title: Small-intestinal histopathology and mortality risk in celiac disease.
abstract: BACKGROUND
  Studies of mortality in celiac disease have not taken small-intestinal pathology into account.
  
  
  OBJECTIVE
  To examine mortality in celiac disease according to small-intestinal histopathology.
  
  
  METHODS
  Retrospective cohort study. We collected data from duodenal/jejunal biopsies taken between July 1969 and February 2008 on celiac disease (Marsh stage 3: villous atrophy; n = 29,096 individuals) and inflammation (Marsh stage 1-2; n = 13,306) from all 28 pathology departments in Sweden. A third cohort consisted of individuals with latent celiac disease from 8 university hospitals (n = 3719). Latent celiac disease was defined as positive celiac disease serology in individuals with normal mucosa (Marsh stage 0). Through linkage with the Swedish Total Population Register, we estimated the risk of death through August 31, 2008, compared with age- and sex-matched controls from the general population.
  
  
  METHODS
  All-cause mortality.
  
  
  RESULTS
  There were 3049 deaths among patients with celiac disease, 2967 with inflammation, and 183 with latent celiac disease. We found an increased hazard ratio (HR) for death in celiac disease (HR, 1.39; 95% confidence interval [CI], 1.33-1.45; median follow-up, 8.8 years), inflammation (HR, 1.72; 95% CI, 1.64-1.79; median follow-up, 7.2 years), and latent celiac disease (HR, 1.35; 95% CI, 1.14-1.58; median follow-up, 6.7 years). The absolute mortality rate was 10.4 (95% CI, 10.0-10.8) per 1000 person-years in celiac disease, 25.9 (95% CI, 25.0-26.8) in inflammation, and 6.7 (95% CI, 5.7-7.6) in latent celiac disease. Excess mortality was 2.9 per 1000 person-years in celiac disease, 10.8 in inflammation, and 1.7 in latent celiac disease. This risk increase was also seen in children. Excluding the first year of follow-up, HRs decreased somewhat.
  
  
  CONCLUSIONS
  Risk of death among patients with celiac disease, inflammation, or latent celiac disease is modestly increased.
authors.affiliation: Department of Pediatrics, Orebro University Hospital, Orebro 70185, Sweden. jonasludvigsson@yahoo.com
authors.forename: Jonas F
authors.initials: JF
authors.lastname: Ludvigsson
authors.forename: Scott M
authors.initials: SM
authors.lastname: Montgomery
authors.forename: Anders
authors.initials: A
authors.lastname: Ekbom
authors.forename: Lena
authors.initials: L
authors.lastname: Brandt
authors.forename: Fredrik
authors.initials: F
authors.lastname: Granath
mesh_terms: D000293:Adolescent; D000328:Adult; D000906:Antibodies / Q000097:blood; D002423:Cause of Death; D002446:Celiac Disease / Q000175:diagnosis / Q000401:mortality* / Q000473:pathology*; D002648:Child; D002675:Child, Preschool; D005260:Female; D005903:Gliadin / Q000276:immunology; D006801:Humans; D007223:Infant; D007249:Inflammation; D007421:Intestine, Small / Q000473:pathology; D008297:Male; D008875:Middle Aged; D016016:Proportional Hazards Models; D012189:Retrospective Studies; D012306:Risk; D012698:Serologic Tests; D013548:Sweden; D011503:Transglutaminases / Q000276:immunology; D055815:Young Adult
chemical_list: D000906:Antibodies; D005903:Gliadin; D011503:Transglutaminases