From the Research
Patients with rheumatoid arthritis often develop anemia of chronic disease due to the ongoing inflammation disrupting normal iron metabolism and red blood cell production, as supported by the study 1. The pathogenesis of anemia in rheumatoid arthritis is complex and involves multiple factors, including the production of pro-inflammatory cytokines such as interleukin-6, tumor necrosis factor-alpha, and interleukin-1, which increase the production of hepcidin, a liver hormone that blocks iron absorption from the gut and prevents iron release from storage sites, as discussed in the study 2. Some key points to consider in the development of anemia in rheumatoid arthritis include:
- The role of hepcidin in blocking iron absorption and preventing iron release from storage sites, creating a functional iron deficiency despite adequate iron stores in the body 1
- The direct suppression of erythropoiesis (red blood cell production) in the bone marrow by inflammatory cytokines, as well as the shortening of the lifespan of circulating red blood cells 3
- The reduction of the body's production of erythropoietin, the hormone that stimulates red blood cell production, due to inflammation 4
- The potential for erythropoiesis-stimulating agents to improve anemia in severe cases, although the evidence is conflicting and these agents may not be effective for all patients 4 Treatment of anemia in rheumatoid arthritis typically focuses on controlling the underlying disease with disease-modifying antirheumatic drugs (DMARDs) like methotrexate, biologics such as TNF inhibitors, or JAK inhibitors, which can improve the anemia by reducing inflammation, as supported by the study 1.