Gout is one of the inflammatory disorder and reported to be very common in type 2 diabetic patients. Previous studies suggested that fenofibrate lowers uric acid and reduces gout attacks. But none of the studies evaluated the efficacy of fenofibrate in diabetic patients. Therefore, the results of the present study showed that fenofibrate significantly reduced the uric acid concentrations in patients with type 2 diabetes. 

Gout is considered one of the painful conditions which prevalent among cases with type 2 diabetes. Some of the small, short-term studies explain the role of Fenofibrate in lowering uric acid and gout attacks. However, whether Fenofibrate provides continued cutbacks in uric acid and gout attacks is unexplored. 

The type 2 diabetic patients of 50–75 years old were randomised to either one 200 mg co-micronised Fenofibrate per day or identical placebo for a median of 5 years follow-up.  A post-hoc analysis of reported on-study gout attacks and plasma uric acid concentrations as per the medication administration. Change in uric acid concentrations and risk of on-study gout attacks were taken as the analysis endpoints. 

Field study involved a total of 9795 participants who were randomly assigned to Fenofibrate or placebo from Feb 23, 1998, to Nov 3, 2000. At the 6-week active Fenofibrate run-in period, uric acid concentrations fell by 20·2% immediately pre-randomisation and persisted at 20·1% lower among subjects receiving Fenofibrate as compared to patients taking placebo in a random subset re-measured at one year. Over five years, there were 151 first gout events with placebo allocation and 81 with Fenofibrate allocation. The cumulative proportion of subjects with first gout event was 7.7% and 13.9% in the placebo group as compared to 3.4% and 5.7% in the fenofibrate group among individuals with baseline uric acid concentration higher than 0·36 and 0.42 mmol/L, respectively. Females and males and those with elevated uric acid concentrations, dyslipidaemia, or on diuretics showed similar risk reductions. No heterogeneity was noticed of the treatment effect of Fenofibrate on gout risk among the subjects with raised baseline uric acid concentrations despite receiving Allopurinol at study entry. By considering all gout events, Fenofibrate medication reduced the risk than with placebo. 

Fenofibrate reduced uric acid concentrations by 20%, and nearly halved first on-study gout events over five years of medication. Fenofibrate might be used as an adjunct for controlling gout in diabetes.