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The Profile of Serum Transferrin Isoforms in Rheumatoid Arthritis

Gudowska, Monika, PhD*; Gruszewska, Ewa, PhD*; Wrona, Alicja, MSc*; Gindzienska-Sieskiewicz, Ewa, PhD; Domyslawska, Izabela, PhD; Lipartowska-Klimuk, Karina, PhD; Cylwik, Bogdan, PhD; Sierakowski, Stanislaw, PhD; Chrostek, Lech, PhD*

JCR: Journal of Clinical Rheumatology: June 2019 - Volume 25 - Issue 4 - p 159–162
doi: 10.1097/RHU.0000000000000808
Original Articles
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Introduction Transferrin, a microheterogeneous iron-transporting N-glycoprotein, is an optimal model for the analysis of the glycosylation profile in rheumatoid arthritis (RA). The aim of this study was to assess the transferrin isoforms profile in RA patients at the time of diagnosis and then look into their associations with disease activity.

Methods Serum samples were collected from 48 patients with RA. The patients were males (6) and females (42) (age range: 33–85 years). Control group consisted of 30 healthy volunteers. Transferrin isoforms were analysed by capillary electrophoresis on MINICAP electrophoretic system.

Results There was a significant decrease in the relative concentrations of trisialo- (mean ± SD; 2.130 ± 1.112) and pentasialotransferrin (13.562 ± 3.088), and significant increase in tetrasialotransferrin (83.640 ± 3.165) in RA patients when compared to the control group (3.615 ± 1.156; 76.840 ± 5.621; 18.610 ± 6.027, respectively) (U Mann–Whitney test: p < 0.001 for all comparisons). There were no significant changes in the disialotransferrin concentrations in RA patients. Trisialotransferrin concentration correlated with RA activity expressed as DAS 28 in RA patients (p < 0.001). The low trisialotransferrin concentration was also associated with high platelet count and high ESR (p < 0.001 for both). Disialo-, tetrasialo- and pentasialotransferrin concentrations did not correlate with DAS 28.

Conclusions In patients with RA the serum profile of transferrin isoforms is altered. We predict that the levels of trisialylated isoforms of transferrin will serve as a useful biochemical marker of the RA activity.

From the *Departments of Biochemical Diagnostics,

Rheumatology and Internal Diseases, and

Pediatric Laboratory Diagnostics, Medical University Bialystok, Bialystok, Poland.

The authors declare no conflict of interest.

Correspondence: Monika Gudowska, PhD, Department of Biochemical Diagnostics, Medical University of Bialystok, Waszyngtona 15A Street, 15-269 Białystok, Poland. E-mail: monika.gudowska@umb.edu.pl.

Online date: May 19, 2018

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