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Anaemia of chronic disease (ACD) is a common feature of active rheumatoid arthritis (RA). Inflammatory cytokines, particularly tumour necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1) and interleukin-6 (IL-6), are thought to contribute to the pathogenesis of ACD, possibly by inhibiting erythropoietin (EPO) production. In this study, we examined the in vivo effects of TNF-alpha blockade with a chimeric monoclonal antibody, cA2, on erythropoiesis in RA patients with ACD. Administration of cA2 led to a dose-dependent increase in haemoglobin levels compared to placebo and these changes were accompanied by a reduction in both EPO and IL-6 levels. The data support the notion that TNF-alpha is important in the causation of ACD, but suggest a mechanism independent of EPO suppression. Instead, TNF-alpha may act directly on bone marrow red cell precursors.

Type

Journal article

Journal

Br J Rheumatol

Publication Date

09/1997

Volume

36

Pages

950 - 956

Keywords

Anemia, Antibodies, Monoclonal, Arthritis, Rheumatoid, C-Reactive Protein, Chronic Disease, Dose-Response Relationship, Drug, Double-Blind Method, Erythropoietin, Female, Hemoglobins, Humans, Interleukin-6, Male, Recombinant Fusion Proteins, Tumor Necrosis Factor-alpha