Differential features of gastric cancer patients, either Helicobacter pylori positive or Helicobacter pylori negative.
BACKGROUND
Helicobacter pylori infection is associated with an increased risk of gastric cancer. In Helicobacter pylori negative patients, factors different from those in Helicobacter pylori positive patients may be involved in gastric carcinogenesis.


METHODS
Thirty-nine recently diagnosed consecutive patients with gastric cancer were investigated. Gastric biopsies were obtained for detection of Helicobacter pylori (by immunohistochemistry), non-Helicobacter pylori flora (by modified Giemsa and culture) and histological assessment according to the Sydney classification by Haematoxylin-Eosin staining. In serum samples, Helicobacter pylori antibodies were determined by IgG enzyme-linked immunosorbent assay, IgA enzyme-linked immunosorbent assay, and Western blotting. Furthermore, serum gastrin, pepsinogen A and C and plasma chromogranin A were 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 serology. Non-Helicobacter pylori flora was detected in 27 of the 39 patients (69.2%) with a similar frequency in Helicobacter pylori positive and negative patients. Helicobacter pylori positivity was found significantly more often in diffuse than intestinal type carcinoma patients (p < 0.05). Elevated gastrin levels and antrum-sparing atrophic gastritis were more frequent 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 previous or current Helicobacter pylori infection could be demonstrated. Non-Helicobacter pylori was found in 69.2% of patients regardless of the Helicobacter pylori status. Further studies are needed to establish the contribution of non-Helicobacter pylori flora as well as antrum-sparing atrophic gastritis with hypergastrinaemia to the development of gastric cancer.
Jonkers
D
D
Department of Gastroenterology, University Hospital Maastricht, Sweden.
Houben
P
P
Hameeteman
W
W
Stobberingh
E
E
de Bruine
A
A
Arends
J W
JW
Biemond
I
I
Lundqvist
G
G
Stockbrügger
R
R
D000368:Aged; D000369:Aged, 80 and over; D000907:Antibodies, Bacterial / Q000097:blood; D053379:Chromogranin A; D002864:Chromogranins / Q000097:blood; D005260:Female; D005755:Gastrins / Q000097:blood; D016480:Helicobacter pylori / Q000276:immunology / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008875:Middle Aged; D020116:Pepsinogen A / Q000097:blood; D020115:Pepsinogen C / Q000097:blood; D011446:Prospective Studies; D013270:Stomach / Q000382:microbiology; D013274:Stomach Neoplasms / Q000097:blood / Q000382:microbiology*
D000907:Antibodies, Bacterial; D053379:Chromogranin A; D002864:Chromogranins; D005755:Gastrins; D020115:Pepsinogen C; D020116:Pepsinogen A