POS0137 CARDIOVASCULAR RISK ASSOCIATED WITH TREATMENT OF ALLOPURINOL AND BENZBROMARONE IN PATIENTS WITH GOUT

2021 
Background: Previous studies have shown that cardiovascular risk is increased in patients with gout. There are many studies on the effect of uric acid lowering therapy on CV risk in gout patients, but few studies have compared allopurinol and benzbromarone. Objectives: A nationwide population-based cohort study is designed to compare cardiovascular risk according to the treatment of allopurinol and benzbromarone in Korean gout patients. Methods: We used South Korea’s database of the Health Insurance Review and Assessment service (HIRA) to identify gout patients 18 years of age or older who newly started allopurinol or benzbromarone between 2009 and 2015. The start date of allopurinol or benzbromarone is defined as the index date. We excluded patients who have been prescribed uric acid lowering agents or have been on dialysis for one year prior to the index date. During the study period, patients who used uric acid lowering agents other than allopurinol and benzbromarone or who used both drugs in combination were also excluded from the study. The primary outcome of the study was the occurrence of a composite cardiovascular endpoint, which included coronary revascularization, hospitalization due to MI, ischemic stroke, and transient ischemic attack (TIA). Cox proportional hazard regression analysis and Kaplan-Meier curves were used for the analysis. Results: 257,097 allopurinol initiators and 7,868 benzbromarone initiators were included in the study. The mean age was 54.4 years, 86% were male. The mean adherence of drug administration was 68.2% for allopurinol initiators and 75.5% for benzbromarone initiators. In baseline, the benzbromarone initiator had more cardiovascular comorbidities and related drug administration than the allopurinol initiator. In allopurinol and benzbromarone initiators, the adjusted hazard ratio (aHR) of the composite CV endpoint was 1.01 (95% CI 0.83-1.21), which was not significantly different. No significant difference was found between the two groups in each of the items of the composite CV endpoint and hospitalization for heart failure. The results did not change even when 1:3 propensity score matching was performed for baseline characteristics. In subgroup analysis of high risk patients with cardiovascular disease, there was no significant difference between allopurinol and benzbromarone initiators. However, when the analysis was limited to the group taking allopurinol ≥200mg and benzbromarone ≥50mg, there was no difference in primary outcome and other outcomes, but the risk of coronary revascularization was higher in benzbromarone initiator (aHR 1.58, 95% CI 1.16-2.14). Conclusion: In our study, there was no significant difference in cardiovascular risk between allopurinol initiator and benzbromarone initiator. In the high risk group of cardiovascular disease, there was no difference in risk between the two drugs. Disclosure of Interests: None declared
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