Abstract
Glucocorticoids are highly effective in many inflammatory rheumatic diseases because of their ability to inhibit the disease process at the local and systemic level. Thereby, they are capable of relieving symptoms and inhibiting the progression of the disease and –in early rheumatoid arthritis– also of joint damage. After the trials
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in rheumatoid arthritis patients who received additional treatment of 7.5 to 10 milligram prednisone daily or placebo, further progression of radiological joint damage was not significantly different for the different treatment groups according to the author’s group meta-analysis on the individual patient level. Nevertheless, the gain acquired during the treatment with glucocorticoids was preserved even 3-4 years after stopping of these trials, supporting the strategy of early intensive treatment. These findings clearly corroborate that treatment with disease-modifying antirheumatic drugs (DMARDs) combined with glucocorticoids is more effective compared to treatment with DMARDs only in early rheumatoid arthritis. At the joint level, it remains hard to predict the clinical response to intra-articular injection of glucocorticoids. Numbers of glucocorticoid receptor positive cells and other steroid hormone receptor positive cells in synovial tissue of the inflamed joint decreased after glucocorticoid injection, but were not predictive of the clinical effect. However, down regulation of estrogen receptor αpositive cells and clinical outcome were associated, indicating an involvement of these receptors in the inflammatory process. Efficacy of glucocorticoids clearly outweighs toxicity if glucocorticoids are used in dosages up to 10 milligram prednisone daily in early rheumatoid arthritis. Few adverse effects are encountered in randomized controlled trials. Both the inflammatory process itself as glucocorticoid therapy are thought to induce negative changes in glucose metabolism and bone. However, during adequate prophylactic medication for osteoporosis in early rheumatoid arthritis patients on methotrexate and 10 mg prednisone daily, even a slight increase instead of decrease of bone mineral density was observed by the author during the first year of treatment. This can be explained by the inhibition of bone loss inducing disease activity by the medication including glucocorticoids, next to the positive effects of the prophylactic medication for osteoporosis. Moreover, author’s group findings were that low dose glucocorticoid therapy for multiple years did not impair glucose metabolism and did not negatively influence physical activity levels. Low dose glucocorticoid therapy thus does not increase cardiovascular risk via these pathways. The author’s group also developed guidelines for the use of glucocorticoids and concluded that optimal choices regarding the use of glucocorticoids in rheumatic diseases are patient specific. The underlying disease, the presence of comorbidity, the response to initial treatment, the dosages used and the development of adverse effects should guide treatment decisions. Monitoring for adverse effect should also be patient tailored: specific aspects of individual patients may warrant a higher frequency of monitoring or a more comprehensive set of adverse effects to monitor. Continuously balancing the benefits and risks of glucocorticoid therapy is recommended. In all, based on these studies, one could conclude that the benefit of especially low dose glucocorticoids, if used adequately to treat an inflammatory rheumatic condition, clearly outweighs the risk
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