Carboxyterminal propeptide of type I procollagen in ELF: elevation in asbestosis, but not in pleural plaque disease

Our plain-English summary of Carboxyterminal propeptide of type I procollagen in ELF: elevation in asbestosis, but not in pleural plaque disease, by L. Lammi, L. Ryhänen, E. Lakari, et al (The European Respiratory Journal, 1999).

The study

• Authors: L. Lammi, L. Ryhänen, E. Lakari, J. Risteli, P. Pääkkö, E.M. Ruotsalainen, S. Lähde, V.L. Kinnula
• Journal: The European Respiratory Journal
• Published: 1999;14(3):560-4
• Cited by: 3 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

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.

In plain English

This study asked whether collagen markers could reveal asbestosis (lung scarring) in people with work-related asbestos exposure. It included 42 consecutive patients; five had asbestosis. The other 37 had no lung-tissue involvement: 25 had pleural plaques, 12 normal chest X-rays. The authors measured two collagen markers, PICP and PIIINP, in lung washing fluid, lung lining fluid estimated from it, and blood. In washing fluid, PICP averaged 9.8 micrograms per litre with asbestosis versus 0.6 without lung-tissue involvement (p less than 0.001). In lining fluid the averages were 488.9 versus 22.6. PICP was detectable in 6 of 25 plaque patients and 2 of 12 with normal X-rays. In washing fluid, PIIINP was detectable in only 1 of 5 asbestosis patients and 3 of 37 others. Blood levels of neither marker differed significantly between groups. After about 7 years, none of the 30 reassessed patients without lung-tissue involvement had developed asbestosis. The authors concluded that lung-fluid PICP could be used to evaluate asbestos-related lung-tissue disease, but not to assess exposure. They noted 7 years could not exclude later asbestosis.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Comparison of consecutive patients examined at diagnosis, with prospective follow-up averaging 7 years
• Who was studied: 42 patients: 5 with asbestosis and 37 without lung-tissue (parenchymal) involvement. Of the 37, 25 had pleural plaques and 12 had no detectable chest X-ray changes.
• Exposure: Occupational exposure to asbestos fibres. Fibre types, jobs and doses were not specified for the patients.
• Main results:
  • PICP was significantly higher in the asbestosis group than in patients without asbestosis. In lavage fluid the means were 9.8 (SD 1.8) versus 0.6 (SD 1.3) micrograms per litre, p less than 0.001. In epithelial lining fluid they were 488.9 (SD 208.8) versus 22.6 (SD 50.6) micrograms per litre, p less than 0.001.
  • Among patients without lung-tissue involvement, PICP was detectable in lavage and lining fluid in 6 of 25 with pleural plaques and 2 of 12 without pleural involvement.
  • PIIINP was detectable in lavage fluid in 1 of 5 asbestosis patients and 3 of 37 patients without parenchymal involvement.
  • Serum PICP, and PIIINP in serum, lavage fluid and lining fluid, did not differ significantly between any of the groups.
  • Among patients without lung-tissue involvement, grouped by the number of asbestos bodies in lavage fluid, PICP and PIIINP levels in lavage fluid did not differ significantly between the three groups.
  • Of the 37 patients without lung-tissue involvement, 30 responded to the follow-up invitation, and none of these had developed asbestosis.
  • FEV1 and carbon monoxide diffusing capacity were significantly decreased in the patients with asbestosis.
• The authors' conclusion: The authors concluded that PICP in lavage fluid and epithelial lining fluid can be used to evaluate asbestos-related parenchymal disease, but is not useful for assessing exposure to asbestos fibres.
• Limitations the authors state:
  • Because asbestos-related disease has a long latency, the 7-year follow-up does not exclude later asbestosis in the 6 patients with pleural plaques and elevated PICP.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis, Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Pleural Plaques, Collagen, Bronchoalveolar Lavage (BAL), Occupational Exposure, Bronchoscopy, Chest X-Ray.

Related studies

• Serum type III procollagen peptide: indicator for pulmonary fibrosis: II. Application in 80 asbestos insulation workers — I. Okazaki, K. Maruyama, et al. (1987)
• Relationship of fiber surface iron and active oxygen species to expression of procollagen, PDGF-A, and TGF-beta(1) in tracheal explants exposed to amosite asbestos — J. Dai, A. Churg (2001)
• Fibronectin and procollagen 3 levels in bronchoalveolar lavage of asbestos-exposed human subjects and sheep — R. Bégin, M. Martel, et al. (1986)
• Asbestosis, pleural plaques and diffuse pleural thickening: three distinct benign responses to asbestos exposure — P.A. Gevenois, V. de Maertelaer, et al. (1998)
• Fractional exhaled nitric oxide concentration is increased in asbestosis and pleural plaques — A. Sandrini, A.R. Johnson, et al. (2006)
• The natural course of lung function decline in asbestos exposed subjects with pleural plaques and asbestosis — M. Barnikel, P.M. Million, et al. (2019)

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