Subclinical Inflammation and Diabetic Polyneuropathy: MONICA/KORA Survey F3 (Augsburg/Germany)

  1. Christian Herder, PHD (christian.herder{at}ddz.uni-duesseldorf.de)1,
  2. Mark Lankisch, MD2,
  3. Dan Ziegler, MD FRCPE1,3,
  4. Wolfgang Rathmann, MD MSPH4,
  5. Wolfgang Koenig, MD5,
  6. Thomas Illig, PHD6,
  7. Angela Döring, MD6,
  8. Barbara Thorand, PHD MPH6,
  9. Rolf Holle, PHD7,
  10. Guido Giani, PHD4,
  11. Stephan Martin, MD1,3 and
  12. Christa Meisinger, MD, MPH6
  1. 1Institute for Clinical Diabetology, German Diabetes Center at Heinrich Heine University, Leibniz Institute for Diabetes Research, Düsseldorf, Germany
  2. 2Department of Medicine 3, Helios Clinic Wuppertal, Wuppertal, Germany
  3. 3Centre for Internal Medicine, Heinrich Heine University Düsseldorf, Düsseldorf, Germany
  4. 4Institute of Epidemiology and Biometrics, German Diabetes Center at Heinrich Heine University, Leibniz Institute for Diabetes Research, Düsseldorf, Germany
  5. 5Department of Internal Medicine II-Cardiology, University of Ulm Medical Center, Ulm, Germany
  6. 6Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany
  7. 7Institute of Health Economics and Health Care Management, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany

    Abstract

    Objective – Subclinical inflammation represents a risk factor for type 2 diabetes and several diabetic complications, but data on diabetic neuropathies are scarce. Therefore, we investigated whether circulating concentrations of acute-phase proteins, cytokines and chemokines differ between diabetes patients with and without diabetic polyneuropathy (DPN).

    Research design and methods – We measured ten markers of subclinical inflammation in 227 DPN patients with type 2 diabetes who participated in the population-based MONICA/KORA Survey F3 (2004/2005; Augsburg/Germany). DPN was diagnosed using the Michigan Neuropathy Screening Instrument (MNSI).

    Results – After adjustment for multiple confounders, high levels of C-reactive protein and interleukin-6 were most consistently associated with DPN, high MNSI score and specific neuropathic deficits, whereas some inverse associations were seen for IL-18.

    Conclusions – This study shows that subclinical inflammation is associated with DPN and neuropathic impairments. This association appears rather specific as only certain immune mediators and impairments are involved.

    Footnotes

      • Received November 7, 2008.
      • Accepted January 3, 2009.

    This Article

    1. Published online before print January 8, 2009, doi: 10.2337/dc08-2011
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