The natural history of gastric atrophy

Glass, George B. Jerzy

doi:10.1007/bf02233429

Cited by 19 publications

(1 citation statement)

References 84 publications

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“…The role of circulating parietal cell antibody in the natural history of atrophic gastritis has long been a matter of dispute (18,(20)(21)(22) …”

Section: Discussionmentioning

confidence: 99%

Effects of Gastric Antibodies on Gastric Secretion

Kawashima

1972

Jpn.J.Pharmacol

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The etiology of atrophic gastritis has not been established. Although the circulating antibody to a constituent of the gastric parietal cell has been demonstrated in a large number of patients with pernicious anemia and atrophic gastritis (1-5), the significance of the pa rietal cell antibody in causing or perpetuating any type of chronic gastritis is unknown. Jacob and Glass (6) have presented direct evidence that the parietal cell antibody is a comple ment fixing antibody, and have supported the concept that the autoimmune mechanism participates in the development of the gastric atrophic lesion in a proportion of patients with pernicious anemia and atrophic gastritis. Fiasse et al. (7) failed to show inhibition of gastric secretion after a single injection of human parietal cell antibody in the rat. On the other hand, Tanaka and Glass (8) have reported that rats injected with human parietal cell antibody for 6 to 8 weeks showed a profound decrease of hydrochloric acid output, and had mild atrophic lesions in the gastric mucosa. Hausamen et al. (9) have shown that the injection of rabbit antisera against antigens from guinea pig gastric mucosa into guinea pigs, resulted in an acute inflammation confined to the stomach. In the present study, short and long-term effects of rabbit antibodies against rat gastric mucosa and gastric juice on gastric secretion in the rat, were investigated. MATERIALS AND METHODS AnimalsMale Donryu strain rats weighing 170-252 g, were used. Antiscra Rabbit antisera, the production and characteristics of which were reported in the pre ceeding paper (10), were used. Three groups of antisera were available and were directed against extract from rat gastric mucosa of the oxyntic area (GM), rat gastric juice (GJ) and extract from rat uterus (Ut). Lyophilized r-globulin fractions, prepared from these antisera and normal rabbit serum, were dissolved in saline and used for animal experiments, after absorption with normal rat serum and a lyophilized homogenate of rat esophagus.

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“…The role of circulating parietal cell antibody in the natural history of atrophic gastritis has long been a matter of dispute (18,(20)(21)(22) …”

Section: Discussionmentioning

confidence: 99%

Effects of Gastric Antibodies on Gastric Secretion

Kawashima

1972

Jpn.J.Pharmacol

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Atrophic chronic gastritis and intestinal metaplasia in gastric carcinoma. Comparison with a representative population sample

Sipponen

Kekki

Siurala

1983

Cancer

112

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The occurrence of chronic gastritis and intestinal metaplasia (IM) was studied in 257 patients with gastric carcinoma (GC). In all cases biopsies were available from the benign mucosal area adjacent to the tumor, and in 139 patients from the antrum and/or body mucosa outside the tumor. The results were compared with endoscopically and bioptically examined noncancer controls representing a large Finnish population sample. For every GC patient, a control subject was matched by age and sex. In addition, a mean age‐adjusted score (AAS) of chronic gastritis, which expresses the progression of gastritis in GC patients as compared with that in the general population, was calculated for GC patients. The prevalences of chronic and atrophic gastritis in the antrum and body mucosa were similar in GC patients and controls when carcinoma cases were not more specifically classified according to histologic type or location of tumors. On the other hand, the location of the tumor showed a significant relation to gastritis: the progression of gastritis was more rapid (high mean AAS value) and the prevalence of atrophic gastritis was higher in the tumor‐affected area (i.e., in the antrum in patients with antral [distal] tumors; in the body in patients with body [proximal] tumors), than in the general population, but were similar in the tumor‐free area in both GC patients and controls. In the intestinal type of GC (IGC), the prevalence of chronic gastritis was higher and its progression was more rapid than in controls. In the diffuse type of GC (DGC), these correlations were less distinct. In GC patients, the IM adjacent to and outside the tumor area was significantly more common and extensive than in the corresponding area of controls, and a significant positive correlation was present between the location of the tumor and the distribution of IM. Like gastritis, the IM showed a closer relationship to IGC than to DGC. In all cases of GC and particularly of IGC, the antral mucosa tended to be more severely affected by gastritis and IM than the body mucosa, i.e., the prevailing type of gastritis found in this GC series was that morphologically corresponding to the so‐called B‐type of chronic gastritis.

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Investigation of two possible modes of action of gastrone, an endogenous inhibitor of gastric secretion

Baume

Law

1966

Digest Dis Sci

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The natural history of gastric atrophy

Cited by 19 publications

References 84 publications

Effects of Gastric Antibodies on Gastric Secretion

Effects of Gastric Antibodies on Gastric Secretion

Atrophic chronic gastritis and intestinal metaplasia in gastric carcinoma. Comparison with a representative population sample

Investigation of two possible modes of action of gastrone, an endogenous inhibitor of gastric secretion

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