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DOI: 10.1055/s-2002-25281
© Georg Thieme Verlag Stuttgart · New York
Comparison Between Magnifying Endoscopy and Histological, Culture and Urease Test Findings from the Gastric Mucosa of the Corpus
Publication History
6 February 2001
15 October 2001
Publication Date:
22 April 2002 (online)
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