OBJECTIVE: To compare the diabetogenic effects of deflazacort (D) versus prednisone (PN) using a dosage ratio of 1.5 mg deflazacort:1 mg prednisone. METHODS:Thirty-three patients suffering from various active connective tissue or chronic inflammatory diseases were randomized to be treated with D or PN, assuming a therapeutic equipotency ratio of 1.5 mg D:1 mg PN. Neither dosage nor glucocorticoid employed were modified during the study. Patients had not received steroid treatment during the month prior to their inclusion date. Fasting glucose, glycosylated haemoglobin and fructosamine were determined before and after 1 month of treatment. Non-diabetic patients were also submitted to an oral glucose tolerance test (OGTT) at entry and after 1 month. Results were compared by univariate, and multivariate tests to correct the effects of age, body mass index and diagnosis. RESULTS: After 1 month of treatment there were no differences between D and PN in fasting glucose, glycosylated haemoglobin, or fructosamine. OGTT performed after treatment showed similar glucose values for both treatment groups. Patients treated with D had insulin levels at min 60 of the post-treatment OGTT which were higher than those treated with PN [114.1 (62.8) mcUI x ml(-1) versus 73.5 (32.7) mcUI x ml(-1), P = 0.049], but the difference lost its statistical significance in the multivariate analysis. CONCLUSION: D and PN have similar effects on glucose tolerance when an equipotency ratio of 1.5 mg D:1 mg PN is employed. Previous studies employing a ratio of 1.2:1 mg may have underestimated the adverse effects of D on glucose metabolism.
RCT Entities:
OBJECTIVE: To compare the diabetogenic effects of deflazacort (D) versus prednisone (PN) using a dosage ratio of 1.5 mg deflazacort:1 mg prednisone. METHODS: Thirty-three patients suffering from various active connective tissue or chronic inflammatory diseases were randomized to be treated with D or PN, assuming a therapeutic equipotency ratio of 1.5 mg D:1 mg PN. Neither dosage nor glucocorticoid employed were modified during the study. Patients had not received steroid treatment during the month prior to their inclusion date. Fasting glucose, glycosylated haemoglobin and fructosamine were determined before and after 1 month of treatment. Non-diabeticpatients were also submitted to an oral glucose tolerance test (OGTT) at entry and after 1 month. Results were compared by univariate, and multivariate tests to correct the effects of age, body mass index and diagnosis. RESULTS: After 1 month of treatment there were no differences between D and PN in fasting glucose, glycosylated haemoglobin, or fructosamine. OGTT performed after treatment showed similar glucose values for both treatment groups. Patients treated with D had insulin levels at min 60 of the post-treatment OGTT which were higher than those treated with PN [114.1 (62.8) mcUI x ml(-1) versus 73.5 (32.7) mcUI x ml(-1), P = 0.049], but the difference lost its statistical significance in the multivariate analysis. CONCLUSION:D and PN have similar effects on glucose tolerance when an equipotency ratio of 1.5 mg D:1 mg PN is employed. Previous studies employing a ratio of 1.2:1 mg may have underestimated the adverse effects of D on glucose metabolism.