The Pyloric Sphincteric Cylinder in Health and Disease

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Chapter 28 (page 133)

By means of fibreoptic gastroscopy Whitehead et al. (l972) obtained fresh, multiple full- thickness biopsy specimens from all parts of the gastric mucosa in a large number of patients. They proposed a classification of chronic gastritis applicable to all zones of the mucosa, based on the following features: First, the mucosal type had to be established, e.g. pyloric mucosa had to be differentiated from pseudopyloric metaplasia of body mucosa. Second, the grade had to be determined; chronic atrophic gastritis (in which there was atrophy of tubules) could be subdivided into mild, moderate and severe grades. Third, the stage of activity had to be established; both superficial and atrophic gastritis could be either active or quiescent. Fourth, the presence and type of metaplasia had to be determined; it was acknowledged that difficulties could arise in recognizing mucosal type when severe gastritis was associated with metaplasia or atrophy. In their classification the degree of atrophy, rather than the degree of chronic cellular infiltration, was graded. It was also established that intestinal metaplasia nearly always occurred in mucosa which was the site of atrophic gastritis.

Strickland and Mackay (l973) reviewed the nature of chronic atrophic gastritis in relation to the structure and function of the pyloric antrum, where "antrum" was equated with the pyloric mucosal zone. Two distinct types of atrophic gastritis were recognized. In Type A, tests for parietal cell autoantibody and intrinsic factor antibody were positive; there was sparing of antral mucosa, with diffuse changes in the corpus, and severe impairment of gastric secretion. In Type B, parietal cell autoantibody and intrinsic factor antibody reactions were negative; there was definite antral involvement with focal changes in the corpus, and moderate impairment of gastric secretion. Benign gastric ulceration of the corpus was found to be associated with Type B atrophic gastritis; the more proximally the ulcer was located in the stomach, the more extensive the gastritis and the more severe the impairment of acid secretion proved to be. Chronic atrophic gastritis persisted after ulcer healing, supporting the view that gastric ulcer originated from chronic gastritis.

Rao et al. (l975) stated that the term chronic gastritis carried different connotations for the clinician, the pathologist and the radiologist. Previously little attention had been given to determining the degree of chronic cellular infiltration involving the full thickness of the gastric mucosa. They supported the use of terms which described the morphological abnormalities found in mucosal biopsies, namely the degree of cellular infiltration of the whole mucosa and the presence or absence of atrophy. A simple descriptive classification of chronic gastritis into mild, moderately severe and severe grades, with or without atrophy or metaplasia, was recommended. Mucosal biopsies in 241 patients with a variety of upper abdominal conditions showed chronic gastritis in 184. Only 3 of the patients were diagnosed as true superficial gastritis, where the cellular infiltration was limited to the lamina propria between the pits.

Op den Orth and Dekker (l976) described erosions as superfical mucosal defects which did not penetrate the muscularis mucosae. A flat erosion was a mucosal defect without reaction in the adjacent parts, while a varioliform or complete erosion indicated a mucosal defect surrounded by an elevated zone; the elevated zone had been variously interpreted as a circular contraction of the muscularis mucosae, oedema, leucocytic infiltration, or fibrosis. It was pointed out that erosions could occur as solitary lesions or in combination with other upper gastro-intestinal pathology, e.g. gastric or duodenal ulceration; whether a gastric erosion itself ever developed into a gastric ulcer was controversial. Because of the raised zone surrounding it, an erosion could be visualized fairly easily with double-contrast radiography as a tiny, constant fleck of barium surrounded by a radiolucent halo; some erosions tended to be linear rather than circular. In some cases erosions in the prepyloric area were associated with prominent or irregular mucosal folds; the radiographic diagnosis of erosions was found to be reliable, and correlated well with their endoscopic demonstration.

Roesch (l978) pointed out that gastric erosions occurred very commonly and were often multiple. In the acute type the epithelial defect was not surrounded by inflammatory reaction, while the chronic type had an elevated, bulging border. Only the chronic type was detectable radiologically, presenting as a small fleck with a surrounding halo. Endoscopy showed that almost 60 percent of chronic erosions occurred in the antral region, and that they were often associated with prominent mucosal folds. Radiological demonstration of these bead-like prepyloric folds was highly suspicious of chronic erosions, even in the absence of a central punctate barium-filled depression. Where erosions were followed-up for 5 years or longer, the transformation of multiple antral erosions into hyperplastic folds could often be seen.

Morson and Dawson (l979) reiterated that the most accurate diagnosis of gastritis was made on biopsies taken under direct vision through a fibrescope. Their classification, which was made on histological grounds, entailed 3 types, namely chronic superfical gastritis, atrophic gastritis (both of which might be either active or quiescent), and gastric atrophy. Active superficial gastritis might be accompanied by small erosions. In atrophic gastritis the essential feature was not the increase in inflammatory cells in the lamina propria, but the reduction or atrophy of the deep glands, accompanied by intestinal metaplasia in the "antrum". Attention was drawn to the fact that in both superficial and atrophic gastritis, submucous fibrosis and thickening of the muscularis externa had been reported, giving rise to "antral" deformity which was recognizable radiologically.

Freise et al. (l979) did four year follow-up studies in 64 patients with gastric erosions. The most common site of multiple erosions was the "antral" region. Erosions were frequently seen in combination with other upper gastrointestinal conditions such as gastric or duodenal ulceration or hiatus hernia. In 10 percent of cases chain-like multiple erosions developed into a persistent, prominent gastric mucosal fold, usually in the "antrum". When such a fold was seen, it could be taken to be the result of a chain of erosions. There was no evidence that erosions led to chronic gastric ulceration, polyps or malignancy.

Karvonen et al. (l983) classified erosions according to their endoscopic morphology. In the complete type there was a surrounding elevated border; incomplete or flat erosions were surrounded by a red halo, and haemorrhagic erosions were punctate bleeding spots. In 86 percent of 117 patients with gastric erosions (but without other upper gastrointestinal pathology), the lesions occurred only in the antral or prepyloric part of the stomach, and in the majority of patients presented as multiple erosions. Some showed features of both the complete and incomplete types, and were characterized by their location on prominent prepyloric mucosal folds.

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