This is a histologic diagnosis and not a clinically recognizable entity because it probably does not cause symptoms. In fact, histologic evidence of gastritis is frequent in asymptomatic individuals, especially as they get older. Thus, the usual clinical assumption that most nonulcer dyspepsia is caused by "gastritis" is not justified. Similarly, gross endoscopic mucosal appearances of erythema, ecchymoses, petechiae, nodularity, or thickened folds do not necessarily indicate histologic changes. Non-erosive gastritis can only be diagnosed by biopsy, and it may or may not be of clinical significance.
The gastric mucosa is divided into two layers: (1) the superficial, nonglandular surface (foveolar) epithelium facing the lumen which is normally replaced every 5 days; and (2) the deeper, glandular layer which is a more stable population of epithelial cells which are replaced very slowly and which have specific functions. These cells include the parietal cells, which make HC1 and intrinsic factor, the chief cells in the fundal glands, which make pepsin, the pylorocardiac glandular cells, which make mucus, and the endocrine G cells in the pyloric glands, which make gastrin. The patterns of gastritis involve both superficial and glandular areas, and the sequence is one of chronic and/or acute inflammation which may cause glandular destruction and may be followed by regeneration, metaplasia, or loss of glands (atrophy). To the pathologist chronic inflammation means the presence of increased plasma cells and lymphocytes in the lamina propria and acute inflammation means the presence of polymorphonuclear leukocytes. This does not necessarily indicate that the process is clinically chronic or acute, and thus morphologic interpretation may be confusing to clinicians. The probable morphologic sequence is that the superficial layer is first inflamed (superficial gastritis) and that epithelial destruction and inflammation within the surrounding lamina propria then penetrates to the deeper glandular areas (atrophic gastritis) leading finally to loss of glands (gastric atrophy) or replacement by metaplastic glands (intestinal metaplasia or pyloric gland metaplasia of fundal glands).
If one cannot ascribe symptoms to these histologic changes, what indeed is their clinical significance? It is known that chronic atrophic gastritis, gastric atrophy, and intestinal metaplasia occur at a younger age, are more widely distributed in the stomach, and are more frequent in populations with a higher incidence of carcinoma of the body and antrum of the stomach. Perhaps this is the "soil" in which this type of cancer develops more easily. But even in the United States, where this type of gastric cancer is decreasing, such gastric changes with aging are common. What is clinically significant in the United States is a completely normal fundal gland area, free of gastritis, in patients 70 years of age or older. These usually are patients with peptic ulcer disease of the hypersecretory, perhaps hereditary, type who commonly have duodenal ulcers and severe reflux esophagitis. The fundal glands of these patients do not undergo the "normal" gastritic changes of aging. Interestingly, such patients often have antral (pyloric gland) gastritis.
What about the patient with a chronic benign gastric ulcer? These patients have chronic gastritis at the edge of their peptic ulcers and secrete normal or less than normal amounts of HC1. Thus, if endoscopic biopsies of the edge of a gastric ulcer show no gastritis, there is a strong likelihood that the ulcer is not a typical peptic ulcer; rather, it is probably associated with aspirin or NSAID ingestion, and discontinuance of the offending drugs will be curative. Atrophic fundal gland gastritis and/or atrophy is often seen in patients with thyroid disease or idiopathic iron deficiency anemia and is regularly seen in pernicious anemia. Perhaps a common denominator in all of these conditions is an autoimmune destruction of the gastric mucosa, but this hypothesis remains unproven.
Severe fundal gland atrophy is invariably present in pernicious anemia where parietal cells secreting intrinsic factor and HC1 are virtually absent. As a result, vitamin B12 in food is not absorbed. Serum gastrin levels are high because the uninvolved antrum secretes gastrin continuously in the absence of acid. The pyloric glands are preserved and relatively free of gastritis. Serum antibodies to parietal cells are present in the serum of about 60 percent of persons with atrophic fundal gastritis and in 80 to 90 percent of those with pernicious anemia. Antibodies to intrinsic factor are present in the serum or gastric juice of most patients with pernicious anemia; they are not found in patients with superficial or atrophic gastritis. The relationship between these immunologic findings and the fundal gland atrophy of pernicious anemia is uncertain.
Antral (pyloric gland) gastritis is common in asymptomatic persons. With age, this type of gastritis probably tends to extend proximally and to replace some fundal glands. If peptic ulcer is located in the upper stomach, pyloric gland gastritis may extend far more proximally. Unlike fundal gastritis, in antral gastritis serum gastrin levels tend to be low and there may be antibodies to gastrin-producing cells rather than to parietal cells. It has been postulated that regurgitation of duodenal contents, particularly bile salts, into the stomach causes pyloric gland gastritis. Spiral bacilli have been isolated from some patients, but their significance is uncertain. Occasionally, pyloric gland gastritis is associated with narrowing of the antrum suggestive of malignancy by x-ray; such patients often complain of ulcer-like pain and may, indeed, prove to have ulcers subsequently. At gastroscopy, normal antral motility suggests pliability, and malignancy can usually be excluded. The symptoms often respond to antacids and inhibitors of H-2 receptors.
Ordinarily, nonerosive gastritis requires no treatment, but it is essential to rule out vitamin B12 malabsorption in persons who are found to be achlorhydric. If pernicious anemia is proved, it is treated as discussed in. Iron-deficiency anemia should not be attributed to atrophic fundal gland gastritis unless other causes are excluded; it responds to oral iron.