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Pathobiochemical Mechanisms Relating Iron Homeostasis with Parameters of Inflammatory Activity and Autoimmune
Katya I Stefanova1, Ginka T Delcheva1, Ana I Maneva1
1Department of Chemistry and Biochemistry, Faculty of Pharmacy, Medical University of Plovdiv, Plovdiv, Bulgaria.
In rheumatoid arthritis (RA), elevated soluble transferrin receptor (sTfR) and prohepcidin indicate tissue iron deficiency driven by inflammation. These markers help assess iron status in RA patients.
Area of Science:
- Rheumatology
- Immunology
- Hematology
Background:
- Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation.
- Iron homeostasis is often disrupted in RA, influenced by inflammation and autoimmune processes.
Purpose of the Study:
- To investigate the correlations between iron homeostasis parameters, inflammatory markers, and autoimmune disease activity in rheumatoid arthritis.
- To identify key biomarkers for assessing iron status and inflammation in RA.
Main Methods:
- Study included 114 RA patients and 42 healthy controls.
- Measured serum iron, TIBC, ferritin, sTfR, CRP, IL-6, prohepcidin, RF, anti-CCP antibodies, and DAS 28.
Main Results:
- RA patients showed higher sTfR, CRP, IL-6, prohepcidin, and lower serum iron compared to controls.
- sTfR positively correlated with inflammatory markers (IL-6, prohepcidin, ESR) and autoimmune parameters (DAS 28, RF, anti-CCP) in RA.
- Prohepcidin positively correlated with inflammation (CRP, ESR) and autoimmune parameters (DAS 28, RF) in RA.
Conclusions:
- Simultaneous measurement of sTfR and prohepcidin is highly informative for evaluating iron homeostasis changes in RA.
- Increased sTfR and prohepcidin suggest inflammation-induced tissue iron deficiency in RA patients.
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