title: Association of subclinical inflammation with polyneuropathy in the older population: KORA F4 study.
abstract: OBJECTIVE
  Inflammatory processes have been implicated in the pathogenesis of diabetic distal sensorimotor polyneuropathy (DSPN), but their possible relationship has not been assessed at the population level.
  
  
  METHODS
  We determined serum concentrations of mediators of subclinical inflammation among 1,047 participants 61-82 years of age from the population-based Cooperative Health Research in the Region of Augsburg (KORA) F4 study (Germany). Logistic and linear regression models were fitted to assess associations between immune mediators (log-transformed) and the presence of clinical DSPN (dichotomous variable) or Michigan Neuropathy Screening Instrument (MNSI) examination score (continuous variable), respectively.
  
  
  RESULTS
  Serum concentrations of the anti-inflammatory interleukin (IL)-1 receptor antagonist (IL-1RA) were positively associated with the presence of DSPN and higher MNSI scores in age-adjusted and sex-adjusted analyses, whereas IL-6, IL-18, and soluble intercellular adhesion molecule-1 were positively associated with only MNSI scores. No associations were observed for adiponectin, C-reactive protein, or tumor necrosis factor-α. Associations for IL-1RA and IL-6 with the MNSI score remained statistically significant after additional adjustment for waist circumference, height, hypertension, cholesterol, smoking, alcohol intake, physical activity, history of myocardial infarction or stroke, presence of neurological conditions, and use of nonsteroidal anti-inflammatory drugs.
  
  
  CONCLUSIONS
  We conclude that DSPN is linked to proinflammatory and anti-inflammatory, possibly compensatory, processes in the older general population. Future studies should clarify the temporal sequence and causality of these associations.
authors.affiliation: Corresponding author: Christian Herder, christian.herder@ddz.uni-duesseldorf.de.
authors.forename: Christian
authors.initials: C
authors.lastname: Herder
authors.forename: Brenda W C
authors.initials: BW
authors.lastname: Bongaerts
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Rathmann
authors.forename: Margit
authors.initials: M
authors.lastname: Heier
authors.forename: Bernd
authors.initials: B
authors.lastname: Kowall
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Koenig
authors.forename: Barbara
authors.initials: B
authors.lastname: Thorand
authors.forename: Michael
authors.initials: M
authors.lastname: Roden
authors.forename: Christa
authors.initials: C
authors.lastname: Meisinger
authors.forename: Dan
authors.initials: D
authors.lastname: Ziegler
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D002097:C-Reactive Protein / Q000032:analysis; D003929:Diabetic Neuropathies / Q000097:blood / Q000188:drug therapy / Q000453:epidemiology*; D005260:Female; D005858:Germany / Q000453:epidemiology; D006801:Humans; D007249:Inflammation / Q000097:blood; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D053590:Interleukin 1 Receptor Antagonist Protein / Q000097:blood; D020382:Interleukin-18 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011115:Polyneuropathies / Q000097:blood / Q000188:drug therapy / Q000453:epidemiology*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D055105:Waist Circumference
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D018836:Inflammation Mediators; D053590:Interleukin 1 Receptor Antagonist Protein; D020382:Interleukin-18; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein