Mills Ch22 Stomach

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CHAPTER 22:  Stomach

metaplasia. Recently it has become recognized that hypo- chlorhydria of the elderly is not simply the result of aging but may also be secondary to chronic gastritis (32).

mucins MUC5AC, MUC1, and MUC6 are detected in the normal stomach (28). Typically, MUC5AC is present in foveolar epithelium and mucus neck cells. MUC1 is present in the foveolar epithelium, chief and parietal cells. MUC6 is present in the antral glands and mucous neck cells. The exact physiologic role of gastric mucin is not determined, although the soluble mucin likely plays a role in lubrica- tion. The mucin forms a surface coating with alternating layers of MUC5AC and MUC6 mucin proteins (29). This forms a barrier that, together with bicarbonate secreted by the superficial epithelial cells, prevents back diffusion of acid and gastric autodigestion. The actual structural barrier is formed by the continuous layer of luminal mucosal cells and the tight junctions between adjacent cells. This pro- cess is likely modulated by prostaglandins which promote mucosal blood flow. SPECIAL TECHNIQUES AND PROCEDURES Relatively few special techniques are applicable to rou- tine diagnosis. Stains that demonstrate the carbohydrate composition of mucin are the most widely used, and the combined PAS/Alcian blue is the most versatile. This com- bination stains neutral mucin magenta, acid mucin light blue, and combinations purple. The combined stain is pre- ferred over a straight PAS because the mucus in some gas- tric carcinomas is PAS negative. A mucicarmine stain is not recommended because it does not permit identification of the mucin type and is also negative with some types of acid mucin. Sialomucin and sulfomucin may be distinguished by a combined high-iron diamine and Alcian blue stain, which stains sulfomucin black and sialomucin light blue. At the present time, however, this distinction is of limited diagnostic utility. Usually, there is no difficulty in distinguishing chief and parietal cells on a good H&E stain (Fig. 22.10). If necessary, special stains, such as a Maxwell stain (30), can aid this distinction. Parietal cells can be recognized and quantified by use of a human milk fat globulin antibody (31). At the present time, the use of cytokeratin 7 and cyto- keratin 20 immunostains to distinguish metaplastic gastric cardiac mucosa from the mucosa of Barrett esophagus is controversial. Different results have been obtained by differ- ent observers, so this methodology cannot be recommended for routine use (15). AGE CHANGES Many older adults have a reduced gastric acid output. His- tologically, this is characterized by a reduction in the area of oxyntic mucosa with expansion of the zone of pyloric mucosa. This results in proximal displacement of the fundo- pyloric junction, a change termed pyloric (or pseudopyloric)

ARTIFACTS A variety of artifacts may occur in gastric biopsy specimens (Fig. 22.15). Most of these artifacts relate to rough han- dling of the specimen, either at the time the biopsy sample is taken or when it is removed from the forceps. Crush- ing is common and can result in compression of the lamina propria, leading to a false impression of an inflammatory infiltrate. Crush artifact also produces telescoping of the foveolar lining cells. Stretching of the mucosa results in separation of the pits and glands, leading to an impression of edema. Hemorrhage into the lamina propria is also com- mon in gastric biopsy samples and has to be distinguished from hemorrhagic gastritis. This can be difficult in small biopsy samples, but usually the microscopic appearances of hemorrhagic gastritis are characteristic. They include superficial epithelial damage and erosions. DIFFERENTIAL DIAGNOSIS One of the problems for pathologists examining gastric biopsy samples is determining whether the specimen is normal or shows minor degrees of gastritis. It is therefore appropriate to review briefly certain aspects of the classifi- cation and diagnosis of gastritis. Specific types of gastritis, for example, acute hemorrhagic gastritis or granulomatous gastritis, are usually so distinct that confusion with a normal stomach is unlikely (33). On the other hand, H. pylori gas- tritis may be patchy and may be associated with atrophy. In the early stage of H. pylori gastritis (chronic superficial gas- tritis), an infiltrate of inflammatory cells is observed in the superficial portion of the mucosa, particularly in the lamina propria between the gastric pits (Fig. 22.16). Later, the inflammation spreads deeply to involve the whole thickness of the mucosa and is accompanied by atrophy of gastric glands (chronic atrophic gastritis). Ultimately, the inflam- mation may burn itself out and all glands are destroyed, leaving only a thinned mucosa containing foveolar structures (gastric atrophy) (33). The superficial gastric lamina propria normally con- tains some chronic inflammatory cells. It is often a mat- ter of judgment whether these are considered normal or increased in number because there is no simple satisfac- tory method of objective measurement. In actual practice, it may be even more difficult to evaluate these cells because the gastric biopsy samples obtained by endoscopists are frequently distorted by crushing or stretching. In assessing possible minor degrees of inflammation, therefore, study should also be made of the superficial and foveolar lining