Introduction: Prior studies comparing abnormalities in pulmonary function between HIV-infected and HIV-uninfected persons in the current era are limited.
Objectives: To determine the pattern and severity of impairment in pulmonary function in HIV-infected compared with HIV-uninfected individuals.
Methods: Cross-sectional analysis of 300 HIV-infected men and 289 HIV-uninfected men enrolled from 2009 to 2011 in 2 clinical centers of the Lung HIV Study. Participants completed pre- and postbronchodilator spirometry, diffusing capacity of the lung for carbon monoxide (DLCO) measurement, and standardized questionnaires.
Results: Most participants had normal airflow; 18% of HIV-infected and 16% of HIV-uninfected men had airflow obstruction. The mean percent predicted DLCO was 69% in HIV-infected vs. 76% in HIV-uninfected men (P < 0.001). A moderately to severely reduced DLCO of ≤60% was observed in 30% of HIV-infected compared with 18% of HIV-uninfected men (P < 0.001), despite the fact that 89% of those with HIV were on antiretroviral therapy. A reduced DLCO was significantly associated with HIV and CD4 cell count in linear regression adjusting for smoking and other confounders. The DLCO was lowest in HIV-infected men with CD4 cell counts <200 cells per microliter compared with those with CD4 cell counts ≥200 cells per microliter and to HIV-uninfected men. Respiratory symptoms of cough, phlegm and dyspnea were more prevalent in HIV-infected patients particularly those with abnormal pulmonary function compared with HIV-uninfected patients.
Conclusions: HIV infection is an independent risk factor for reduced DLCO, particularly in individuals with a CD4 cell count below 200 cells per microliter. Abnormalities in pulmonary function among HIV-infected patients manifest clinically with increased respiratory symptoms. Mechanisms accounting for the reduced DLCO require further evaluation.
*Department of Medicine, University of Washington, Seattle, WA;
†Department of Medicine, University of Pittsburgh, Pittsburgh, PA;
‡Department of Medicine, University of California, Los Angeles, Los Angeles, CA;
§Department of Medicine, Atlanta Veterans Affairs Medical Center (VAMC) and Emory University, Atlanta, GA;
‖Department of Medicine, West Los Angeles VAMC and David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA;
¶Department of Medicine, James J. Peters Bronx VAMC, Bronx, NY;
#Department of Medicine, Michael E. DeBakey Houston VAMC and Baylor College of Medicine, Houston, TX;
**Department of Medicine, University of California, San Francisco, San Francisco, CA;
††Department of Medicine, Clinical Trials and Survey Corporation, Owings Mills, MD;
‡‡Department of Medicine, Ohio State University Medical Center, Columbus, OH;
§§Department of Medicine, Johns Hopkins University, Baltimore, MD;
‖‖Department of Medicine, New York University School of Medicine, New York, NY;
¶¶Departments of Infectious Diseases and Microbiology; and Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA; and
##Departments of Medicine and Immunology, University of Pittsburgh, Pittsburgh, PA.
Correspondence to: Kristina Crothers, MD, University of Washington, Harborview Medical Center, 325 9th Avenue, Seattle, WA 98104 (e-mail: firstname.lastname@example.org).
Supported by NIH/NHLBI R01-HL090342 (K.C.); K24-HL087713 (L.H.); HL090335 (L.H.); R01-HL090313 (P.T.D.), R01-HL090483 (G.K.), R01-HL090316 (W.N.R.), R01-HL090331 (B.W.T.), R01-HL090339 (A.M.).
Presented in part, at the Conference on Retrovirus and Opportunistic Infections (CROI), March 7, 2012, Seattle, WA.
The authors have no conflicts of interest to disclose.
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Received April 21, 2013
Accepted August 01, 2013