title: Helicobacter pylori associated antigastric autoantibodies: role in Sjögren's syndrome gastritis.
abstract: BACKGROUND
  Previous studies have shown that Helicobacter pylori seroprevalence in Sjögren's syndrome is comparable with that of the general population. However, the origin of the chronic gastropathy associated with this syndrome and the role of local autoimmunity--possibly triggered by bacterial infection--in its pathogenesis remain unclear.
  
  
  METHODS
  We initially determined the prevalence of IgG anti H. pylori in dyspeptic subjects with and without Sjögren's syndrome. In subsets of both groups we then determined anti CagA and human tissue-tested anticanalicular/antifoveolar autoantibodies. We also compared activity, atrophy and Mucosa Associated Lymphoid Tissue (MALT) scores, as well as symptoms, before and after bacterial eradication.
  
  
  RESULTS
  Prevalence of H. pylori in Sjögren's syndrome patients was similar to controls: 31/54 (57%) vs. 93/150 (62%). Anti CagA prevalence was also similar in the two groups. Twenty weeks after H. pylori eradication, histological activity decreased in both groups, however, atrophy and MALT decreased significantly only in controls. Sixteen months after H. pylori eradication, 75% of Sjögren's syndrome patients still complained of dyspepsia compared with 13% of controls. Finally, antigastric autoantibodies were present in 29% of tested Sjögren's syndrome patients vs. 28% of controls.
  
  
  CONCLUSIONS
  H. pylori infection was equally prevalent among dyspeptic Sjögren's syndrome patients and dyspeptic controls. Likewise, there were no differences regarding anti CagA prevalence or antigastric autoantibodies among the two groups. The persistence of symptoms as well as of the lymphocytic infiltration and atrophy after H. pylori eradication in Sjögren's syndrome may underlie the 'endogenous' and still unknown nature of the gastropathy in this condition.
authors.affiliation: Gastrointestinal Unit/Internal Medicine, School of Medicine, University of Udine, Italy.
authors.forename: Dario
authors.initials: D
authors.lastname: Sorrentino
authors.forename: Gerhard
authors.initials: G
authors.lastname: Faller
authors.forename: Salvatore
authors.initials: S
authors.lastname: DeVita
authors.forename: Claudio
authors.initials: C
authors.lastname: Avellini
authors.forename: Antonella
authors.initials: A
authors.lastname: Labombarda
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Ferraccioli
authors.forename: S
authors.initials: S
authors.lastname: Kahlow-Toussaint
mesh_terms: D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000276:immunology; D001323:Autoantibodies / Q000097:blood*; D001426:Bacterial Proteins / Q000276:immunology; D004415:Dyspepsia / Q000276:immunology / Q000382:microbiology; D016099:Endoscopy, Gastrointestinal; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology* / Q000382:microbiology / Q000473:pathology*; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology; D016480:Helicobacter pylori / Q000187:drug effects / Q000276:immunology* / Q000302:isolation & purification / Q000472:pathogenicity; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D008221:Lymphoid Tissue / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012859:Sjogren's Syndrome / Q000150:complications* / Q000276:immunology / Q000382:microbiology / Q000473:pathology
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001323:Autoantibodies; D001426:Bacterial Proteins; D007074:Immunoglobulin G; C080866:cagA protein, Helicobacter pylori