Overview
- Editors:
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Nicolas Bazan
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LSU Neuroscience Center, Louisiana State University Medical Center, School of Medicine, New Orleans, USA
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Jack Botting
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The William Harvey Research Institute, St Bartholomew’s Hospital Medical College, Charterhouse Square, London, UK
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John Vane
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The William Harvey Research Institute, St Bartholomew’s Hospital Medical College, Charterhouse Square, London, UK
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Table of contents (16 papers)
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- J. R. Vane, R. M. Botting
Pages 1-12
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- M. Pairet, L. Churchill, G. Engelhardt
Pages 23-38
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- N. G. Bazan, V. M. Marcheselli, G. Allan, K. Van Meter, J. P. Moises
Pages 47-53
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- S. G. Morham, R. Langenbach
Pages 63-70
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- B. F. McAdam, G. A. Fitzgerald
Pages 117-123
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- R. N. Dubois, A. Radhika, J. Shao, M. Tsujii, H. Sheng, O. Kobyashi et al.
Pages 125-130
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- P. E. Lipsky, A. F. Kavanaugh, H. Schulze-Koops, L. S. Davis
Pages 139-144
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Back Matter
Pages 145-147
About this book
For the past 100 years the mainstay of therapy for rheumatoid arthritis (RA) has been aspirin or other drugs of the non-steroid anti-inflammatory group. In 1971 Vane pro posed that both the beneficial and toxic actions of these drugs was through inhibition of prostaglandin synthesis. The recent discovery that prostaglandins responsible for pain and other symptoms at inflammatory foci are synthesized by an inducible cyclooxygenase (COX-2) that is encoded by a gene distinct from that of the consti tutive enzyme (COX-I) provided a new target for therapy of RA. A drug that would selectively inhibit COX-2 would hopefully produce the symptomatic benefit provided by existing NSAIDs without the gastrointestinal and renal toxicity due to the inhibition of COX-I. Drugs selective for COX-2 are now available. Experimental studies have shown them to be effective with minimal toxicity, and in clinical trials gastric and renal toxicities are less. Highly selective COX-2 inhibitors, perhaps designed with knowledge of the crystal structures of COX-I and COX-2, are also available. Other experimental studies, including those in animals lacking effective genes for COX-lor COX-2 and in experimental carcinomas, suggest there is still much to be learned of the pathophysiological functions of these enzymes. The inflammatory response is a complex reaction involving many mediators that derive from white blood cells, endothelial cells and other tissues. Preliminary data have revealed that inhibitors of the cytokines and adhesion molecules that play a crucial role in the migration of white cells to inflammatory sites may be useful in RA.
Editors and Affiliations
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LSU Neuroscience Center, Louisiana State University Medical Center, School of Medicine, New Orleans, USA
Nicolas Bazan
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The William Harvey Research Institute, St Bartholomew’s Hospital Medical College, Charterhouse Square, London, UK
Jack Botting,
John Vane
About the editors
Jack Botting is Consultant at the William Harvey Research Institute, an independent charitable foundation within Queen Mary and Westfield College of the University of London, UK.
Sir John Vane is the Director General at the William Harvey Research Institute, an independent charitable foundation within Queen Mary and Westfield College of the University of London, UK.
Sir John Vane shared the Nobel Prize in Physiology or Medicine in 1982 for his discoveries of the mechanism of action of aspirin and of prostacyclin, as well as his work on other prostanoids.
