Serum levels of type III collagen aminopropeptide in patients with systemic scleroderma

Circulating type I collagen degradation products: a new serum marker for clinical severity in patients with scleroderma?

“…Furthermore, a similar increase in ICTP has been found in two patients with a generalized form of morphoea, supporting the correlation between the extent of connective tissue involvement and ICTP levels in SSc. The finding of an increased turnover of type I collagen in SSc may be further supported by the increased levels of the amino terminal propeptide of type III procollagen in this disease reported by several authors, 6,23,24 as recent studies indicate that some of the assays used previously also measure degradation products of type III collagen. 21 Moreover, a recent study reporting increased urinary excretion of two mature cross-links of collagen, hydroxylysyl and lysyl pyridinoline, in patients with SSc, suggests that in SSc more fibrillar collagens are degraded than in the normal state.…”

Evidence for protein oedema, neutrophil influx, and enhanced collagen production in lungs of patients with systemic sclerosis.

“…26 Our results indicate that the measurement of serum procollagen N peptide does not distinguish patients with clinical evidence of pulmonary fibrosis from those without. By contrast, our results for bronchoalveolar lavage fluid suggest a progressive increase in type III collagen synthesis with the development of pulmonary fibrosis, though these data do not necessarily indicate that type III collagen is laid down as mature collagen fibrils in the lung interstitium.…”

“…Lavage was also performed on 10 healthy, non-smoking volunteers who acted as controls. The median age of the control group was 29 (range [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36] years.…”

Markers of collagen and basement membrane metabolism in sera of patients with progressive systemic sclerosis.

“…Raised serum concentrations of the amino terminal propeptide of type III procollagen have earlier been found in patients with systemic sclerosis.14 [25][26][27] The results of our study indicate that the increases in both the larger forms of PIIINP, as measured by the antibody PIIINP assay, and in the degradation products of this antigen, as detected by the PIIINP-Fab assay, occur during active phases of the disease, as indicated by the presence of immune complexes and antinuclear antibodies. Active arthritis, in particular, was associated with increased PIIINP concentrations; a similar finding has previously been made in rheumatoid arthritis .28 In contrast with a previous study on scleroderma,14 in our series of patients PIIINP-Fab was not pathological more often than PIIINP.…”