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Eighty-three patients treated with cyclosporine were included in the analysis of efficacy.
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The pathophysiology behind this excessive activation, although apparent mainly in the monocytic lineage, involves the interactions of T cells and macrophages.
NSAIDs have evolved from blocking both COX-1 and COX-2 to selectively only blocking COX-2 in order to inhibit the inflammatory response and reduce the production of inflammatory prostaglandins and thromboxanes.
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By contrast, we should be in a position to define quite precisely what we expect of such therapy in terms of the metabolic outcome.
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