimating equations were used to determine the effects of markers of HIV infection on adjusted annual change in forced expiratory volume in one second (FEV1) and forced vital capacity (FVC).
Results: A total of 1064 participants contributed 4555 spirometry measurements over a median follow-up time of 2.75 years. The mean age of the cohort was 48 years; nearly, two-thirds were men and 85% current smokers. After adjustment, the overall annual decline of FEV1 and FVC between HIV-infected and uninfected persons did not differ. However, there was a 76 ml/year greater rate of decline in FEV1 and 86 ml/year greater rate of decline in FVC among HIV-infected participants with viral load more than 75 000 copies/ml compared with HIV-uninfected individuals (P < 0.01). Similarly, HIV-infected individuals with CD4 cell count less than 100 cells/μl had a 57 ml/year more rapid decline in FEV1 and 86 ml/year more rapid decline in FVC than HIV-uninfected participants (P = 0.018 and P = 0.001, respectively).
Conclusion: Markers of poorly controlled HIV disease are independently associated with accelerated annual lung function decline, with decrements in both FEV1 and FVC. These findings highlight the need for optimized HIV antiretroviral therapy in addition to smoking cessation among HIV-infected individuals with tobacco dependence.
Introduction
The advancement of antiretroviral therapy (ART) has led to improved survival and longer life expectancy for persons living with HIV infection. Subsequently, there is an increased recognition of development of age-associated chronic diseases (e.g. cardiovascular, metabolic, renal, neurological) and non-AIDS-defining malignancies occurring in these individuals. Emerging data suggest an increased prevalence of chronic lung disease in HIV-infected individuals, the spectrum of which includes both chronic airflow obstruction and restrictive lung disease. HIV infection has been shown to increase the diagnosis of self-reported and administratively diagnosed COPD. We have previously shown that the odds of airflow obstruction were increased more than three-fold among HIV-infected individuals with the highest plasma viral load independent of smoking compared with epidemiologically similar HIV-negative individuals. Respiratory infections, increased in HIV-infected individuals, are associated with restrictive lung disease. Beyond these cross-sectional reports, few studies have evaluated longitudinal lung function decline among HIV-infected persons. Because earlier studies were prior to widespread ART availability and recent studies were limited by small numbers of persons, short duration of follow-up and lack of HIV-negative comparator groups, the independent effect of HIV disease markers on lung function decline remains unanswered.
The AIDS Linked to the Intravenous Experience (ALIVE) study is a longitudinal cohort of persons with a history of injecting drugs with or at-risk for HIV infection followed in Baltimore, Maryland, since 1988. The ALIVE study collects behavioural, clinical and laboratory data at regular 6-month intervals and recently instituted serial spirometric measures into the data collection protocol. With nearly ubiquitous cigarette smoking and substantial prevalence of respiratory symptoms and obstructive lung disease (OLD), ALIVE represents an appropriate population to examine the effect of HIV infection on changes in lung function. In the current study, we used longitudinal data from ALIVE to determine the independent association of HIV infection on lung function decline over almost 3 years of observations. We hypothesized that HIV infection, particularly more advanced HIV disease, would be associated with accelerated lung function decline. Some of these results have been previously presented at the 19th Conference on Retroviruses and Opportunistic Infections and published in an abstract form.
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