The pathophysiology of pulmonary diffusion impairment in human immunodeficiency virus infection

Citation
Pt. Diaz et al., The pathophysiology of pulmonary diffusion impairment in human immunodeficiency virus infection, AM J R CRIT, 160(1), 1999, pp. 272-277
Citations number
33
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073449X → ACNP
Volume
160
Issue
1
Year of publication
1999
Pages
272 - 277
Database
ISI
SICI code
1073-449X(199907)160:1<272:TPOPDI>2.0.ZU;2-R
Abstract
Numerous reports have demonstrated that prior to the development of acquire d immunodeficiency syndrome (AIDS)-related pulmonary complications, human i mmunodeficiency virus-positive (HIV+) individuals commonly develop unexplai ned reductions in pulmonary diffusing capacity (DLCO). The potential releva nce of this observation is underscored by recent data demonstrating that re ductions in DLCO independently predict the subsequent development of opport unistic pneumonia. To delineate the alterations in gas exchange associated with HIV, we investigated a group of HIV+ subjects with unexplained reducti ons in DLCO, using high-resolution computed tomography (HRCT) of the chest and a separation of diffusing capacity into its membrane (Dm) and capillary blood volume (Vc) components. We compared this abnormal group with HIV+ su bjects with more normal gas exchange and also with a group of HIV- voluntee rs matched for age and smoking history. Compared with other groups, the HIV + group with diffusion impairment demonstrated prominent reductions in Vc, despite a well-preserved total lung capacity (TLC). HRCT demonstrated virtu ally no evidence of interstitial fibrosis in any HIV- subject, but evidence of early emphysema that significantly correlated with DLCO. Our results su ggest that the previously reported impairment in pulmonary gas exchange in the HIV+ population involves loss of Vc and likely represents the developme nt of early emphysema.