New evidence shows Rituximab halts damage to joints
A significant finding in previously unstudied group of rheumatoid arthritis patientsNew data, presented today at the Annual European Congress of Rheumatology show for the first time that a rheumatoid arthritis (RA) treatment, rituximab, is able to significantly inhibit the structural damage to joints caused by RA in patients who have long-standing disease and an inadequate response to one or more TNF (Tumour Necrosis Factor) inhibitors.
Prevention of joint structural damage in rheumatoid arthritis is a critical therapeutic outcome. Many patients respond well to the TNF inhibitors, a relatively new class of therapy which prevents TNF protein causing inflammation in rheumatoid arthritis, however approximately 30% - 40% of patients treated with this therapy experience either an inadequate response or are intolerant to such therapies. As such, the study was designed to investigate the effect at 1 year of rituximab (a new therapy targeting B-cells – cells which create abnormal antibodies causing rheumatoid arthritis symptoms) plus methotrexate (an antimetabolite drug which inhibits the synthesis of DNA, RNA and protein, previously the gold standard in the treatment of rheumatoid arthritis) on joint structural damage, compared to methotrexate alone in rheumatoid patients with inadequate response to one or more TNF inhibitors.
The results reveal bone erosions in patients in the rituximab group were reduced by over half during the course of a year compared to patients receiving placebo (erosion scores of 0.59 and 1.32 respectively), as were the narrowing of joint spaces (scores of 0.41 and 0.99 respectively). In addition the proportion of patients with no change in erosion score was significantly higher in the rituximab group compared to placebo.
"These findings suggest that treatment with rituximab plus methotrexate is associated with significant inhibition of joint structural damage, an important finding in patients who do not currently respond to other treatments" explained Professor Edward Keystone, Rheumatology Department at the University of Toronto, Canada, one of the studies principle investigators. "Stopping joint damage indicates that the disease pathway has been interrupted, a goal we strive for in the treatment of rheumatoid arthritis. As such, today's results have the potential to offer many patients a new hope".
For further information on this study, or to request an interview with the study lead, please do not hesitate to contact the EULAR congress press office on:
Jim Baxter - Onsite tel: +44 (0) 7900 605652
Jo Spadaccino - Onsite tel: +44 (0) 7773 271930
Mia Gannedahl - Office tel: +44 (0) 20 7331 2325
Abstract number: OP0016
- The European League Against Rheumatism (EULAR) is the organization which represents the patient, health professional and scientific societies of rheumatology of all the European nations.
- The aims of EULAR are to reduce the burden of rheumatic diseases on the individual and society and to improve the treatment, prevention and rehabilitation of musculoskeletal diseases. To this end, EULAR fosters excellence in education and research in the field of rheumatology. It promotes the translation of research advances into daily care and fights for the recognition of the needs of people with musculoskeletal diseases by the governing bodies in Europe.
- Diseases of bones and joints, such as rheumatoid arthritis and osteoarthritis cause disability in 4 - 5 % of the adult population and are predicted to rise as people live longer.
- As new treatments emerge and cellular mechanisms are discovered, the 7th Annual European Congress of Rheumatology in Amsterdam (EULAR 2006) brings together more than 10,000 experts - scientists, clinicians, healthcare workers, pharmaceutical companies and patients - to share their knowledge in a global endeavour to challenge the pain and disability caused by musculo-skeletal disorders.
- To find out more information about the activities of EULAR, visit: www.eular.org.
Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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