ELASTIN AND COLLAGEN DEGRADATION PRODUCTS IN URINE OF SMOKERS WITH AND WITHOUT CHRONIC OBSTRUCTIVE PULMONARY-DISEASE

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.