Galectin-3 level in scleroderma

Scleroderma is a chronic inflammatory disease characterized by vascular injury, immunological abnormalities and widespread fibrosis of the skin and internal organs. At scleroderma, fibroblasts that responsible for fibrosis development; interact with inflammatory cells such as T lenfosits, macrophages, B lenfosits, mast cells and natural killer cells and than converts to myofibroblasts that can synthesis collagen. As a result extracellüler matrix increases and fibrosis grows up.Galectin-3, is a member of beta galaktozid binding lectins and mediate interaction between T cells, macrofages and fibroblasts. In addition, in experimental studies, galectin-3 inhibition has been shown to prevent development of fibrosis. This research, galectin-3 levels in scleroderma patients and the relationship between galectin-3 levels and disease activity and disease severity scors were evaluated.Thirty seven scleroderma patients, 23 systemic lupus erythematosus (SLE) patients (patient control group) and 28 healthy volunteers were included to research. Disease activity and severity scors were detected with Valentini disease activity index and Medsger disease severity scale in scleroderma group and SLE Disease Activity Index (SLEDAI) and Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) damage index in SLE group. İn addition to routine laboratory parameters, galectin-3, vascular endothelial growth factor (VEGF), transforming growth factor- ß (TGF-ß) and interleukin-6 (IL-6) levels were exemined.Compared with control group, in scleroderma and SLE groups, galectin-3 levels were higher (in orderly p<0,05, p<0,001). However, both two disease groups, galectin-3 level has no corelation with disease activity and severity scors but has corelation with TGF-ß level. (in orderly r=0.474, p=0.017 and r=0.503 p=0.014).At the result, galectin-3 level has increased as well as at an inflamatuar disease SLE and fibrotic disease skleroderma. In the future, targeted therapies that focused at galectin-3 may be important as a potential treatment method.Key words: Scleroderma, galectin-3, fibrosis, TGF-ß, VEGF