In rheumatoid arthritis and many other chronic inflammatory diseases, many cellular and molecular processes contribute towards an immunological disequilibrium, in which normal homeostatic processes are unable to restore a healthy state and prevent the perpetuation of inflammatory processes. The success of TNF- blockade in therapy suggests that this molecule occupies such a critical position in the pathogenic process. However, blockade of TNF or any other key physiological molecules may have the downside of negating their beneficial role in generating protective immune responses. For TNF- antagonists, the key safety considerations include infection, both common and opportunistic, cytopenias, demyelinating disease, lupus-like syndromes, congestive heart failure and malignancies, particularly lymphomas.
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