Be. Orsida et al., Effect of a long-acting beta(2)-agonist over three months on airway wall vascular remodeling in asthma, AM J R CRIT, 164(1), 2001, pp. 117-121
There are few data regarding the potential effects of antiasthma treatment
on indices of airway remodeling, such as the increased subepithelial airway
vascularity in patients with asthma. We studied 45 symptomatic subjects wi
th asthma who were receiving treatment with low dose inhaled corticosteroid
s (ICS) (range 200-500 mug twice a day) and 28 normal subjects without asth
ma as a control population. Subjects underwent bronchoscopy with airway bio
psy and subjects with asthma were then randomized to receive supplementary
inhaled salmeterol 50 mug twice a day, fluticasone propionate 100 mug twice
a day, or placebo for 3 mo in addition to their baseline ICS. Biopsy of th
e airway was then repeated. The biopsies were analyzed for vascular structu
res in the subepithelial lamina propria, Sufficient biopsy material was ava
ilable for analysis of vascularity in 34 of the subjects with asthma and 28
of the normal subjects. We confirmed that airways of subjects with asthma
had a significant increase in the number of vessels/mm(2) of lamina propria
compared with airways of normal subjects (524 +/- 137 vessels/mm(2), n = 3
4 versus 425 +/- 130 vessels/mm(2), n = 28; p = 0.004). There was a decreas
e in the density of vessels of lamina propria after treatment only in the s
almeterol group compared with baseline (before, 535 +/- 153 vessels/mm(2) v
ersus after, 400 +/- 142 vessels/mm(2). n = 12; p = 0.04). There was Mo sig
nificant change within the fluticasone (n = 11) or placebo (n = 11) treatme
nt groups, but also no significant differences between the groups. Notably,
no treatment was associated with increased airway wall vascularity. The de
monstrated fall in vessel number within the salmeterol-treated group may su
ggest an advantageous effect of long-acting beta (2)-agonists on this manif
estation of airway remodeling over the 3-mo time scale of this study, which
is complementary to the action of ICS on airway vascularity.