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BMJ Open Diabetes Res Care. 2017 Oct 10;5(1):e000438. doi: 10.1136/bmjdrc-2017-000438. eCollection 2017.

Statin use and risk of developing diabetes: results from the Diabetes Prevention Program.

Author information

1
Department of Medicine and Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, USA.
2
Division of Endocrinology and Metabolism, Indiana University School of Medicine, Indianapolis, Indiana, USA.
3
Diabetes Research Institute, University of Miami School of Medicine, Miami, Florida, USA.
4
UCLA Research Center at Alhambra, UC Los Angeles Alhambra, Alhambra, California, USA.
5
Medicine, St Luke's-Roosevelt Hospital, New York, NY, USA.
6
Diabetes and Endocrinology, MedStar Health Research Institute, Hyattsville, Maryland, USA.
7
Department of Family and Preventive Medicine, University of California, San Diego, California, USA.
8
Biostatistics Center and Department of Epidemiology and Biostatistics, Milken Institute School of Public Health, George Washington University, Rockville, Maryland, USA.

Abstract

OBJECTIVE:

Several clinical trials of cardiovascular disease prevention with statins have reported increased risk of type 2 diabetes (T2DM) with statin therapy. However, participants in these studies were at relatively low risk for diabetes. Further, diabetes was often based on self-report and was not the primary outcome. It is unknown whether statins similarly modify diabetes risk in higher risk populations.

RESEARCH DESIGN AND METHODS:

During the Diabetes Prevention Program Outcomes Study (n=3234), the long-term follow-up to a randomized clinical trial of interventions to prevent T2DM, incident diabetes was assessed by annual 75 g oral glucose tolerance testing and semiannual fasting glucose. Lipid profile was measured annually, with statin treatment determined by a participant's own physician outside of the protocol. Statin use was assessed at baseline and semiannual visits.

RESULTS:

At 10 years, the cumulative incidence of statin initiation prior to diabetes diagnosis was 33%-37% among the randomized treatment groups (p=0.36). Statin use was associated with greater diabetes risk irrespective of treatment group, with pooled HR (95% CI) for incident diabetes of 1.36 (1.17 to 1.58). This risk was not materially altered by adjustment for baseline diabetes risk factors and potential confounders related to indications for statin therapy.

CONCLUSIONS:

In this population at high risk for diabetes, we observed significantly higher rates of diabetes with statin therapy in all three treatment groups. Confounding by indication for statin use does not appear to explain this relationship. The effect of statins to increase diabetes risk appears to extend to populations at high risk for diabetes.

TRIAL REGISTRATION NUMBER:

NCT00038727; Results.

KEYWORDS:

Hmg Coa reductase inhibitors; lipids; pre-diabetes

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