Introduction

Systemic sclerosis is a connective tissue disease of unknown etiology characterized by endothelial cell injury, inflammation and fibrosis. Beta-trace protein (BTP) catalyzes conversion of prostaglandin H2 to prostaglandin D2. Prostaglandin D2 stimulates the vascular response by DP1 and allergic reactions by CRTH2.

Objective

To evaluate serum BTP in systemic sclerosis and correlate it with systemic sclerosis subtype, C-reactive protein, disease duration, skin fibrosis, and vascular and internal organ involvement.

Material and methods

Forty-six patients with systemic sclerosis and 30 healthy volunteers were included in the study. Clinical and laboratory data were collected including specific antibodies, interstitial lung disease, esophageal involvement, digital pitting scars, disease duration, Raynaud’s phenomenon and modified Rodnan skin score. BTP levels were analyzed by ELISA. Statistical analysis was performed by c2, Student’s t-test and Mann-Whitney-U test. Pearson and Spearman correlation analyses were used to establish variables’ association. The significance threshold was set at p < 0.05.

Results

Patients with systemic sclerosis had significantly higher serum BTP concentration in comparison to healthy controls at p = 0.0003. No association between BTP levels and C-reactive protein, internal organ involvement, disease duration, autoantibodies and Raynaud’s phenomenon onset was found. Patients who developed pitting scars and fingertip ulcerations had significantly higher BTP serum levels than those without these symptoms (p = 0.03).

Conclusions

Significantly elevated BTP in systemic sclerosis at p < 0.001 may indicate the role of BTP in disease pathogenesis, since a BTP-dependent effect can be involved in three main features of systemic sclerosis: inflammation/autoimmunity, vasocontraction and fibrosis. Further studies with larger numbers of patients are required to fully establish the prognostic and diagnostic significance of BTP in systemic sclerosis.