Hypertrophic gastritis is a histologic misnomer. The individual mucosal epithelial cells are not enlarged (hypertrophic), but there are more of them (hyperplasia), and thus the mucosa is thickened. There are three causes for gastric mucosal hyperplasia: Menetrier's disease, hypersecretory gastropathy, and Zollinger-Ellison syndrome (gastrinoma). Most hyperplastic mucosal conditions produce enlarged gastric folds which may be indistinguishable by x-ray or endoscopy from infiltrative cancer, lymphoma, or a functional abnormality.
Menetrier's disease The cause of this uncommon type of gastric mucosal hyperplasia is unknown. It is characterized grossly by tortuous enlargement of the gastric mucosal folds resembling cerebral convolutions, and histologically by a thickened mucosa with hyperplasia of mucous cells and loss of most parietal and chief cells. The gastric pits are markedly elongated and tortuous and often exhibit cystic dilatation; these cysts may penetrate through the muscularis mucosae into the submucosa. The lamina propria often contains increased numbers of lymphocytes. Intestinal metaplasia may be present. The mucosal involvement may be localized or diffuse and tends to be most prominent on the greater curvature. The antrum is uninvolved in more than 50 percent of patients. Occasionally the gross appearance suggests diffuse polyposis.
Epigastric pain is the most common complaint. Anorexia, nausea, vomiting, weight loss, or diarrhea are other symptoms. Bleeding is not uncommon because of superficial erosions. Some patients develop a gastric ulcer. Carcinoma may develop rarely. Loss of protein through the mucosa often causes hypoalbuminemia, and sometimes peripheral edema. Widening of tight junctions between surface epithelial cells revealed by electron microscopy may explain the protein loss. The gastric juice contains little or no hydrochloric acid but often excessive mucus. X-ray shows very large folds and sometimes hypomotility. The diagnosis can usually be made from clinical, radiologic, and laboratory data supplemented by gastroscopy (preferably using one of the newer, larger biopsy forceps to get the deeper biopsy needed for diagnosis), and brash cytology to rule out cancer. Occasionally, laparotomy with full-thickness biopsy of the stomach is necessary to establish the diagnosis and to exclude malignancy.
There is no specific treatment, but frequent small meals may give some symptomatic relief. Those with gastric ulcers should receive antacids or H-2 receptor antagonists. A high-protein diet should be given to patients with hypoalbuminemia, but diuretics or intravenous albumin may be necessary for those with severe edema. Treatment with anticholinergic drugs or cimetidine reduces protein loss in some patients. Partial gastrectomy may be helpful for intractable symptoms if the disease is sufficiently well localized. Rarely, total gastrectomy may be necessary. The latter should be deferred as long as possible because spontaneous improvement or complete reversal of chronic disease has been documented.
Hypersecretory gastropathy Patients with this rare syndrome differ from those with classical Menetrier's disease because the thickened mucosa secretes gastric acid normally or excessively but not at the high rate seen in gastrinoma; furthermore, blood gastrin levels are normal. The mucosa is histologically indistinguishable from that seen in Zollinger's syndrome with an excess of parietal and chief cells. Many of these patients may represent the upper end of the spectrum of increased fundal gland mass seen in patients with duodenal ulcer. Some have a protein-losing gastropathy. Ulcer symptoms may improve after antacids or H-2 receptor inhibitors, but some patients may require surgery. Protein loss, when present, may be difficult to control unless the disease remits spontaneously.
Gastrinoma (Zollinger-Ellison syndrome) This is a fundal gland hyperplasia caused by excessive gastrin secretion by a gastrinoma, usually located in the pancreas.