Carboxyterminal propeptide of type I procollagen in ELF: elevation in asbestosis, but not in pleural plaque disease.
Markers of collagen metabolism may possibly be used in the assessment of pulmonary involvement in asbestosis-related pulmonary diseases. In this study the levels of the carboxyterminal propeptide of type I procollagen (PICP) and the aminoterminal propeptide of type III procollagen (PIIINP) were evaluated in bronchoalveolar lavage fluid (BALF), epithelial lining fluid (ELF) and serum from patients with asbestos related pulmonary and pleural involvement. Forty-two consecutive patients with occupational exposure to asbestos fibres, who underwent bronchoscopy and bronchoalveolar lavage (BAL) at the time of the diagnosis were investigated. Five patients were diagnosed as having asbestosis, while 37 showed no parenchymal involvement. Of the latter group, 25 had pleural plaques, while 12 had no detectable changes in chest radiographs. The patients were followed-up for an average of 7 yrs. The PICP in BALF and ELF was detectable in all patients with asbestosis and in 8/37 subjects without parenchymal involvement. The levels of PICP in BALF and ELF were significantly higher in the asbestosis group compared to the patients without asbestosis (9.8+/-1.8 microg x L(-1) versus 0.6+/-1.3 microg x L(-1), p<0.001 and 488.9+/-208.8 microg x L(-1) versus 22.6+/-50.6 microg x L(-1), p<0.001, respectively). Only 1 patient with asbestosis and 3 patients without parenchymal involvement had detectable levels of PIIINP in BALF. The serum levels of PICP and PIIINP did not differ between the patients with asbestosis and those with exposure to asbestos fibres without asbestosis and were within the normal range. None of the 37 patients exposed to asbestos fibres without parenchymal involvement at the baseline developed asbestosis during the follow-up period of 7 yrs. In conclusion, the data show that the carboxyterminal propeptide of procollagen type I, but not the aminoterminal propeptide of type III procollagen is highly elevated in bronchoalveolar lavage fluid and epithelial lining fluid in patients with asbestosis, but not in those without parenchymal involvement. This suggests that the determination of carboxyterminal propeptide of procollagen type I in bronchoalveolar lavage fluid could be used as a marker of parenchymal involvement in patients exposed to asbestos fibres.
Lammi
L
L
Dept of Pulmonary Medicine, Vaasa Central Hospital, Finland.
Ryhänen
L
L
Lakari
E
E
Risteli
J
J
Pääkkö
P
P
Ruotsalainen
E M
EM
Lähde
S
S
Kinnula
V L
VL
D001194:Asbestos / Q000009:adverse effects; D001195:Asbestosis / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology; D015415:Biomarkers; D001706:Biopsy; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D003937:Diagnosis, Differential; D004847:Epithelial Cells / Q000378:metabolism*; D015633:Extravascular Lung Water / Q000378:metabolism*; D005500:Follow-Up Studies; D006801:Humans; D008875:Middle Aged; D010446:Peptide Fragments / Q000378:metabolism*; D010995:Pleural Diseases / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology; D011347:Procollagen / Q000378:metabolism*; D011658:Pulmonary Fibrosis / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D013902:Radiography, Thoracic; D012189:Retrospective Studies
D015415:Biomarkers; D010446:Peptide Fragments; D011347:Procollagen; C041876:procollagen Type III-N-terminal peptide; C042813:procollagen type I carboxy terminal peptide; D001194:Asbestos