Diabetes mellitus and insulin resistance in patients with rheumatoid arthritis: Risk reduction in a chronic inflammatory disease

Authors

  • Mary Chester Wasko,

    Corresponding author
    1. University of Pittsburgh, Pittsburgh, Pennsylvania
    • University of Pittsburgh School of Nursing, Room 453B, 440 Victoria Street, Pittsburgh, PA 15261
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    • Dr. Wasko has received consultancy fees (less than $10,000 each) from UCB and Centocor.

  • Jonathan Kay,

    1. UMass Memorial Medical Center and University of Massachusetts Medical School, Worcester
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    • Dr. Kay has received consultancy fees (less than $10,000 each) from Array Biopharma, Bristol-Myers Squibb, Celgene, Centocor, Eisai, Genentech, Roche, Sanofi-Aventis, UCB, and Wyeth.

  • Elizabeth C. Hsia,

    1. Centocor Research and Development, Malvern, Pennsylvania and University of Pennsylvania, Philadelphia
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    • Drs. Hsia and Rahman own stock and/or hold stock options in Johnson & Johnson.

  • Mahboob U. Rahman

    1. Centocor Research and Development, Malvern, Pennsylvania and University of Pennsylvania, Philadelphia
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    • Drs. Hsia and Rahman own stock and/or hold stock options in Johnson & Johnson.


Abstract

Objective

To perform a systematic literature review of the potential association among molecular markers of inflammation, alterations in body composition, and insulin resistance (IR), a precursor to type 2 diabetes mellitus (DM), in rheumatoid arthritis (RA) patients. To determine the impact of tumor necrosis factor α (TNFα) as a pivotal proinflammatory cytokine in the pathophysiology of type 2 DM and RA, and the effect of antirheumatic drugs on glycemic control.

Methods

We performed a search of PubMed to identify articles on IR and body habitus in patients with RA.

Results

Patients with RA had characteristics placing them at high risk for IR and type 2 DM. The incidence and prevalence of type 2 DM in RA was not clearly increased compared with the general population; however, studies suggested that patients with RA are likely to have IR and have increased risk of cardiovascular disease (CVD). The prevalence of type 2 DM and IR could be estimated from reports of risk factors for CVD in RA patients. The TNFα antagonists provided rapid and effective control of RA-related inflammation. Evidence indicated that extended use of TNFα antagonists in RA may provide the additional benefit of improving insulin sensitivity. These treatment-related changes may contribute to an overall reduction in the risk of type 2 DM and CVD in RA patients.

Conclusion

Controlling inflammation may improve insulin sensitivity and subsequently reduce the risk of developing type 2 DM in RA patients. This may also reduce the risk of CVD in this high-risk group. Future studies are required to elucidate the relationships between inflammation, body composition, IR, TNFα antagonist use, and the risk of developing type 2 DM in RA patients.

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