B-Cell monoclonality in Helicobacter pylori-associated chronic atrophic gastritis

Citation
T. Hiyama et al., B-Cell monoclonality in Helicobacter pylori-associated chronic atrophic gastritis, VIRCHOWS AR, 438(3), 2001, pp. 232-237
Citations number
30
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
VIRCHOWS ARCHIV-AN INTERNATIONAL JOURNAL OF PATHOLOGY
ISSN journal
09456317 → ACNP
Volume
438
Issue
3
Year of publication
2001
Pages
232 - 237
Database
ISI
SICI code
0945-6317(200103)438:3<232:BMIHPC>2.0.ZU;2-9
Abstract
B-cell monoclonality has been reported not only in gastric lymphoma, but al so in 1.3-21% of Helicobacter pylori-associated chronic gastritis (Hp-CG) c ases. The aim of this study was to determine the significance of B-cell mon oclonality in Hp-CG. We examined 134 gastric biopsy specimens from 99 patie nts with Hp-CG. The density of Hp, polymorphonuclear neutrophil activity, c hronic inflammation, glandular atrophy, and intestinal metaplasia (IM) were scored according to the updated Sydney System. B-cell monoclonality was an alyzed for immunoglobulin heavy chain gene rearrangement using polymerase c hain reaction amplification. B-cell monoclonality was detected in 6% of inf ormative samples. B-cell monoclonality was found in 18% of the samples from Hp-CG patients with marked glandular atrophy but in none of the samples fr om Hp-CG patients with none to moderate glandular atrophy. Monoclonality wa s also detected in 20% of the samples from Hp-CG patients with marked TM, i n 11% of the samples from Hp-CG patients with moderate IM, and in none of t he samples from Hp-CG patients without IM. Therefore, B-cell monoclonality was significantly more frequent in Hp-CG patients with marked glandular atr ophy than in Hp-CG patients with none to moderate atrophy. It was also more significantly frequent in Hp-CG patients with moderate or marked IM than i n Hp-CG patients without IM (P<0.05). Of 35 Hp-CG patients, 26 (74%) had id entical B-cell populations in the antrum and the corpus, and all were polyc lonal. The remaining nine (26%) Hp-CG patients had B-cell populations that differed in the antrum and the corpus. Four of the nine (44%) showed monocl onal B-cell populations in at least one gastric biopsy specimen. There were no patients with monoclonal B-cell populations in both the antrum and the corpus. These data suggest that glandular atrophy and IM in gastric biopsy specimens may be markers for gastric mucosa-associated lymphoid tissue (MAL T) lymphomagenesis and that multiple gastric biopsy specimens from both the antrum and the corpus may be needed to assess the risk of gastric MALT lym phoma.