Background and Study Aims: The incidence of Helicobacter pylori infection in Japan is high. Unlike the case in Western countries, H. pylori-induced gastritis in Japanese patients has a tendency to spread to the corpus. H. pylori-induced gastritis is characterized by a number of specific endoscopic findings. In a previous study, the endoscopic features and a magnified view of the gastric mucosa of the corpus of H. pylori-negative normal stomach were described. This report describes the specific histological features and magnified views of the H. pylori-negative stomach and compares them with those seen during H. pylori-induced gastritis.
Patients and Methods: The anterior wall or greater curvature of the middle body of the stomachs of 297 patients were observed by magnifying endoscopy (× 80). Forceps biopsy was performed at the following locations: i) the magnified site, for histological examination; ii) the antral mucosa, for culture/urease test, and histology; and iii) greater curvature of the upper body for culture/urease test.
Results: 72 patients were diagnosed as having H. pylori-negative normal stomach and 225 as having H. pylori-positive gastritis. The magnified views were classified into four types: i) collecting venules, with true capillaries forming a network, and gastric pits resembling pinholes (type Z-0; n = 80); ii) irregular true capillaries but no collecting venules observed (type Z-1; n = 36); iii) white gastric pits and sulci, with neither collecting venules nor true capillaries being seen (Z-2; n = 110); and iv) dilated pits with surrounding redness (Z-3; n = 71). All cases of H. pylori-negative normal stomach were type Z-0, whereas H. pylori-induced gastritis was present in all cases where the classification was Z-1, Z-2, or Z-3. Type Z-0 differed significantly from types Z-1, Z-2, and Z-3 with regard to the grade of inflammation, activity, and presence of H. pylori.
Conclusions: Collecting venules and true capillaries forming a network with gastric pits in the center (type Z-0) were observed in the H. pylori-negative normal mucosa. The magnified views of H. pylori-related gastritis clearly differed from type Z-0.
References
-
1
Price A B.
The Sydney system. Histological division.
J Gastroenterol Hepatol.
1991;
6
209-222
-
2
Dixon M F, Genta R M, Yardley J H. et al .
Classification and grading of gastritis: the updated Sydney system.
Am J Surg Pathol.
1996;
20
1161-1181
-
3
Satoh K, Kimura K, Taniguchi Y. et al .
Distribution of inflammation and atrophy in the stomach of Helicobacter pylori-positive and -negative patients with chronic gastritis.
Am J Gastroenterol.
1996;
91
963- 969
-
4
El-Omar E M, Oien K, El-Nujimi A. et al .
Helicobacter pylori infection and chronic gastritis acid hyposecretion.
Gastroenterology.
1997;
113
15-24
-
5
Tucci A, Blasco G, Paparo G F.
Effect of eradication of Helicobacter pylori in patients with fundic atrophic gastritis.
N Engl J Med.
1997;
336
957-958
-
6
Khakoo S I, Lobo A J, Shepherd N A. et al .
Histological assessment of the Sydney classification of endoscopic gastritis.
Gut.
1994;
35
1172-1175
-
7
Bah A, Saraga E, Armstrong D. et al .
Endoscopic features of Helicobacter pylori-related gastritis.
Endoscopy.
1995;
27
593-596
-
8
Yagi K, Nakamura A, Sekine A. et al .
Endoscopic features of the normal gastric mucosa without Helicobacter pylori infection (in Japanese with English abstract).
Gastroenterol Endosc.
2000;
10
1977-1987
-
9
Sakaki N, Iida Y, Okazaki Y. et al .
Magnifying endoscopic observation of the gastric mucosa, particularly in patients with atrophic gastritis.
Endoscopy.
1978;
10
269-274
-
10
Laine L, Cohen H, Sloane R. et al .
Interobserver agreement and predictive value of endoscopic findings for H. pylori and gastritis in normal volunteers.
Gastrointest Endosc.
1995;
42
420-423
-
11 Tsuchihashi Y. Structural alterations of mucosal microvascular system in human chronic gastritis. In: Manabe H, Zweifach BW, Messmer K (eds) Microcirculation in circulatory disorders. Springer-Verlag 1988: 161-169
-
12
Kitadima M, Wolfe R R, Trelstad R L. et al .
Gastric mucosal lesions after burn injury:relationship to H+ back-diffusion and the microcirculation.
J Trauma.
1978;
18
644-650
-
13
Parsonnet J, Freedman G D, Vandersteen D P. et al .
Helicobacter pylori infection and risks of gastric carcinoma.
N Engl J Med.
1991;
325
1127-1131
-
14
Asaka M, Kimura T, Kato M. et al .
Possible role of Helicobacter pylori infection in early gastric cancer development.
Cancer.
1994;
73
2691-2694
-
15
Haruma K, Komoto K, Kamada T. et al .
Helicobacter pylori infection is a major risk factor for gastric carcinoma in young patients.
Scand J Gastroenterol.
2000;
35
255-259
K. Yagi, M.D.
Dept. of Internal Medicine · Niigata Prefectural Yoshida Hospital
Yoshidamachi · Nishikanbaragun · Niigataken 959-0242 · Japan
Fax: + 81-256-92-2610
Email: yagikazu@pop12.odn.ne.jp
