Pj. Stone et al., ELASTIN AND COLLAGEN DEGRADATION PRODUCTS IN URINE OF SMOKERS WITH AND WITHOUT CHRONIC OBSTRUCTIVE PULMONARY-DISEASE, American journal of respiratory and critical care medicine, 151(4), 1995, pp. 952-959
Citations number
45
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
It has been hypothesized that emphysema results from damage to the ela
stic fiber network of the lungs as a result of elastase-antielastase i
mbalance. We used a new assay for urinary desmosine (DES) and isodesmo
sine (IDES), specific markers for the degradation of mature crosslinke
d elastin, and hydroxylysylpyridinoline (HP) and lysylpyridinoline (LP
), specific markers for the degradation of mature crosslinked collagen
, in order to examine elastin and collagen degradation in relation to
current cigarette smoking and the presence of chronic obstructive pulm
onary disease (COPD). The study sample consisted of 22 never-smokers (
NSM group), 13 current smokers without airflow obstruction (SM group),
and 21 patients with COPD (COPD group), including both current and fo
rmer smokers. The relation between the creatinine-height index and FEV
(1) was used to correct for possible loss of muscle mass and decreased
excretion of creatinine in the COPD group. Mean urinary excretion of
elastin-derived crosslinks in the COPD group (DES, 11.8 +/- 5.1 [mean
+/- SD]; IDES, 11.3 +/- 5.0 mu g/g creatinine) and in the SM group (DE
S, 11.0 +/- 4.2; IDES, 10.2 +/- 2.5 mu g/g creatinine) was significant
ly higher than in the NSM group (DES, 7.5 +/- 1.4; IDES, 6.9 +/- 1.3 m
u g/g creatinine). In multivariate analysis, current smoking and the p
resence of COPD were significantly and independently associated with h
igher urinary excretion of elastin degradation products, and there was
no significant interaction between current smoking and the presence o
f COPD. Urinary excretion of HP and LP in the COPD group was significa
ntly higher than in the SM and the NSM groups (51.5 +/- 24.9, 31.1 +/-
8.3, and 24.9 +/- 6.1 nmol/mmol creatinine, respectively, for HP and
12.9 +/- 5.9, 7.0 +/- 1.5, and 4.9 +/- 2.0 nmol/mmol creatinine, respe
ctively, for LP). After adjusting for the effect of sex, urinary HP ex
cretion in the SM group was significantly greater than in the NSM grou
p. Because urinary LP is almost exclusively derived from bone collagen
degradation, urinary LP can be used to calculate the relative amounts
of bone and soft-tissue-derived HP. The excess HP excretion in the SM
and the COPD groups was derived from bone collagen turnover. We concl
ude that COPD and current smoking are independently associated with el
evated elastin and collagen degradation. The excess elastin and collag
en degradation associated with COPD appears to persist even after the
cessation of smoking.