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Crystal arthropathies
Gout risk in adults with pre-diabetes initiating metformin
  1. Javier Marrugo1,2,3,
  2. Leah M Santacroce1,
  3. Misti L Paudel1,3,
  4. Sho Fukui1,3,
  5. Alexander Turchin3,4,
  6. Sara K Tedeschi1,3,
  7. Daniel H Solomon3,5
  1. 1 Department of Medicine, Division of Rheumatology Immunology and Allergy Research, Brigham and Women's Hospital, Boston, Massachusetts, USA
  2. 2 Department of Medicine, Division of Rheumatology, University of Sherbrooke and Centre Intégré Universitaire de Santé et de Services Sociaux de l’Estrie-CIUSSSE-CHUS, Sherbrooke, QC, Canada
  3. 3 Harvard Medical School, Boston, Massachusetts, USA
  4. 4 Department of Medicine, Division of Endocrinology, Brigham and Women's Hospital, Boston, Massachusetts, USA
  5. 5 Department of Medicine, Division of Pharmacoepidemiology, Division of Rheumatology Immunology and Allergy Research, Brigham and Women's Hospital, Boston, Massachusetts, USA
  1. Correspondence to Dr Javier Marrugo; javiermarrugo{at}hms.harvard.edu; Professor Daniel H Solomon; dsolomon{at}bwh.harvard.edu

Abstract

Objective Despite the strong association between gout and pre-diabetes, the role of metformin in gout among individuals with pre-diabetes remains uncertain. We compared the incidence rates of gout in adults with pre-diabetes starting metformin with those not using antidiabetic treatments.

Methods We conducted a new-user, propensity score-matched cohort study using electronic health records from an academic health system (2007–2022). Pre-diabetes was defined based on haemoglobin A1c levels. Metformin users were identified and followed from the first metformin prescription date. Non-users of antidiabetic medications were matched to metformin users based on propensity score and the start of follow-up. The primary outcome was incident gout. Cox proportional hazards models estimated the HR for metformin. Linear regression analyses assessed the association between metformin use and changes in serum urate (SU) or C-reactive protein (CRP).

Results We identified 25 064 individuals with pre-diabetes and propensity score-matched 1154 metformin initiators to 13 877 non-users. Baseline characteristics were well balanced (all standardised mean differences <0.1). The median follow-up was 3.9 years. The incidence rate of gout per 1000 person-years was lower in metformin users 7.1 (95% CI 5.1 to 10) compared with non-users 9.5 (95% CI 8.8 to 10.2). Metformin initiation was associated with a reduced relative risk of gout (HR 0.68, 95% CI 0.48 to 0.96). No relationship was found between metformin and changes in SU or CRP.

Conclusions Metformin use was associated with a reduced risk of gout among adults with pre-diabetes, suggesting that metformin may be important in lowering gout risk in individuals with pre-diabetes.

  • Gout
  • Incidence
  • Crystal arthropathies

Data availability statement

No data are available. Data is not publicly available due to regulations in our institution.

https://doi.org/10.1136/ard-2024-225652

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    Data availability statement

    No data are available. Data is not publicly available due to regulations in our institution.

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    Footnotes

    • Handling editor Josef S Smolen

    • Contributors JM and DHS contributed to the original conception and design of this study. JM conducted the data analyses with supervision from DHS, MLP and SKT, which AT, LMS and SF reviewed. JM, DHS, SKT, SF, MLP, AT and LMS interpreted the data. JM prepared the original draft of the manuscript, which was critically reviewed by all other authors. All authors approved the final version after being involved in drafting and revising the article for important intellectual content. The corresponding authors (JM and DHS) attest that all listed authors meet authorship criteria and that no others meeting the criteria have been omitted. JM and DHS serve as the guarantors of this manuscript.

    • Funding This work was supported by the National Institutes of Health (NIH-NIAMS P30AR072577). Source of funding had no role in the study design or execution, data interpretation or writing of the manuscript.

    • Competing interests Disclosure of interests: DHS receives salary support from unrelated research contracts to Brigham and Women’s Hospital from CorEvitas, Janssen and Novartis. AT receives salary support from unrelated research contracts to Brigham and Women’s Hospital from Eli Lilly. AT serves as a consultant in areas unrelated to this research to Novo Nordisk and Proteomics International. SKT reports consulting fees from Novartis. JM: None declared. SF: None declared. MLP: None declared. LMS: None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.