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Impact of diabetes against the future risk of developing gout
  1. García Rodríguez1,
  2. Lucia Cea Soriano1,
  3. Hyon K Choi2
  1. 1Spanish Centre for Pharmacoepidemiological Research (CEIFE), Madrid, Spain
  2. 2Section of Rheumatology and the Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA
  1. Correspondence to Dr Hyon K Choi, Section of Rheumatology and the Clinical Epidemiology Unit, Boston University School of Medicine, 650 Albany Street, Suite 200, Boston, Massachusetts 02118, USA; hchoius{at}bu.edu

Abstract

Objective Although hyperuricaemia and gout are associated with an increased future risk of diabetes, diabetes may reduce the future risk of gout through the uricosuric effect of glycosuria or the impaired inflammatory response. The present work evaluates the impact of diabetes on the future risk of developing gout.

Methods A case-control study nested in a UK general practice database (the health improvement network) was conducted by identifying all incident cases of gout (N=24 768) and randomly sampling 50 000 controls who were 20–89 years between 2000 and 2007. The independent effect of type 1 and type 2 diabetes on the development of incident gout was examined.

Results After adjusting for age, sex, body mass index, general practitioner visits, smoking, alcohol intake, ischaemic heart disease and presence of cardiovascular risk factors, the RR for incident gout among patients with diabetes, as compared with individuals with no diabetes was 0.67 (95% CI 0.63 to 0.71). The multivariate RRs with the duration of diabetes of 0–3, 4–9 and ≥10 years were 0.81 (95% CI 0.74 to 0.90), 0.67 (95% CI 0.61 to 0.73) and 0.52 (95% CI 0.46 to 0.58), respectively. The inverse association was stronger with type 1 diabetes than with type 2 diabetes (multivariate RR, 0.33 vs 0.69) and stronger among men than women (p value for interaction <0.001).

Conclusions Individuals with diabetes are at a lower future risk of gout independent of other risk factors. These data provide support for a substantial role of the pathophysiology associated with diabetes against the risk of developing gout.

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Footnotes

  • Competing interests HKC has received research funding from TAP Pharmaceuticals for other research projects. In addition, HKC has received honoraria from, and serves on advisory boards to, Takeda Pharmaceuticals and Savient.

  • Funding This work was supported in part by grants from the National Institute of Health (AR47785). Spanish Centre for Pharmacoepidemiological Research has received an unrestricted research grant from Novartis to work on other projects related to gout. The funding sources had no role in the design, conduct, or reporting of the study or in the decision to submit the manuscript for publication.

  • Ethics approval This study was conducted with the approval of the NHS South-East Multi-Centre Research Ethics Committee.

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

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