FROM AIDS

HIV infection is an independent risk factor for an acute exacerbation of chronic obstructive pulmonary disease (AECOPD), particularly in those with severe immune suppression, new research shows.

The longitudinal study, led by Dr. Kristina Crothers, a pulmonary and critical care specialist at Harborview Medical Center in Seattle, compared the incidence of AECOPD in 43,618 HIV-infected patients with 86,492 uninfected patients participating in the Veterans Aging Cohort Study ( AIDS. 2016 Jan 28;30[3]:455-63 ).

Over 234,099 person-years of follow-up, the research team found that HIV-infected individuals had an increased rate of AECOPD compared with uninfected individuals (18.8 vs. 13.3 per 1,000 person-years, P less than .001).

Adjusted models showed that AECOPD risk was greater in HIV-infected individuals overall (IRR 1.54; 95% CI 1.44-1.65), particularly in those with more severe immune suppression when stratified by CD4+ cell count (cells/mcL) compared with uninfected individuals (HIV-infected CD4+ <200: IRR 2.30, 95% CI 2.10-2.53, HIV-infected CD4+ ≥ 200-349: IRR 1.32, 95% CI 1.15-1.51, HIV-infected CD4+ ≥350: IRR 0.99, 95% CI 0.88-1.10).

“These findings support that severity of immune suppression increases risk for AECOPD, likely through greater risk of infection,” Dr. Crothers and her coauthors wrote.

The researchers also found a significant interaction between HIV infection and current smoking and alcohol use, with both conferring a substantially greater risk for AECOPD. This suggests that the increased risk of AECOPD in HIV may be related to enhanced susceptibility to harms from the modifiable risk factors of smoking and unhealthy alcohol use.

Infection with HIV coupled with alcohol use could serve as a ‘double hit’ to increase susceptibility to exacerbations of lung disease, the authors suggested.

“Intervening on these contributing factors may decrease morbidity and costs associated with COPD, particularly in a vulnerable HIV-infected population,” they concluded.

The authors declared no conflicts of interest.

imnews@frontlinemedcom.com

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