Differential features of gastric cancer patients, either Helicobacter pylori positive or Helicobacter pylori negative

Citation
D. Jonkers et al., Differential features of gastric cancer patients, either Helicobacter pylori positive or Helicobacter pylori negative, ITAL J GAST, 31(9), 1999, pp. 836-841
Citations number
51
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
ITALIAN JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
ISSN journal
11258055 → ACNP
Volume
31
Issue
9
Year of publication
1999
Pages
836 - 841
Database
ISI
SICI code
1125-8055(199912)31:9<836:DFOGCP>2.0.ZU;2-3
Abstract
Background: Helicobacter pylori infection is associated with an increased r isk of gastric cancer In Helicobacter pylori negative patients, factors dif ferent from those in Helicobacter pylon: positive patients may be involved in gastric carcinogenesis. Methods: Thirty-nine recently diagnosed consecutive patients with gastric c ancer were investigated Gastric biopsies were obtained for detection of Hel icobacter pylori (by immunohistochemistry), non-Helicobacter pylori flora ( by modified Giemsa and culture) and histological assessment according to th e Sydney classification by Haematoxylin-Eosin staining. In serum samples, H elicobacter pylori antibodies were determined by IgG enzyme-linked immunoso rbent assay, IgA enzyme-linked immunosorbent assay, and Western blotting. F urthermore, serum gastrin, pepsinogen A and C and plasma chromogranin A wer e determined. Results: Helicobacter pylori was detected by immunohistochemistry in 53.8%, by IgG; in 56.4%, by IgA in 33.3%, and by Western blotting in 74.4% of the 39 patients. Ten patients (25.6%) were negative by both histology and sero logy. Non-Helicobacter pylori flora was detected in 27 of the 39 patients ( 69.2%) with a similar frequency in Helicobacter py lori positive and negati ve patients. Helicobacter pylori positivity was found significantly more of ten in diffuse than intestinal type carcinoma patients (p<0.05). Elevated g astrin levels and antrum-sparing atrophic gastritis were more fre quent in Helicobacter pylori negative than in Helicobacter pylori positive patients (p<0.05). Conclusions: In 10 out of 39 gastric cancer patients, no evidence of previo us or current Helicobacter pylori infection could be demonstrated. Non-Heli cobacter pylori was found in 69.2% of patients regardless of the Helicobact er pylori status. Further studies are needed to establish the contribution of non-Helicobacter pylori flora as well as antrum-sparing atrophic gastrit is with hypergastrinaemia to the development of gastric cancer.