title: Autoimmune gastritis in autoimmune thyroid disease.
abstract: BACKGROUND
  Autoimmune gastritis leads to oxyntic gastric atrophy, a condition at increased risk for gastric cancer. Autoimmune gastritis in conjunction with autoimmune thyroid disease has been reported previously.
  
  
  OBJECTIVE
  In a case-control study in patients with autoimmune thyroid disease to evaluate the usefulness of serum pepsinogens for the identification of oxyntic gastric atrophy, and to determine the relationship of Helicobacter pylori with oxyntic gastric atrophy.
  
  
  METHODS
  Patients with autoimmune thyroid disease (cases) and goitre (controls) were prospectively enrolled in the study. Pepsinogen (PG) I levels ≤25 μg/mL and PG I/II ratio ≤3 were indicative for oxyntic gastric atrophy. Antibodies against H. pylori, CagA and parietal cells were also determined. Esophagogastroduodenoscopy with biopsies was offered to patients with serological oxyntic gastric atrophy.
  
  
  RESULTS
  In total, 34 autoimmune thyroid disease patients and 30 controls were enrolled. Serological oxyntic gastric atrophy was present only in autoimmune thyroid disease patients (8/34, 23.5%, OR 8.3, 95% CI = 1.9-36.2). In all eight patients oxyntic gastric atrophy was confirmed by histology. OLGA stage I, II, III and IV was described in 0%, 33%, 50% and 17% of the cases, respectively. About, 89% and 11% of oxyntic gastric atrophy patients were seropositive for antibodies against parietal cells or H. pylori infection, respectively. Gastric atrophy involved the angulus/antrum in 50% of patients with autoimmune gastritis.
  
  
  CONCLUSIONS
  The seroprevalence of oxyntic gastric atrophy is high in patients with autoimmune thyroid disease, and testing of serum pepsinogens should be included in the clinical assessment of these patients. H. pylori infection is unlikely to be a principal factor in the pathogenesis of oxyntic gastric atrophy in patients with autoimmune thyroid disease. In autoimmune gastritis, gastric atrophy can spread from the oxyntic towards the antral mucosa.
authors: Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University, Magdeburg, Germany.
authors: M
authors: M
authors: Venerito
authors: M
authors: M
authors: Radünz
authors: K
authors: K
authors: Reschke
authors: D
authors: D
authors: Reinhold
authors: K
authors: K
authors: Frauenschläger
authors: D
authors: D
authors: Jechorek
authors: F
authors: F
authors: Di Mario
authors: P
authors: P
authors: Malfertheiner
mesh_terms: D000328:Adult; D000368:Aged; D001327:Autoimmune Diseases / Q000453:epidemiology* / Q000276:immunology; D015415:Biomarkers; D001706:Biopsy; D016022:Case-Control Studies; D005260:Female; D005757:Gastritis, Atrophic / Q000175:diagnosis / Q000453:epidemiology* / Q000276:immunology; D006042:Goiter / Q000453:epidemiology; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010295:Parietal Cells, Gastric / Q000276:immunology; D020116:Pepsinogen A / Q000097:blood; D020115:Pepsinogen C / Q000097:blood; D016036:Seroepidemiologic Studies; D013959:Thyroid Diseases / Q000453:epidemiology* / Q000276:immunology
chemical_list: D015415:Biomarkers; D020115:Pepsinogen C; D020116:Pepsinogen A