CROI 2018 Abstract eBook

Abstract eBook

Poster Abstracts

COPD, but HIV infection has also been identified as an independent COPD risk factor. There are scant longitudinal data on the pulmonary effects of smoking in HIV. We measured baseline and annual spirometry in the Strategic Timing of Antiretroviral Treatment (START) Pulmonary Substudy and found no difference in lung function decline between persons living with HIV (PLWH) randomized to immediate versus deferred antiretroviral therapy. We used these data to determine the impact of smoking on rate of lung function decline and incident COPD in PLWH. Methods: We included individuals who contributed at least two spirometry measures during the study, and we restricted this analysis to spirometry data meeting international quality control standards. Slope of forced expiratory volume in 1 second (FEV1) was estimated using a repeated measures model with random intercept and slope and AR(1) covariance matrix adjusted for treatment group (immediate vs. deferred treatment arm of START), age, sex, race, and region. COPD was defined as an FEV1/Forced Vital Capacity (FVC) 12 years, mean CD4 of HIV+ subjects was 454. 27% of HIV+ subjects reported ≥1 year of daily or weekly marijuana smoking, compared with 18% of HIV- subjects (p<0.001). During 25,788 person-years of follow-up, 407 HIV+ subjects had one or more infectious pulmonary diagnosis (27%, median follow-up 9 years), compared with 262 HIV- subjects (18%, median follow-up 11 years) (p<0.001), while non-infectious pulmonary

diagnoses occurred at similar frequency between groups (19%, n=269 vs. 17%, n=232; p=0.19). Daily or weekly marijuana smoking in the prior 6 months was associated with higher adjusted hazard ratio (HR) for both infectious (HR 1.31, 95% CI 1.01-1.71) and non-infectious (HR 1.39, 95% CI 1.02-1.89) pulmonary diagnoses, independent of tobacco smoking and other risk factors. 2-year prior average marijuana use was associated with increased risk for both infectious and non-infectious pulmonary diagnoses when modeled as a continuous variable (HR 1.06, 95% CI 1.02-1.07, and HR 1.07, 95% CI 1.02-1.11, respectively, per 10 days use/month increase). There was no significant association between marijuana use and infectious or non-infectious events in HIV- participants. Conclusion: Frequent marijuana smoking is a risk factor for infectious and non-infectious pulmonary disease in HIV-infected men, independent of tobacco smoking and other risk factors.

Poster Abstracts

748 HIV INFECTION, SYSTEMIC INFLAMMATION AND LUNG FUNCTION IN RURAL UGANDA Crystal North 1 , Bernard Kakuhikire 2 , Alexander C. Tsai 1 , David C. Christiani 3 , Douglas Kwon 4 , Samson Okello 2 , Mark J. Siedner 1 , Russell Tracy 5 1 Massachusetts General Hospital, Boston, MA, USA, 2 Mbarara University of Science and Technology, Mbarara, Uganda, 3 Harvard University, Boston, MA, USA, 4 Ragon Institute of MGH, MIT and Harvard, Cambridge, MA, USA, 5 University of Vermont, Colchester, VT, USA Background: Systemic inflammation is associated with impaired lung function in people living with HIV (PLWH) in high-income settings. Little is known about the relationship between systemic inflammation and lung function in PLWH in sub-Saharan Africa. Methods: We measured lung function and serum hsCRP, IL-6, sCD14 and sCD163 in 126 PLWH at least 40 years of age who were on stable antiretroviral therapy (ART) and 111 age and gender matched HIV uninfected controls in rural Uganda. We modeled the relationship between lung function and systemic inflammation using linear regression, stratified by HIV serostatus, controlling for age, gender, height and smoking history. Results: All 237 participants completed ATS-acceptable spirometry and 225 (95%) underwent phlebotomy for serum inflammatory markers. Those without phlebotomy results were slightly older than those with results (58 vs. 52 years, p = 0.01), otherwise there were no differences between those who did and did not have phlebotomy results. Median cohort age was 52 years (IQR 48-55), 46% (n=110) were women, and average lung function was normal, with no differences by HIV serostatus. HIV negative participants were more likely than PLWH to be current or former smokers (57%, n=63 vs. 43%, n=54; P=0.03). Most PLWH (92%, n=116) were virally suppressed, median CD4 count was 475 cells/mm 3 (IQR 374-627), and median time on first-line ART was 9 years (IQR 8-10). Median IL-6 and sCD163 concentrations were 0.3795pg/mL (IQR 0.273-0.568) and 454.695ng/mL (IQR 350.19-615.16), with no difference by HIV serostatus. Median hsCRP and sCD14 concentrations were higher among PLHW than HIV negative controls (hsCRP 1.325mg/L (IQR 0.6-3.15) vs. 0.44 (IQR 0.19-0.99), P<0.0001); sCD14 1458.09ng/mL (IQR 1162.735-1720.312) vs. 1213.82 (IQR 1005.92-1406.19), P<0.0001, respectively). In regression models controlled for age, gender, height, and smoking, increased IL-6 and sCD163 were associated with lower lung function among PLWH only, while increased hsCRP was associated with lower lung function in both PLWH and HIV negative controls. There was no association between sCD14 and lung function.

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