title: Seroprevalence of Helicobacter pylori infection in inflammatory bowel disease: is Helicobacter pylori infection a protective factor?
abstract: BACKGROUND
  The mechanisms for the observed low prevalence of Helicobacter pylori infection in inflammatory bowel disease (IBD) are unknown, but might be important for the pathogenesis of IBD. We have studied the seroprevalence of H. pylori in different categories of IBD and evaluated the role of medical therapy, smoking and social status. We also analysed the effect of seropositivity on the age of onset of IBD in order to find possible evidence for the protective effect of the infection.
  
  
  METHODS
  We studied 296 (mean age 43 years, range 18-79; women 144) unselected patients with IBD, including 185 with ulcerative colitis (UC). 94 with Crohn disease (CD), and 17 with indeterminate colitis (IC). Seventy healthy age- and sex-matched subjects served as controls. Serum samples were studied for H. pylori antibodies. Detailed clinical history was obtained from patient records and by face-to-face interview.
  
  
  RESULTS
  The prevalence of H. pylori infection was lower in IBD patients (24%) than in controls (37%; P = 0.029), and in CD lower (13%) than in UC (30%; P = 0.002). Seropositivity was not related to sulphasalazine treatment or smoking. Age of onset of IBD was higher in seropositive (mean 40 years) than in seronegative patients (30 years: P < 0.001). The age of onset of IBD showed unimodal distribution in H. pylori seronegative patients, with a peak between 30 and 40 years, although there was some evidence of bimodality in CD. In contrast, H. pylori seropositive patients had clear bimodal pattern with peaks at 20-40 and 50-60 years of age.
  
  
  CONCLUSIONS
  Our results confirm the low prevalence of H. pylori infection in IBD, and in particular in CD. The significantly higher age of onset and bimodal pattern of age-specific incidence in seropositive IBD patients suggest that H. pylori infection significantly modifies the development of IBD and may have a protective effect.
authors.affiliation: Dept. of Pathology, University of Oulu, Finland.
authors.forename: P O
authors.initials: PO
authors.lastname: Väre
authors.forename: B
authors.initials: B
authors.lastname: Heikius
authors.forename: J A
authors.initials: JA
authors.lastname: Silvennoinen
authors.forename: R
authors.initials: R
authors.lastname: Karttunen
authors.forename: S E
authors.initials: SE
authors.lastname: Niemelä
authors.forename: J K
authors.initials: JK
authors.lastname: Lehtola
authors.forename: T J
authors.initials: TJ
authors.lastname: Karttunen
mesh_terms: D000328:Adult; D017668:Age of Onset; D016022:Case-Control Studies; D003092:Colitis / Q000453:epidemiology / Q000382:microbiology / Q000517:prevention & control; D003093:Colitis, Ulcerative / Q000453:epidemiology / Q000382:microbiology* / Q000517:prevention & control; D003424:Crohn Disease / Q000453:epidemiology / Q000382:microbiology* / Q000517:prevention & control; D005260:Female; D016481:Helicobacter Infections / Q000150:complications / Q000453:epidemiology*; D016480:Helicobacter pylori; D006801:Humans; D015994:Incidence; D008297:Male; D016036:Seroepidemiologic Studies; D012907:Smoking / Q000453:epidemiology; D012923:Social Class