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. 2014 Jan;43(1):195-203.
doi: 10.1183/09031936.00157712. Epub 2013 Feb 21.

Contributors to diffusion impairment in HIV-infected persons

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Contributors to diffusion impairment in HIV-infected persons

Matthew R Gingo et al. Eur Respir J. 2014 Jan.

Abstract

Abnormal diffusing capacity is common in HIV-infected individuals, including never smokers. Aetiologies for diffusing capacity impairment in HIV are not understood, particularly in those without a history of cigarette smoking. Our study was a cross-sectional analysis of 158 HIV-infected individuals without acute respiratory symptoms or infection with the aim to determine associations between a diffusing capacity of the lung for carbon monoxide (D(LCO)) % predicted and participant demographics, pulmonary spirometric measures (forced expiratory volume in 1 s (FEV1) and FEV1/forced vital capacity), radiographic emphysema (fraction of lung voxels < -950 Hounsfield units), pulmonary vascular/cardiovascular disease (echocardiographic tricuspid regurgitant jet velocity, N-terminal pro-brain natriuretic peptide) and airway inflammation (induced sputum cell counts), stratified by history of smoking. The mean D(LCO) was 65.9% predicted, and 55 (34.8%) participants had a significantly reduced D(LCO) (<60% predicted). Lower D(LCO) % predicted in ever-smokers was associated with lower post-bronchodilator FEV1 % predicted (p<0.001) and greater radiographic emphysema (p=0.001). In never-smokers, mean±SD D(LCO) was 72.7±13.4% predicted, and D(LCO) correlated with post-bronchodilator FEV1 (p=0.02), sputum neutrophils (p=0.03) and sputum lymphocytes (p=0.009), but not radiographic emphysema. Airway obstruction, emphysema and inflammation influence D(LCO) in HIV. Never-smokers may have a unique phenotype of diffusing capacity impairment. The interaction of multiple factors may account for the pervasive nature of diffusing capacity impairment in HIV infection.

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Figures

Figure 1
Figure 1
Distribution of DLCO % predicted. Dashed line represents 60% predicted DLCO. Solid line represents the mean. (light gray) = never smokers; (dark gray) = ever smokers.
Figure 2
Figure 2
Scatterplots and regression lines for DLCO % predicted by a) post-bronchodilator (BD) FEV1 % predicted, b) Tricuspid regurgitant velocity, c) sputum neutrophil percent, d) post-BD FEV1/FVC, and e) natural logarithm (ln) of the fraction of lung <-950 for ever smokers (positive symbols,+, and solid lines) and never smokers (open squares, □, and dashed lines). Pearson correlation coefficients (r) and significance values (p) are shown nearest to the regression lines of smokers (bottom) and never smokers (top) for correlations between the independent variable in each graph and DLCO % predicted.

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