Role of Fetuin-A in Systemic Sclerosis-associated Calcinosis

Abstract

To the Editor: Calcinosis, a soft-tissue calcification occurring in the setting of normal serum calcium and phosphate levels, has been observed in connective tissue diseases, including systemic sclerosis (SSc)1, more frequently in the limited form (lcSSc) and in patients who are anticentromere antibody (ACA)-positive1. Calcinosis may be exceedingly painful and cause major clinical problems, including ulceration, infection, and joint contractures1. Hypovascularity, hypoxia, and tissue damage seem to favor its development, with genetic factors also playing a role. No treatment exists so far, and even surgical removal is unsatisfactory, since recurrences are common1. Fetuin-A (α-2-Heremans-Schmid glycoprotein, AHSG) is a major inhibitor of systemic calcification, and low serum levels have been associated with vascular and soft-tissue calcifications2. Any situation that lowers serum fetuin-A, including inflammatory conditions, could increase the risk of calcification, because fetuin-A is a negative acute-phase protein. AHSG gene variations seem to influence fetuin-A serum concentration3. Forty-one consecutive Italian patients with SSc [40 women, age 63 ± 13 years, 16 diffuse SSc (dcSSc), 25 lcSSc] were … Address correspondence to Dr. L. Belloli, Via Manzoni 56, Rozzano 20089, Italy. E-mail: laurabelloli{at}tiscali.it