title: Serological evidence of infections and Type 2 diabetes: the MultiEthnic Study of Atherosclerosis.
abstract: OBJECTIVE
  Prospective studies have identified chronic inflammation as a risk factor for Type 2 diabetes. However, it is not known whether infection by specific pathogens or having a greater 'pathogen burden' is associated with diabetes. The aim of this study was to examine the cross-sectional relation of seropositivity to five pathogens (Chlamydia pneumoniae, cytomegalovirus, Helicobacter pylori, hepatitis A virus, herpes simplex virus) and prevalent diabetes.
  
  
  METHODS
  Baseline data from a random sample of MultiEthnic Study of Atherosclerosis (MESA) participants (n = 1000; age 45-84 years) were used. Diabetes was defined by American Diabetes Association 2003 criteria, and 'pathogen burden' by the number of pathogens (0-5) for which an individual was seropositive. Logistic regression was used to test differences in diabetes prevalence by seropositivity. Linear regression was used to explore associations between pathogen seropositivity and the inflammation markers C-reactive protein, interleukin-6 and fibrinogen.
  
  
  RESULTS
  Diabetes prevalence was 12.7%, whereas seropositivity for C. pnuemoniae was 76%, cytomegalovirus 77%, H. pylori 45%, hepatitis A 58% and herpes simplex virus 85%. Seventy-two percent were seropositive for three or more pathogens. In crude analyses, the prevalence of diabetes was higher among those with a pathogen burden of three or more, and with seropositivity to cytomegalovirus, H. pylori, hepatitis A and herpes simplex virus. After adjustment for demographic covariates (particularly race), all associations became non-significant. Pathogen seropositivity was also not related to inflammation marker levels.
  
  
  CONCLUSIONS
  Following demographic adjustments, no associations were observed between infection by several pathogens and diabetes status, suggesting no aetiological role for them in the occurrence of diabetes.
authors.affiliation: Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN, USA. lutsey@umn.edu
authors.forename: P L
authors.initials: PL
authors.lastname: Lutsey
authors.forename: J S
authors.initials: JS
authors.lastname: Pankow
authors.forename: A G
authors.initials: AG
authors.lastname: Bertoni
authors.forename: M
authors.initials: M
authors.lastname: Szklo
authors.forename: A R
authors.initials: AR
authors.lastname: Folsom
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000378:metabolism; D023521:Chlamydophila Infections / Q000453:epidemiology* / Q000276:immunology; D016993:Chlamydophila pneumoniae / Q000276:immunology; D003430:Cross-Sectional Studies; D003587:Cytomegalovirus / Q000276:immunology; D003586:Cytomegalovirus Infections / Q000453:epidemiology* / Q000276:immunology; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology* / Q000276:immunology; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D016481:Helicobacter Infections / Q000453:epidemiology* / Q000276:immunology; D016480:Helicobacter pylori / Q000276:immunology; D006506:Hepatitis A / Q000453:epidemiology* / Q000276:immunology; D017957:Hepatitis A Virus, Human / Q000276:immunology; D006561:Herpes Simplex / Q000453:epidemiology* / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D016036:Seroepidemiologic Studies; D018139:Simplexvirus / Q000276:immunology; D014481:United States / Q000453:epidemiology
chemical_list: D007074:Immunoglobulin G; D015850:Interleukin-6; D005340:Fibrinogen; D002097:C-Reactive Protein