title: A close relationship between Helicobacter pylori infection and gastric xanthoma.
abstract: BACKGROUND
  Although the pathogenesis of gastric xanthoma (GX) remains unclear, an association of GX with atrophic gastritis has been reported. Helicobacter pylori is closely related to atrophic gastritis. The aim of this study was to investigate the relationship among GX, H. pylori, and atrophic gastritis.
  
  
  METHODS
  Sixty-seven patients with GX were assessed for H. pylori infection by serum anti-H. pylori IgG antibody, in addition to the rapid urease test, culture, and histologic examination using biopsy specimens of the antrum and corpus. The findings were compared with 67 age- and sex-matched control subjects without GX. The distribution of atrophic gastritis was assessed endoscopically. The severity of atrophic gastritis was determined endoscopically and histologically. Serum pepsinogen (PG) levels were also measured. Immunohistochemical staining of GX samples for H. pylori antigen was performed. H. pylori clinical isolates from patients with GX and controls were assessed for cagA by means of polymerase chain reaction.
  
  
  RESULTS
  The prevalence of H. pylori was significantly higher in patients with GX than in controls (94% and 72%, respectively). A significantly more extensive atrophic gastritis was present in patients with GX, as determined endoscopically and histologically, than in controls. Serum PG-I levels and the PG-I/PG-II ratio were significantly lower in the GX group than in the control group. H. pylori antigens were frequently identified in the cytoplasm of xanthoma cells in H. pylori-positive specimens of GX (54 of 63 specimens, 86%), whereas no immunoreactivity for H. pylori antigens was detected in H. pylori-negative specimens of GX. There was no significant difference in the positive rate of cagA between the two groups.
  
  
  CONCLUSIONS
  Our results identified a close relationship among H. pylori infection, GX, and atrophic gastritis. A proportion of GXs may be provoked by H. pylori infection.
authors.affiliation: Second Dept. of Internal Medicine, Nagasaki University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Isomoto
authors.forename: Y
authors.initials: Y
authors.lastname: Mizuta
authors.forename: K
authors.initials: K
authors.lastname: Inoue
authors.forename: T
authors.initials: T
authors.lastname: Matsuo
authors.forename: T
authors.initials: T
authors.lastname: Hayakawa
authors.forename: M
authors.initials: M
authors.lastname: Miyazaki
authors.forename: K
authors.initials: K
authors.lastname: Onita
authors.forename: F
authors.initials: F
authors.lastname: Takeshima
authors.forename: K
authors.initials: K
authors.lastname: Murase
authors.forename: I
authors.initials: I
authors.lastname: Shimokawa
authors.forename: S
authors.initials: S
authors.lastname: Kohno
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology; D005757:Gastritis, Atrophic / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications* / Q000175:diagnosis / Q000473:pathology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008875:Middle Aged; D013272:Stomach Diseases / Q000382:microbiology* / Q000473:pathology; D014973:Xanthomatosis / Q000382:microbiology* / Q000473:pathology