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Therapy in Rheumatoid Arthritis1
*
Department of Rheumatology, Charing Cross Hospital, London, United Kingdom;
The Kennedy Institute of Rheumatology, London, United Kingdom;
Institute of Clinical Immunology and Rheumatology, Erlangen, Germany;
Department of Rheumatology, University Hospital, Leiden, The Netherlands;
¶
University Klinik fur Innere Medizin III, Vienna, Austria; and
||
Centocor, Malvern, PA 19335
Treatment with a chimeric mAb to TNF-
has been shown to suppress
inflammation and improve patient well-being in rheumatoid arthritis
(RA), but the mechanisms of action of such treatment have not been
fully explored. Here we show that in vivo administration of
anti-TNF- Ab, using a longitudinal analysis, results in the
rapid down-regulation of a spectrum of cytokines, cytokine inhibitors,
and acute-phase proteins. Marked diurnal variation in the serum levels
of some of these were detected. These results were consistent with the
concept of a cytokine-dependent cytokine cascade, and the degree of
clinical benefit noted after anti-TNF- therapy is probably due
to the reduction in many proinflammatory mediators apart from TNF-,
such as IL-6, which reached normal levels within 24 h. Serum
levels of cytokine inhibitors such as soluble p75 and p55 TNFR were
reduced as was IL-1 receptor antagonist. Reductions in acute-phase
proteins occurred after serum IL-6 fell and included serum amyloid A,
haptoglobin, and fibrinogen. The latter reduction could be of
importance, as it is a risk factor for atherosclerosis, which is
augmented in RA patients.
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