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Increased levels of amino terminal propeptide of type III procollagen are an unfavourable predictor of survival in systemic sclerosis

Z. Nagy, L. Czirják

Department of Immunology and Rheumatology, Medical School, Hungarian Brothers of St. John of God and University of Pécs, Pécs, Hungary

ABSTRACT
Objective
Investigation of the impact on survival of inflammatory parameters (C-reactive protein, ESR), markers of immune activation (serum soluble IL-2 receptor, soluble CD30), and N-terminal propeptide of type III procollagen levels (PIIINP) in systemic sclerosis (SSc).

Methods
In a prospective follow up study, clinical and laboratory data of 80 patients with SSc were evaluated. Kaplan-Meier survival curves and Cox proportional hazards model were used. Eighty cases with SSc were evaluated. Female/male ratio was 8/72. The mean (±SD) age was 49.3 (±12.3) years, 16 patients died during our mean follow up of 58.1 months.

Results
In the univariate analysis, the presence of a C-reactive protein level above 20 mg/l was an unfavourable prognostic sign (p<0.001). Increased level of PIIINP level also caused an unfavourable outcome of disease (p<0.001).
Conversely, increased ESR, soluble IL-2 receptor, soluble CD30 levels, presence of anaemia, did not influence the prognosis. Male gender (p<0.005), diffuse cutaneous SSc, clinically significant lung involvement (p<0.001), kidney (p<0.0001), cardiac (p<0.05) manifestations including pericarditis (p<0.02) were unfavourable prognostic signs
by univariate Kaplan–Meier method. Multivariate analysis by Cox proportional hazards model showed that the increased level of PIIINP (RR: 6.98), and presence of diffuse cutaneous SSc (RR: 5.14) were independent unfavourable prognostic signs.

Conclusions
An increased collagen metabolism unfavourably influences the outcome of SSc. This parameter may also be a potential candidate as a disease activity marker.

Key words
Prognosis, survival, systemic sclerosis, C-reactive protein, aminoterminal type III collagen propeptide.

This work was supported by the Hungarian NKFP grant (1/026/2001), the Hungarian Ministry of Health and Social Welfare grant (ETT 643/2003), and by the National Foundation for Scientific Research grants (OTKA T046701).
Please address correspondence to: Prof. László Czirják, MD, PhD, Hungarian Brothers of St. John of God
and University of Pécs, Medical School, Department of Immunology and Rheumatology, H-7621 Pécs, Irgalmasok u. 1.
E-mail: <laszlo.czirjak@aok.pte.hu>