Anaemia of chronic disease in rheumatoid arthritis: in vivo effects of tumour necrosis factor alpha blockade.
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 erythro...
| Main Authors: | , , , , , |
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| Format: | Journal article |
| Language: | English |
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1997
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| _version_ | 1826300385991589888 |
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| author | Davis, D Charles, P Potter, A Feldmann, M Maini, R Elliott, M |
| author_facet | Davis, D Charles, P Potter, A Feldmann, M Maini, R Elliott, M |
| author_sort | Davis, D |
| collection | OXFORD |
| description | 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. |
| first_indexed | 2024-03-07T05:16:22Z |
| format | Journal article |
| id | oxford-uuid:dd54a6b8-db9c-48d9-9a97-8aaed3d2694e |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T05:16:22Z |
| publishDate | 1997 |
| record_format | dspace |
| spelling | oxford-uuid:dd54a6b8-db9c-48d9-9a97-8aaed3d2694e2022-03-27T09:24:19ZAnaemia of chronic disease in rheumatoid arthritis: in vivo effects of tumour necrosis factor alpha blockade.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:dd54a6b8-db9c-48d9-9a97-8aaed3d2694eEnglishSymplectic Elements at Oxford1997Davis, DCharles, PPotter, AFeldmann, MMaini, RElliott, MAnaemia 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. |
| spellingShingle | Davis, D Charles, P Potter, A Feldmann, M Maini, R Elliott, M Anaemia of chronic disease in rheumatoid arthritis: in vivo effects of tumour necrosis factor alpha blockade. |
| title | Anaemia of chronic disease in rheumatoid arthritis: in vivo effects of tumour necrosis factor alpha blockade. |
| title_full | Anaemia of chronic disease in rheumatoid arthritis: in vivo effects of tumour necrosis factor alpha blockade. |
| title_fullStr | Anaemia of chronic disease in rheumatoid arthritis: in vivo effects of tumour necrosis factor alpha blockade. |
| title_full_unstemmed | Anaemia of chronic disease in rheumatoid arthritis: in vivo effects of tumour necrosis factor alpha blockade. |
| title_short | Anaemia of chronic disease in rheumatoid arthritis: in vivo effects of tumour necrosis factor alpha blockade. |
| title_sort | anaemia of chronic disease in rheumatoid arthritis in vivo effects of tumour necrosis factor alpha blockade |
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