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Metformin prescribed to prediabetes patients reduces risk of developing gout
Last reviewed: 02.07.2025
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Metformin given to patients with prediabetes also reduced the risk of developing gout, a new study has found.
Among 1,154 people with elevated hemoglobin A1c (HbA1c) levels, just below the threshold for type 2 diabetes, who started taking metformin, gout was diagnosed at a rate of 7.1 per 1,000 person-years (95% CI 5.1-10.0) during a median follow-up of 4 years, according to data presented by Javier Marrugo, MD, of Brigham and Women's Hospital in Boston, and colleagues.
Gout developed at an incidence of 9.5 per 1,000 person-years (95% CI 8.8-10.2) among nearly 14,000 similar patients who did not start metformin, yielding a relative risk of 0.68 (95% CI 0.48-0.96) with metformin use, the researchers reported in the journal Annals of the Rheumatic Diseases.
Interestingly, however, metformin did not seem to have an effect on either serum uric acid or C-reactive protein (CRP) levels, complicating the interpretation of the results.
This is not the first study to find a link between antidiabetic drugs and a reduced risk of gout. Such a link has previously been noted for so-called gliflozin drugs, which increase the excretion of glucose in the urine, although in these cases uric acid levels were reduced.
Metformin, of course, is the most common first-line treatment for type 2 diabetes, and its relative safety has made it the drug of choice for people with prediabetes (defined in this study as HbA1c 5.7%-6.4%). Marrugo and colleagues noted that many studies of metformin have documented its anti-inflammatory effects. “Thus, in addition to its established role in reducing diabetes risk, metformin may also be associated with a lower risk of gout in individuals with prediabetes,” they explained.
In the current study, Marrugo’s team examined data from 50,588 patients treated at the Mass General Brigham Health System from 2007 to 2022 for prediabetes. Half were excluded because they were quickly diagnosed with type 2 diabetes or gout, or because they had less than a year of missing data. Of the roughly 25,000 remaining, the researchers identified 1,172 metformin users and 23,892 other patients treated differently. Eighteen metformin users and 10,015 nonusers could not be matched for propensity, leaving 1,154 and 13,877, respectively, for analysis.
About two-thirds of the participants were women, and the average age was 57 years. Just over 60% were white. The average body mass index was about 32; HbA1c averaged 6.0%. Participants not using metformin were not receiving other glucose-lowering medications. In both groups, 10% to 12% were taking aspirin, and about the same number were taking antihypertensive medications.
Kaplan-Meier analysis covering 5 years of follow-up showed a difference in gout incidence between groups starting after just a few months. After 5 years, 30 metformin users (2.6%) developed gout compared with 546 (3.9%) in the nonuser group (P=0.032 for trend). Most of those who developed gout were men.
Serum uric acid levels were slightly lower in the metformin group, but not to a significant level (P=0.73); levels decreased over time at a similar rate in both groups. The same was true for CRP. As expected, metformin was effective in reducing HbA1c levels, with a decrease of 0.14 percentage points after one year.
Marrugo and colleagues did not attempt to explain how metformin might reduce gout risk without explicitly lowering uric acid levels, but noted that the drug lowers HbA1c and appears to cause some weight loss; these effects have previously been linked to reduced systemic inflammation (although the current study did not find an effect on CRP). The researchers also noted that earlier studies showing the uric acid-lowering effects of gliflozin drugs were conducted in people with advanced diabetes, whereas the new study looked only at people with less pronounced increases in HbA1c.
Limitations of the study include the predominance of women in the sample, whereas gout predominantly affects men. The retrospective, observational design and lack of data on lifestyle factors also mean that unaccounted for confounders may have influenced the results.