OBJECTIVE: Prior research demonstrates that hydroxychloroquine (HCQ) lowers glycosylated hemoglobin (HbA(1c) ) in diabetes patients without rheumatic disease. We examined medical records of patients with diabetes mellitus (DM) and concomitant rheumatic illness to measure changes in HbA(1c) after starting HCQ or methotrexate (MTX). METHODS: We used electronic medical records to identify patients beginning treatment with either HCQ or MTX who had a diagnosis of DM (or a pretreatment HbA(1c) value of ≥7%) and at least 1 HbA(1c) measurement both before and within 12 months after initiation of treatment. Using a structured medical record abstraction, we examined rheumatic disease diagnosis, cumulative steroid use, duration (months) between drug initiation and lowest HbA(1c) value, a change in DM medication, body mass index (BMI), age, and sex. Adjusted linear regression models determined changes in HbA(1c) from pretreatment values to the lowest posttreatment values within 12 months. RESULTS: We identified 45 patients taking HCQ and 37 patients taking MTX who met the inclusion criteria. Rheumatoid arthritis had been diagnosed in approximately half of the patients in each group. Age, sex, and mean pretreatment HbA(1c) levels were similar across groups. The mean BMI of those taking HCQ (35.4 kg/m(2) ) was slightly higher than that of those taking MTX (32.2 kg/m(2) ) (P = 0.13). Glucocorticoid use appeared more common in those taking MTX (46%) than in those taking HCQ (29%) (P = 0.17). The mean reduction in HbA(1c) from pretreatment values to the lowest posttreatment values was 0.66% (95% confidence interval [95% CI] 0.26, 1.05) in those taking HCQ compared with 0.11% (95% CI -0.18, 0.40) in those taking MTX. In fully adjusted analyses, the reduction in HbA(1c) among those taking HCQ was 0.54% greater than the reduction among those taking MTX (P = 0.041). CONCLUSION: HCQ initiation was associated with a significantly greater reduction in HbA(1c) as compared with MTX initiation among diabetes patients with rheumatic disease.
OBJECTIVE: Prior research demonstrates that hydroxychloroquine (HCQ) lowers glycosylated hemoglobin (HbA(1c) ) in diabetespatients without rheumatic disease. We examined medical records of patients with diabetes mellitus (DM) and concomitant rheumatic illness to measure changes in HbA(1c) after starting HCQ or methotrexate (MTX). METHODS: We used electronic medical records to identify patients beginning treatment with either HCQ or MTX who had a diagnosis of DM (or a pretreatment HbA(1c) value of ≥7%) and at least 1 HbA(1c) measurement both before and within 12 months after initiation of treatment. Using a structured medical record abstraction, we examined rheumatic disease diagnosis, cumulative steroid use, duration (months) between drug initiation and lowest HbA(1c) value, a change in DM medication, body mass index (BMI), age, and sex. Adjusted linear regression models determined changes in HbA(1c) from pretreatment values to the lowest posttreatment values within 12 months. RESULTS: We identified 45 patients taking HCQ and 37 patients taking MTX who met the inclusion criteria. Rheumatoid arthritis had been diagnosed in approximately half of the patients in each group. Age, sex, and mean pretreatment HbA(1c) levels were similar across groups. The mean BMI of those taking HCQ (35.4 kg/m(2) ) was slightly higher than that of those taking MTX (32.2 kg/m(2) ) (P = 0.13). Glucocorticoid use appeared more common in those taking MTX (46%) than in those taking HCQ (29%) (P = 0.17). The mean reduction in HbA(1c) from pretreatment values to the lowest posttreatment values was 0.66% (95% confidence interval [95% CI] 0.26, 1.05) in those taking HCQ compared with 0.11% (95% CI -0.18, 0.40) in those taking MTX. In fully adjusted analyses, the reduction in HbA(1c) among those taking HCQ was 0.54% greater than the reduction among those taking MTX (P = 0.041). CONCLUSION:HCQ initiation was associated with a significantly greater reduction in HbA(1c) as compared with MTX initiation among diabetespatients with rheumatic disease.
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