Anemia in rheumatoid arthritis is a process associated with chronic inflammatory disease. It occurs as iron deficiency, mostly due to drug-induced gastrointestinal bleeding and disorders as well as iron redistribution into inflamed joint structure. Oxidative stress plays an important role in neuronal injuries caused by cerebral ischemia. It is known that free iron increases significantly during ischemia and is responsible for oxidative damage in the brain. For a period of two years 46 patients (8 male and 38 female), diagnosed with rheumatoid arthritis from the Department of Rheumatology at “St. Ivan Rilski” hospital were observed. Acute stroke were diagnosed in Neurology Dept. at University “Aleksandrovska” hospital. Thalassemia patients were monitored in Intensive Cardiology Dept. at the same hospital. Serum hepcidin levels statistically differ in three RA groups: RA no anemia 15.8 ± 0.7 µg/L (in the reference ranges), RA with IDA 0.7 ± 0.2 µg/L and RA with ACD 96.7 ± 1.9 µg/L (P < 0.001). In patients with acute stroke hepcidin concentrations were significantly elevated compared to thalassemia cases 87.8 ± 1.6 µg/L to 0.95 ± 0.3 µg/L (P < 0.001). Our study in patients with rheumatoid arthritis and different anemia plus additional acute stroke cases confirms the ability of verified immunochemical method to differentiate the increase and decrease in serum hepcidin in patients with RA. It provides a basis for choosing the correct therapeutic approach in the treatment of anemia.
 

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