5.4. Procollagen I carboxyterminal propeptide and procollagen III aminoterminal propeptide in bronchoalveolar lavage fluid and serum in asbestos-related lung diseases (III)
Forced expiratory volume in one second and diffusion capacity were significantly decreased in asbestosis compared with the patients without parenchymal involvement (Table 3). The numbers of asbestos bodies in the four of five patients with asbestosis without open biopsy were 2.4 AB/ml, 12.4 AB/ml, 130 AB/ml and 772 AB/ml in BALF. Twelve patients without parenchymal changes had no AB, 14 had 0-1 AB/ml and 11 had more than one AB/ml in BALF.
All of the five patients with asbestosis had significantly higher levels of PICP in BALF and ELF than the 37 patients without parenchymal involvement (Table 10, Fig. 2). In the latter group, 6 of the 25 patients with pleural plaques and two of the 12 patients without pleural involvement had detectable PICP in BALF and ELF. The levels of the procollagen markers of these two groups did not differ significantly (Fig. 2). The serum level of PICP and the levels of PIIINP in serum, BALF and ELF did not show significant differences between any of these groups (Table 10). PIIINP was detectable in BALF in one of the 5 patients with asbestosis, in three of the 25 patients with pleural involvement and in none of those without pleural involvement (Not shown). The levels of PICP or PIIINP in patients with no parenchymal involvement did not differ in relation to the amount of asbestos bodies in BALF (Fig. 3). One patient of the asbestosis group had an elevated S-ALAT value, suggesting a possible hepatic lesion. As liver diseases are known to elevate S-PIIINP, the value of this patient was excluded.
There was no statistically significant difference in the levels of PICP in BALF between the asbestosis and fibrosing alveolitis (II) patients, but the difference between the asbestosis patients and the controls (I) was highly significant (p<0.0001). BALF-PICP but not BALF-PIIINP was significantly higher in the subjects exposed to asbestos fibres without parenchymal involvement than in the controls. In the sarcoidosis patients (I) the level of PIIINP in BALF was higher (p<0.05) but the level of PICP in BALF lower (p<0.01) than in the patients with asbestosis.
Table 10. Concentrations of PIIINP and PICP in serum, BALF, and ELF in the patients with asbestosis and those without parenchymal involvement (III).
| Asbestosis | No parenchymal involvement | |||||
|---|---|---|---|---|---|---|
| Mean ± SD | Median | Mean ± SD | Median | |||
| S-PIIINP# | µg/ | 2.3 ± 0.7 | 2.5## | 2.8 ± 0.8 | 2.7 | |
| S-PICP# | µg/ | 108.6 ± 28.2 | 104.5 | 120.4 ± 33.7 | 114.0 | |
| BALF-PIIINP | µg/ | 0.2 ± 0.4 | 0 | 0.1 ± 0.6 | 0 | |
| BALF-PICP | µg/ | 9.8 ± 1.8 | 10.8 | 0.6 ± 1.3 | 0. *** | |
| ELF-PIIINP | µg/ | 11.6 ± 25.9 | 0 | 5.4§ ± 33.8 | 0 | |
| ELF-PICP | µg/ | 488.9 ± 208.8 | 423.9 | 22.6§ ± 50.6 | 0. *** | |
| # Available from 36 patients with no parenchymal involvement. ## One patient excluded because of elevated S-ALAT. § ELF value not available for one patient with no parenchymal involvement because of missing BALF-urea. The significance of the difference was tested with the Mann-Whitney U-test. ***: p<0.001. | ||||||
All the patients with exposure to asbestos fibres without parenchymal involvement were invited for a control visit after a follow-up period of 7 years. Three patients had died from causes unrelated to asbestos. Thirty (81 %) of the 37 patients responded. None of these patients had developed asbestosis when assessed with chest radiography and diffusion capacity. One patient had an infiltrate caused by a lung carcinoma, and one patient had a previously diagnosed pulmonary metastasis due to a thyroid malignancy. The pleural plaques had only progressed in one patient. None of those with normal chest radiographs had developed plaques.
