The Pyloric Sphincteric Cylinder in Health and Disease

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Chapter 28 (page 132)

Chapter 28

Gastritis and Erosions in the Pyloric Sphincteric Cylinder

Holsti (l931) stated that inflammatory alterations of gastritis usually affected the mucosa, but that changes also occurred in the deeper layers of the wall in 66 percent of cases, and even the serous layer might be involved. He performed detailed histological studies of the intramural ganglia in gastric resection specimens affected by chronic gastritis (in the absence of peptic ulceration). Compared with normal controls, the ganglia of gastritis showed marked changes affecting the periganglionar, capsular and intraganglionar structures. The outstanding feature was an increase in connective tissue both in the periganglionar and intraganglionar regions, coupled with intraganglionar infiltration of inflammatory cells and degeneration of ganglion cells; in some ganglia hardly a single normal cell was seen. The changes were more marked in Auerbach's than in Meissner's plexus and more advanced in the pyloric than in the fundic zone. The intensity of the condition varied from case to case, from ganglion to ganglion, and even from one part of a ganglion to another. The spatial spread of the process was uneven, but two components of the wall, namely the mucosa and Auerbach's plexuses, were always involved.

Schindler et al. (l937) pointed out that at that time the normal histological picture of the gastric mucosa was still being debated. Specimens for examination were rarely obtained from healthy stomachs as postmortem changes altered the picture and healthy stomachs were not resected. Minor histological changes did not indicate active disease but were the normal reaction to external irritants, such as hot or cold food; those changes were not due to chronic gastritis. Gastroscopy could be carried out in normal persons, and on the basis of systematic gastroscopic investigations it was suggested that chronic gastritis could be divided into 3 types: superficial, atrophic and hypertrophic. Demonstrating the mucosal folds by means of radiological relief techniques was of little value in the diagnosis of chronic gastritis.

Golden (l937) defined gastritis as inflammation of the gastric wall of unknown etiology, which began in and might be limited to the mucosa, but which frequently extended to the deeper layers and even to the serosa. It could be generalized, but was often patchy and not infrequently it was limited to, or had its maximum effect in, the antrum. The term "antrum" was used synonymously with the canalis egestorius as described by Forssell (l913), while antral systole and diastole indicated contraction and relaxation of the canalis respectively. As the canalis egestorius was the most important part of the stomach as far as motility was concerned, inflammatory change here could be expected to produce serious disturbances in gastric motive function.

Golden (l937) agreed with Schindler et al. (l937) and other previous authors that in many cases of gastritis the change in the mucous membrane could not be demonstrated by radiology, and the condition could only be diagnosed by gastroscopy. In other cases, however, the canalis exhibited motility disorders which were readily apparent during the radiological examination; in some there was absence of contraction (absence of "antral systole"), while in others a greater or lesser degree of "antral" spasm was seen. The spasm could vary from marked contraction to failure of full relaxation of the canalis. Involvement of the deeper layers of the wall by inflammatory infiltration and fibrosis could hamper or prevent normal movements of the muscularis mucosae and consequently of the mucosal folds (Chaps. 2, 13); as a result the folds failed to change in direction as they normally did during antral systole, causing them to appear exaggerated. These features enabled Golden (l937) to make a radiological diagnosis of "antral gastritis and spasm" in appropriate cases. The prepyloric narrowing was sometimes associated with mucosal erosions which at that time were only demonstrable by gastroscopy or histological examination.

In histological studies of 100 partial gastrectomy specimens, Magnus (l946) found that inflammatory gastritis affecting the pyloric region consisted of two types. The first type, acute erosive pyloric gastritis, was characterized by polymorphonuclear infiltration of the mucosa, with lesser numbers of lymphocytes, plasma cells and eosinophils. The glandular epithelium showed degenerative changes, there was capillary hyperaemia with mucosal oedema, and erosions were visible on the surface. The typical erosion had the size of a pin's head and involved only the superficial part of the mucosa, i.e. it did not extend through the mucosa and muscularis mucosae into the submucosa; erosions varied in number from a few to over a hundred in individual cases. The second type, chronic atrophic gastritis, was characterized by atrophy of the glandular parenchyma, fibrosis in the mucosa and submucosa, intense infiltration of the interstitial tissue by plasma cells and lymphocytes, and intestinal metaplasia of the gastric epithelium. There was a transition from acute erosive to chronic atrophic pyloric gastritis, and the two types were sometimes found together.

MacDonald and Rubin (l967) found that gastric suction biopsy studies of gastritis had been disappointing; blind suction biopsy often missed the pyloric mucosal zone and specimens of pyloric mucosa were seldom obtained. Examination of the entire length of gastrectomy specimens by means of the Swiss roll technique afforded better results. For a variety of reasons the definition and classification of chronic gastritis remained unsatisfactory. Correlation between the radiological mucosal fold pattern and histological findings was poor.

Studies by Gear et al. (l97l), (Chap. 29), showed that ulcers of the body of the stomach were associated with more extensive and more severe gastritis than ulcers of the prepyloric region. In the latter gastritis was usually localized to the distal stomach, it was often superficial and showed little evidence of atrophic change or metaplasia. The fact that gastritis persisted in spite of healing of the gastric ulceration, indicated that it was the basic disease process and not simply a zonal change secondary to the ulcer.

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