CIRCULATING GALECTIN-1 AND GALECTIN-3 IN SERA FROM PATIENTS WITH SYSTEMIC SCLEROSIS: ASSOCIATIONS WITH CLINICAL FEATURES AND TREATMENT

VICTORIA SUNDBLAD; RAMIRO GOMEZ; JUAN STUPIRSKI; PABLO HOCKL; MARIA PINO; HUGO LABORDE; GABRIEL RABINOVICH

FRONTIERS IN PHARMACOLOGY

FRONTIERS

Año: 2021

1663-9812

Systemic Sclerosis (SSc) is a rheumatic disease characterized by fibrosis, microvasculardamage and immune dysregulation. Two major subsets, limited cutaneous systemicsclerosis (lcSSc) and diffuse cutaneous systemic sclerosis (dcSSc) can be defined,according to the extent of skin involvement. Increasing evidence indicates a role forgalectins in immune and vascular programs, extracellular matrix remodeling and fibrosis,suggesting their possible involvement in SSc. Here, we determined serum levels of galectin(Gal)-1 and Gal-3 in 83 SSc patients (dcSSc n 17; lcSSc n 64; ssSSc n 2), andevaluated their association with clinical manifestations of the disease. Patients with dcSScshowed lower Gal-3 levels, compared to lcSSc (p 0.003), whereas no considerabledifference in Gal-1 levels was detected between groups. Remarkably, higherconcentrations of Gal-1 were associated with the presence of telangiectasias (p 0.015), and higher concentrations Gal-3 were associated with telangiectasias (p 0.021), diarrhea (p 0.039) and constipation (p 0.038). Moreover, lower Gal-3 levelswere associated with the presence of tendinous retractions (p 0.005). Patients receivingcalcium blockers (p 0.048), methotrexate (p 0.046) or any immunosuppressivetreatment (p 0.044) presented lower concentrations of Gal-3 compared to those notreceiving such treatments. The presence of telangiectasia and the type of SSc maintainedtheir statistical association with Gal-3 (β 0.25; p 0.022 and β 0.26; p 0.017,respectively) in multiple linear regression models. In conclusion, serum levels of Gal-3are associated with clinical manifestations of SSc. Among them, the presence oftelangiectasias could be explained by the central role of this lectin in the vascularizationprograms.