EDITORIAL
Low dose methotrexate
Going with the flow: methotrexate, adenosine, and blood flow
Correspondence to:
Correspondence to:
Professor B N Cronstein
Department of Medicine, Pathology, and Pharmacology, NYU School of Medicine, 550 First Ave, New York, NY 10016, USA; Cronsb01@med.nyu.edu
Accepted 7 January 2006
Methotrexate treatment modulates adenosine metabolism in patients with rheumatoid arthritis
Keywords: adenosine; adenosine receptors; caffeine; methotrexate; blood flow
| The first 150 words of the full text of this article appear below. |
Since its reintroduction for the treatment of rheumatoid arthritis (RA) in the 1980s,1,2 low dose methotrexate has become the favoured second line treatment for patients with RA and other forms of inflammatory arthritis. It is safe and effective; indeed, it is nearly as effective as the biological agents that seem to have transformed the treatment of RA, and the effects of biological agents combined with methotrexate are clearly better than either alone.3–7 Low dose methotrexate was introduced into the therapeutic armamentarium for RA on the basis of its ability to inhibit cellular proliferation, although the doses required for the antiproliferative effect in patients with cancer are considerably higher than those commonly used to treat RA (1–5 g in a bolus for cancer v 10–25 mg/week for RA). Thus, the mechanism by which methotrexate suppresses inflammation has been an area of some interest.
Several mechanisms of action have
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(2009). Methotrexate, rheumatoid arthritis and infection risk--what is the evidence?. Rheumatology (Oxford)
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