Objective To compare the efficacy and safety of benzbromarone vs. allopurinol for primary gout. Methods Searching PubMed, Cochrane Library, EMbase, CNKI, VIP and CBM, randomized controlled trials were collected and the quality of RCTs was evaluated using Cochrane systematic review. Meta-analysis was performed. Results 6 RCTs were included in this study,with a total of 350 patients. Meta-analysis showed that there was no statistical significance in total effective rate between two groups (Pgt;0.05). 4 RCTs were enrolled in comparison of ADR. There was statistical significance between two groups (Plt;0.05). Conclusion There is no significant difference in the efficacy between benzbromarone and allopurinol for the primary gout.But benzbromarone is safe than allopurinol for primary gout .
Objective To systematically review the effect of allopurinol on renal function in patients with chronic kidney disease (CKD). Methods The PubMed, EMbase, Cochrane Library, WanFang Data, CNKI, and VIP databases were searched for randomized controlled trials (RCTs) of the effect of allopurinol on renal function in patients with CKD. Databases for articles published between establishment of the database and April 28, 2021 were searched. Two evaluators independently screened the literature, extracted data and evaluated the risk of bias of the included studies. RevMan 5.4 was then used for meta-analysis. Results A total of 20 RCTs comprising 2 338 patients were included. The results of meta-analysis showed that compared with the control group, allopurinol substantially reduced the serum uric acid (MD=?2.48, 95%CI ?3.08 to ?1.89, P<0.01). In addition, the effect of allopurinol on slowing the decline in eGFR was influenced by the serum uric acid concentration. Participants taking allopurinol whose serum uric acid concentrations were maintained at >6 mg/dL showed a slower decline in eGFR (MD=5.03, 95%CI 1.76 to 8.31, P<0.01). However, there was no difference in the decline in eGFR between the two groups when the serum uric acid concentration of the participants was <6 mg/dL. Among participants with CKD and moderate renal dysfunction at baseline, those taking allopurinol showed a slower decline in eGFR than controls (MD=3.33, 95%CI 1.14 to 5.52, P<0.01). A further subgroup analysis showed that those who maintained their serum uric acid concentration above 6 mg/dL experienced a slower decline in eGFR (MD=5.46, 95%CI 2.06 to 8.86, P<0.01). However, when the serum uric acid concentration was <6 mg/dL, there was no difference between the allopurinol and control groups. Moreover, the serum creatinine concentration of the allopurinol group was lower than that of the control group after the intervention (MD=?0.39, 95%CI ?0.58 to ?0.19), P<0.01). However, there was no significant difference in the incidence of progression to end-stage kidney disease between the two groups (RR=0.96, 95%CI 0.65 to 1.42, P=0.85). Conclusion Allopurinol can substantially reduce serum uric acid and may protect the kidneys of patients with CKD when the serum uric acid concentration is maintained above 6 mg/dL.
