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Journal of Clinical Pathology 2001;54:774-777
Copyright © 2001 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.
J Clin Pathol 2001; 54:774-777
© 2001 Journal of Clinical Pathology

Helicobacter heilmannii gastritis: a histological and immunohistochemical trait

E Ierardi, R A Monno, A Gentile, R Francavilla, O Burattini, S Marangi, L Pollice and A Francavilla

Department of Emergency and Organ Transplantation, Section of Gastroenterology, University of Bari, 70124 Bari, Italy
Department of Internal Medicine and Public Health, Section of Hygiene, University of Bari
Department of Human Pathology, University of Bari
Department of Paediatrics, University of Bari

Correspondence to:
Professor Francavilla Cattedra di Gastroenterologia, Università di Bari, Policlinico V.le Ennio, 70124 Bari, Italy afrancavilla{at}gastro.uniba.it

Aim—Biopsies of the gastric antrum were reviewed over a period of 10 years to determine the prevalence of Helicobacter heilmannii in symptomatic subjects from this geographical area and to relate its presence to distinctive histopathological and immunohistochemical features.

Methods—Biopsies from 7926 symptomatic patients were reviewed. Ten serial sections were stained with haematoxylin and eosin for conventional histology. Another 10 sections were stained with the Gram method for spiral bacteria. When H heilmannii was suspected, 10 additional serial sections were stained with methylene blue to obtain homogeneous colouring. An equal number of sections from patients affected by isolated H heilmannii or H pylori gastritis were analysed by immunohistochemistry to evaluate lymphoid aggregate/mucosal lymphocyte clonality (CD20 and CD3) and tumour necrosis factor alpha (TNF-{alpha}) in stromal cells.

Results—The prevalence of H heilmannii was 0.1% (eight of 7926), whereas H pylori was present in 60.7% of patients (4813 of 7926). In two of the eight H heilmannii positive patients both helicobacters were found. In all subjects infected by H heilmannii only, distinctive histology (lymphocyte exudation into gastric foveolae) was seen. Lymphoid aggregates, chronic mucosal inflammation with patchy activity, and the absence of epithelial mucus depletion were regular features of H heilmannii gastritis. Immunohistochemistry did not reveal different lymphocyte clonal patterns between H pylori and H heilmannii gastritis: CD20 positive cells were predominant in the centre of aggregates and mucosal infiltrates, whereas CD3 positive cells were prevalent at the periphery of follicles. Only H pylori gastritis showed a significant increase in TNF-{alpha} positive stromal cells.

Conclusion—These data suggest that an unusual lymphocyte reaction, with the tendency to invade the foveolar lumen, is a distinctive histopathological aspect of H heilmannii chronic gastritis, although further studies in a larger series are necessary to confirm this fact. Nevertheless, lymphocyte clones do not differ qualitatively from those found in H pylori infection. Moreover, compared with H heilmannii, H pylori provokes a more intense release of TNF-{alpha}, suggesting that different inflammatory responses exist to these two organisms.

Key Words: Helicobacter heilmanniiHelicobacter pylori • tumour necrosis factor {alpha}


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