Arthritis & Rheumatism, Volume 63,
November 2011 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Chicago, Illinois November 4-9, 2011.

Serum Galectin-3 Level in Patients with Scleroderma.

Ozgen1,  Metin, Koca1,  Suleyman Serdar, Akbas1,  Fatma, Ilhan2,  Nevin, Gundogdu1,  Baris, Isik1,  Ahmet

Department of Rheumatology, Faculty of Medicine, Firat University, Elazig, Turkey
Department of Biochemistry, Faculty of Medicine, Firat University, Elazig, Turkey


Scleroderma (systemic sclerosis [SSc]) is an autoimmune disease of unknown etiology characterized by progressive multiorgan fibrosis. Activated fibroblasts are mainly responsible for fibrosis in SSc. Galectin-3, a b-galactoside binding lectin, plays many important regulatory roles in both physiological and pathological processes including proliferation, apoptosis, inflammation and fibrosis. Previous studies have demonstrated that galectin-3 contributes significantly to fibroblast activation and the development of fibrosis.

The purpose of this study was to asses the serum galectin-3 level and its association with disease activity and severity indexes in patients with SSc.


Thirty seven SSc patients, 23 systemic lupus erythematosus (SLE) patients (serving as patient control group) and 28 healthy volunteers were enrolled in this study. Disease activity and severity scores were detected with Valentini disease activity index and Medsger disease severity scale in the SSc group, and SLE Disease Activity Index (SLEDAI) and Systemic Lupus International Collaborating Clinics/American Collage of Rheumatology (SLICC/ACR) damage index in the SLE group. The serum levels of galectin-3, vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-b and interleukin (IL)-6 were determined.


Compared with the control group, the galectin-3 levels were higher (Table) in the SSc and SLE groups. The galectin-3 levels were not correlated with the disease activity and severity indexes in both patient groups. But, the serum galectin-3 levels were higher in the active SSc and SLE subgroups than in the inactive SSc (4.6 ng/mL vs. 1.3 ng/mL p=0.015) and SLE (17.4 ng/mL vs. 6.5 ng/mL p=0.019) subgroups.

Table. Demographics and laboratory data in the study groups

Age (years)46 ± 1337 ± 1042 ± 140.110*
Gender (Female/Male)32/521/222/60.302**
BMI (kg/m2)24.2/5.125.2 ± 4.126.9 ± 4.80.980*
Disease duration (years)4.19 ± 4.575.13 ± 4.380.079*
ESR (mm/h)26 ± 20b32 ± 26c9 ± 40.001*
CRP (mg/L)12 ± 206 ± 63 ± 00.056*
IL-6 (pg/mL)11.4 ± 5.618.5 ± 20.414.9 ± 26.10.116*
TGF-b (ng/mL)42.7 ± 14.832.8 ± 11.735.5 ± 12.20.085*
VEGF (pg/mL)337 ± 242210 ± 175a330 ± 1950.023*
Galectin-3 (ng/mL)3.5 ± 4.9a,d14.0 ± 11.6c1.25 ± 1.080.001*
Data were presented as mean ± standard deviation. SSc: Systemic sclerosis, SLE: Systemic lupus erythematosus, HC: Healthy control, BMI: Body mass index, ESR: Erythrocyte sedimentation rate, CRP: C-reactive protein, IL: Interleukin, TGF: Transforming growth factor, VEGF: Vascular endothelial growth factor.
* ANOVA and** Chi-square p value; Compared with control group:a p<0.05,b p<0.01,c p<0.001; Compared with SLE group:d p<0.001.


These results suggest that galectin-3 is involved in the pathogenesis of SSc characterized by fibrosis and SLE characterized by inflammation. Galectin-3, which is proposed as biomarker of fibrosis and inflammation by previous studies, may be a novel biomarker for activities of SSc and SLE.

To cite this abstract, please use the following information:
Ozgen, Metin, Koca, Suleyman Serdar, Akbas, Fatma, Ilhan, Nevin, Gundogdu, Baris, Isik, Ahmet; Serum Galectin-3 Level in Patients with Scleroderma. [abstract]. Arthritis Rheum 2011;63 Suppl 10 :1837

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