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Author Notes:

Corresponding Author: Kristina Crothers, MD, University of Washington, Harborview Medical Center, 325 9th Avenue, PO Box 359762, Seattle, WA 98104, 206 744 9870, crothk@uw.edu.

Substantial contributions to the conception or design of the work (TBD, KAM, KLK, KC); the acquisition, analysis, or interpretation of data for the work (TBD, KAM, KLK, KMA, EJE, DAF, AAB, SC, AJG, MF, CLG, DR, KJB, KC); drafting the work or revising it critically for important intellectual content (all authors); final approval of the version to be published (all authors); agreement to be accountable for all aspects of the work (all authors).

Presented in abstract form at the 2013 American Thoracic Society International Conference, Philadelphia, PA


Research Funding:

NIH/NHLBI R01 HL090342, NIAAA U24-AA020794


  • Science & Technology
  • Life Sciences & Biomedicine
  • Immunology
  • Infectious Diseases
  • Virology
  • acute exacerbation
  • chronic obstructive pulmonary disease
  • cigarette smoking
  • COPD
  • tobacco use
  • unhealthy alcohol use
  • CARE

Risk factors associated with acute exacerbation of chronic obstructive pulmonary disease in HIV-infected and uninfected patients

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Journal Title:



Volume 30, Number 3


, Pages 455-463

Type of Work:

Article | Post-print: After Peer Review


Objective: To determine the association between HIV infection and other risk factors for acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Design: Longitudinal, national Veterans Aging Cohort Study including 43 618 HIV-infected and 86 492 uninfected veterans. Methods: AECOPD was defined as an inpatient or outpatient COPD ICD-9 diagnosis accompanied by steroid and/or antibiotic prescription within 5 days. We calculated incidence rate ratios (IRR) and 95% confidence intervals (CI) for first AECOPD over 2 years and used Poisson regression models to adjust for risk factors. Results: Over 234 099 person-years of follow-up, 1428 HIV-infected and 2104 uninfected patients had at least one AECOPD. HIV-infected patients had an increased rate of AECOPD compared with uninfected (18.8 vs. 13.3 per 1000 person-years, P < 0.001). In adjusted models, 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/ml) compared with uninfected (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). HIV infection also modified the association between current smoking and alcohol-related diagnoses with risk for AECOPD such that interaction terms for HIV and current smoking or HIV and alcohol-related diagnoses were each significantly associated with AECOPD. Conclusion: HIV infection, especially with lower CD4+ cell count, is an independent risk factor for AECOPD. Enhanced susceptibility to harm from current smoking or unhealthy alcohol use in HIV-infected patients may also contribute to the greater rate of AECOPD.

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