OBJECTIVE: To investigate the efficacy of bromocriptine in suppressing active systemic lupus erythematosus (SLE) in a therapeutic trial. METHODS: We conducted an open label investigation of bromocriptine treatment in 7 patients with active non-life threatening SLE. Patients received bromocriptine daily during the treatment phase of 6 to 9 months and were followed for 5 months after bromocriptine was discontinued. Disease activity was assessed by determination of the SLE activity Measure (SLAM) and the Toronto SLE Disease Activity Index (SLEDAI). Serum prolactin concentrations and a battery of serologic and urine tests were obtained at baseline and at monthly intervals during and after bromocriptine treatment. RESULTS: Serum prolactin concentration was suppressed from (mean +/- SEM) 11.2 ng/ml +/- 1.9 to 3.1 ng/ml +/- 1.7 after 6 months of bromocriptine treatment. The mean pretreatment SLAM score was 11.3 +/- 0.9;6 months of bromocriptine treatment significantly decreased the mean SLAM score to 6.0 +/- 1.6 (p = 0.03 compared to pretreatment measure). The mean SLEDAI score decreased from 16.0 +/- 2.0 to 5.9 +/- 0.8 (p = 0.02) during the same period. Bromocriptine treatment was associated with transient suppression of anti-dsDNA, and serum cholesterol was reduced significantly through the treatment period. After bromocriptine was discontinued, all patients had increased disease activity associated with rising serum prolactin concentrations. CONCLUSION: These findings justify controlled trials to study the efficacy of bromocriptine in treating patients with active SLE.
OBJECTIVE: To investigate the efficacy of bromocriptine in suppressing active systemic lupus erythematosus (SLE) in a therapeutic trial. METHODS: We conducted an open label investigation of bromocriptine treatment in 7 patients with active non-life threatening SLE. Patients received bromocriptine daily during the treatment phase of 6 to 9 months and were followed for 5 months after bromocriptine was discontinued. Disease activity was assessed by determination of the SLE activity Measure (SLAM) and the Toronto SLE Disease Activity Index (SLEDAI). Serum prolactin concentrations and a battery of serologic and urine tests were obtained at baseline and at monthly intervals during and after bromocriptine treatment. RESULTS: Serum prolactin concentration was suppressed from (mean +/- SEM) 11.2 ng/ml +/- 1.9 to 3.1 ng/ml +/- 1.7 after 6 months of bromocriptine treatment. The mean pretreatment SLAM score was 11.3 +/- 0.9;6 months of bromocriptine treatment significantly decreased the mean SLAM score to 6.0 +/- 1.6 (p = 0.03 compared to pretreatment measure). The mean SLEDAI score decreased from 16.0 +/- 2.0 to 5.9 +/- 0.8 (p = 0.02) during the same period. Bromocriptine treatment was associated with transient suppression of anti-dsDNA, and serum cholesterol was reduced significantly through the treatment period. After bromocriptine was discontinued, all patients had increased disease activity associated with rising serum prolactin concentrations. CONCLUSION: These findings justify controlled trials to study the efficacy of bromocriptine in treating patients with active SLE.
Authors: F Magro; E Cunha; F Araujo; E Meireles; P Pereira; M Dinis-Ribeiro; F Tavarela Veloso; R Medeiros; P Soares-da-Silva Journal: Dig Dis Sci Date: 2006-09-15 Impact factor: 3.199