The profile of adipokines associated with fibrosis and impaired microcirculation in systemic sclerosis

Adipokines belong to a group of molecules mostly produced by adipose tissue. Abnormalities in the secretion of several adipokines have already implicated to play a pathogenic role in systemic sclerosis (SSc). However, the possible role of numerous molecules still needs to be clarified. The aim of the study was to determine whether the altered level of selected circulating adipokines might correlate with the intensity of fibrosis and vasculopathy in the course of SSc.

Serum concentrations of chemerin, adipsin, retinol-binding protein 4, apelin, visfatin, omentin-1, and vaspin were determined with ELISA in the sera of patients with SSc (n ​= ​55) and healthy controls (n ​= ​25).

The serum concentration of adipsin (p ​= ​0.03) and visfatin (p ​= ​0.04) was significantly increased and the level of retinol-binding protein 4 (p ​= ​0.03) was decreased in diffuse compared to limited cutaneous SSc. Moreover, serum adipsin level correlated positively with the intensity of skin fibrosis measured with the modified Rodnan skin score (r ​= ​0.31, p ​= ​0.02) and was significantly higher in patients with pulmonary arterial hypertension than in those without the condition (p ​= ​0.03). The concentrations of adipsin (p ​= ​0.01) and visfatin (p ​= ​0.04) were significantly increased and the level of apelin (p ​= ​0.02) was decreased in patients with active digital ulcerations compared to individuals without this complication.

Adipsin may be considered a pivotal protein in the development of both fibrosis and impaired microcirculation. Its abnormal concentration reflects the intensity of skin thickening and the presence of pulmonary arterial hypertension. Adipsin, visfatin, and apelin are adipose tissue-derived molecules associated with digital vasculopathy.