Galectin-3 Protein May Be Blood Biomarker for Scleroderma and Like Diseases

Galectin-3 Protein May Be Blood Biomarker for Scleroderma and Like Diseases
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Elevated blood levels of a protein called galectin-3 can help diagnose people with rheumatic diseases that include scleroderma, rheumatoid arthritis, and systemic lupus erythematosus, a study suggests.

The study, “Diagnostic Power of Galectin-3 in Rheumatic Diseases,” was published in the Journal of Clinical Medicine.

Chronic inflammation characterizes the progression of rheumatic diseases such as scleroderma, accompanied by high levels of inflammatory proteins in the bloodstream.

Galectin-3 is found across diverse organs and types of cells, including those of the immune system. The protein is involved in processes that include cell-to-cell recognition, cell growth and differentiation, and the formation of blood vessels.

Elevated blood levels of galectin-3 have been reported in several disorders and associated with fibrosis (scarring) in the liver and lungs, supporting the protein’s role as an active marker of fibrosis in disease settings.

Researchers at the Medical University of Bialystok, in Poland, analyzed the levels of galectin-3 in blood samples of rheumatic patients to assess its diagnostic potential.

Blood samples from 149 patients — 82 with rheumatoid arthritis (RA), 49 with scleroderma (39 women and 10 men), and 18 with lupus — were analyzed, as were samples from 30 healthy subjects, who served as controls. Patients were a median age of 51 (range 19 to 85); the control group’s median age was 25.

Results showed that the median blood levels of galectin-3 were significantly higher in the three groups of patients — 19.4 nanogram per milliliter (ng/mL) in scleroderma, 18.75 ng/mL in RA, and 19.2 ng/mL in lupus — compared with those of the controls (9.45 ng/mL).

Levels of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and platelets — all markers of inflammation — were also significantly elevated in RA and scleroderma patients compared with controls.

In RA, higher galectin-3 levels correlated with more advanced age, but not with the disease activity scores on DAS28, which rates RA activity based on measures that include joint swelling and sensitivity, pain, and ESR and CRP levels.

In both scleroderma and RA, higher galectin-3 levels correlated with higher ESR levels. No association between galectin-3 and these inflammation markers were found among lupus patients.

Galectin-3 blood levels in the blood had a high diagnostic specificity (95%) for the three rheumatic diseases, and a sensitivity comparable to ESR and CRP values. (A marker’s sensitivity is its ability to correctly identify those with a given disease, while specificity refers to correctly identifying those without it.)

The researchers considered the diagnostic accuracy of galectin-3 to be high — about 80% — and similar across these three  diseases.

Study results “showed that galectin-3 had a high diagnostic specificity in all rheumatic diseases accompanied by diagnostic sensitivity placed between ESR and CRP values,” they wrote.

The positive predictive value (PPV) of galectin-3 was also higher than that of CRP and ESR in these three disorders. PPV measures the proportion of patients who tested positive and actually have the condition.

Further analyses showed that galectin-3 levels had excellent diagnostic power for RA and scleroderma, and a very good power for a lupus diagnosis.

“The results obtained in our study suggest that determination of serum [blood] galectin-3 concentration may be a useful tool in the diagnosis and treatment of these diseases,” the scientists concluded.

Patricia holds a Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She has also served as a PhD student research assistant at the Department of Microbiology & Immunology, Columbia University, New York.
Total Posts: 27
José holds a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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Patricia holds a Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She has also served as a PhD student research assistant at the Department of Microbiology & Immunology, Columbia University, New York.
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