| Summary: | 碩士 === 臺北醫學大學 === 藥學系(碩博士班) === 102 === Background
Coronary artery disease (CAD), caused by narrowing or obstruction of coronary artery, has been recently reported to be associated with gout. However, studies on the preventive effect of urate-lowering agents on CAD are still limited. The present study, therefore, attempted to preliminarily observe the change in risk of CAD in gout patients prescribed with allopurinol and/or benzbromarone, and further to analyze the dose-response relationship of the both drugs.
Methods
This retrospective cohort study was conducted using the claims data provided by the National Health Insurance Research Database. Both inpatients and outpatients diagnosed with gout between 2001 and 2008 were enrolled in our study. Patients were excluded from this study if they had history of CAD, heart failure, chronic kidney disease, cancer, or gout; or took either allopurinol or benzbromarone prior to diagnosis of gout. Each disease required at least two separate outpatient diagnostic codes or one inpatient diagnostic code, be it defined in an inclusion criterion, an exclusion criterion, or as a covariate. Besides, prescription with a medication was regarded as exposure to the medication in our study, irrespective of the patients’ medication adherence. To ascertain the effects of allopurinol and benzbromarone on lowering the risks of CAD, we excluded those who were prescribed with allopurinol or benzbromarone after December 31, 2008, who were identified as having CAD before or within 180 days of administration of either allopurinol or benzbromarone, and who took either allopurinol or benzbromarone for fewer than 90 days within 180 days of starting either of the medications. A total of 8,227 gout patients remained and were regarded as the experimental groups. Each patient of the experimental groups was exclusively matched with a gout patient who had never been prescribed with either drug by age and gender in the ratio of 1:1. The matched non-allopurinol-or-benzbromarone- exposed patients were categorized as the comparison group (Group C). We further divided the experimental groups into allopurinol-treated (Group A, N = 1,437), benzbromarone-treated (Group B, N = 4,241), and both-treated groups (Group A+B, N = 2,549). The index date was defined as the date newly prescribed with either drug for the experimental groups or newly diagnosed with gout for Group C.
Results
Patients of the experimental groups, in general, had no statistically significant change in risk of CAD with the covariates adjusted in comparison with those who were not exposed to either drug (Group C). However, the risk of CAD was negatively correlated with the number of doses in Group A and Group A+B. Each experimental group, in fact, had a lower risk of CAD than Group C after receiving over 360 defined daily doses (DDDs), after which Group A presented the lowest risk of CAD.
Conclusion
Our findings indicated that a considerable number of doses of allopurinol and benzbromarone are required for CAD prophylaxis, and hence the two drugs might be recommended for gout patients only as an adjuvant medication against the onset of CAD.
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