4.2 Article

Metabolic mediators determine the association of antinuclear antibody subtypes with specific clinical symptoms in systemic sclerosis

Journal

ADVANCES IN MEDICAL SCIENCES
Volume 66, Issue 1, Pages 119-127

Publisher

ELSEVIER URBAN & PARTNER SP Z O O
DOI: 10.1016/j.advms.2020.12.007

Keywords

Adipokines; Adipose tissue; Antinuclear antibodies; Endothelium; Systemic sclerosis

Funding

  1. Medical University of Warsaw, Poland [1M4/N/19/19]

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The study aimed to investigate the possible link between different types of systemic sclerosis-specific antinuclear antibodies, adipokines, and endothelial molecules. The results showed associations between specific antibodies and increased serum concentrations of certain molecules, indicating metabolic and vascular factors may serve as mediators between immunological abnormalities and non-immune driven clinical symptoms in systemic sclerosis.
Purpose: The aim of this study was to investigate the possible link between different types of systemic sclerosis-specific antinuclear antibodies, adipokines and endothelial molecules which were recently found to have a pathogenic significance in systemic sclerosis. Materials/methods: Serum concentration of adiponectin, resistin, leptin, endothelin-1, fractalkine and galectin-3 were determined in the sera of patients with systemic sclerosis (n = 100) and healthy controls (n = 20) using ELISA. Results: The following associations between antinuclear antibodies and increased serum concentrations were identified: anticentromere antibodies with endothelin-1 (p < 0.0001; mean level in patients 2.21 vs control group 1.31 pg/ml), anti-topoisomerase I antibodies with fractalkine (p < 0.0001; 3.68 vs 1.68 ng/ml) and galectin-3 (p = 0.0010, 6.39 vs 3.26 ng/ml). Anti-RNA polymerase III antibodies were associated with increased resistin (p < 0.0001; 15.13 vs 8.54 ng/ml) and decreased adiponectin (p < 0.0001; 2894 vs 8847 ng/ml). Conclusion: In systemic sclerosis metabolic and vascular factors may serve as mediators between immunological abnormalities and non-immune driven clinical symptoms.

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