Remission-inducing therapy in rheumatoid arthritis

Rheumatoid arthritis is characterized by immunologically mediated chronic inflammation of synovial structures. Remission-inducing drugs, such as gold compounds, antimalarials, and D-penicillamine, have been shown to suppress disease activity in rheumatoid arthritis while having minimal nonspecific anti-inflammatory properties. The possibility that these agents are effective because they modulate the underlying immunologic reactivity prompted an examination of the immunosuppressive properties of these drugs. The evidence indicates that immunosuppression is an action that is shared by these agents and thus supports the view that remission induction may result from suppression of the immunologic activity that underlies rheumatoid inflammation. Despite the fact that these agents can function as immunosuppressives, each appears to have a unique site of action, specifically inhibiting the function of only one of the populations of cells likely to be involved in chronic immunologically mediated inflammation. Gold compounds and anti-malarials appear to be active by virtue of their capacity to depress various functions of mononuclear phagocytes, while D-penicillamine acts by inhibiting a number of the activities of T lymphocytes. These results imply that the means by which these drugs suppress rheumatoid inflammation are fundamentally different. This suggests the conclusion that the remission-inducing drugs may be classified as T cell-active and mononuclear phagocyte-active agents. A better understanding of the pathophysiology of rheumatoid arthritis should thus be helpful in deciding which of these classes of drugs is appropriate in individual cases.