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
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.