Impaired fibrinolysis linked to new digital ulcers in SSc

Impaired fibrinolysis appears to play a role in underlying digital vasculopathy and its progression in systemic sclerosis (SSc), suggests a study.

A group of researchers examined the variables of endothelial dysfunction, thrombin generation, overall haemostatic potential, and fibrin clot turbidity in plasma from 58 patients with SSc (39 with digital ulcer [DU] history and 19 DU-naïve) and 46 matched healthy controls. Scanning electron microscopy (SEM) was used to visualize the fibrin structure.

The researchers followed 39 patients with DU history for 1.5 years and explored the predictive value of all examined markers for new DU onset.

Results revealed significantly enhanced endogenous thrombin potential (ETP) and prolonged clot lysis time (CLT) in patients with DUs relative to healthy controls.

CLT was prolonged in DU patients compared to those without, signifying good validity in identifying DUs with an area under the curve of 0.7 (95 percent confidence interval [CI], 0.6‒0.8). ETP and intercellular adhesion molecule 1 levels each correlated with CLT.

Twenty patients developed new DUs over the follow-up period. These patients had prolonged CLT (p<0.001), particularly those with recurrent DUs. On regression analysis, the Raynaud phenomenon visual analogue scale (odds ratio [OR], 1.1, 95 percent CI, 1.0‒1.1) and CLT (OR, 1.2, 95 percent CI, 1.1‒1.3) predicted new DUs. Moreover, SEM confirmed denser fibrin clots in patients with new DUs.