SAT0247 Higher Fibrinogen Plasma Levels at Baseline Are Associated with A Faster Development of New Digital Pitting Scars/ulcers at Follow-Up in Systemic Sclerosis Patients
Authors: S. Vettori, V. Giacco, D. Capocotta, B. Russo, G. Valentini
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> The -455 G&gt;A polymorphism in the proximal promoter region of β-fibrinogen gene is known to increase fibrinogen plasma levels and to promote arterial and venous thrombosis in the general population (1). We previously showed that systemic sclerosis (SSc) patients with pitting scars and/or ulcers have a higher frequency of the β-fibrinogen -455 A allele and higher plasma levels of fibrinogen (2). <h3>Objectives</h3> We aimed to investigate fibrinogen plasma levels in a prospective cohort of SSc patients and to search for associations with features of vascular involvement at follow-up (FU). <h3>Methods</h3> SSc patients meeting the 2013 ACR/EULAR criteria for disease classification with measurement of fibrinogen plasma levels and at least one FU visit with complete clinical evaluation were enrolled. The comparison of fibrinogen levels in different patient groups was performed using the Mann-Whitney U test; differences between patients with fibrinogen levels higher or equal/lower than the median value were analyzed by Kaplan-Maier curves applying the log-rank test. <h3>Results</h3> One-hundred and thirty-three SSc patients, aged 51±13 years, were investigated (91% females; median disease duration 8 years, range 1–49). Seventy-six % of patients had a limited SSc subset (lcSSc); 24% had a diffuse subset (dcSSc). All patients were ANA positive (40% had anti-centromere antibodies, 35% anti-Scl70+; 3% anti-RNApolymerase III; 2.3% anti-PmScl; 1.5% anti-U1RNP). All patients were under low-dose aspirin and oral vasodilators. Forty-one % of patients had already pitting scars and/or ulcers at baseline; 13% developed new digital ischemic injury during observation (median FU 3 years; range 0.7–22). Baseline fibrinogen levels were higher in patients who developed digital ischemic lesions during FU (385 mg/dl, range 180–688 versus 344 mg/dl, range 81–765; p&lt;0.05). SSc patients with levels higher than the median value developed new ischemic lesions in the digits faster than patients with values lower or equal to the median (χ<sup>2</sup>=4.3; p&lt;0.05). <h3>Conclusions</h3> Consistently with our previous findings, here we first show that higher fibrinogen levels at baseline in SSc patients are associated with a faster development of new digital ischemic lesions over time. Of note, all our patients were taking aspirin, which, however, does not affect platelet-fibrinogen interaction. In addition, all of them were taking an oral vasodilator, that is recommended for the treatment of peripheral vasculopathy in SSc (3). Randomized controlled clinical trials in larger SSc cohorts to explore the potential benefit of gpIIb/IIIa inhibitors± low-dose aspirin in these patients are needed. <h3>References</h3> van9t Hooft FM et al.Arterioscler Thromb Vasc Biol 1999;19:3063–70 Vettori S et al. Clin Exp Rheumatol 2010;28:923–4 Kowal-Bielecka O et al. Ann Rheum Dis 2009; 68:620–628 <h3>Disclosure of Interest</h3> None declared