Endoscopic Appearance

Atrophy causes a progressive thinning of the mucosa of the gastric corpus; this explains why few folds are left and why fine submucosal vessels are easily recognized on endoscopic examination, especially in advanced disease. The antral mucosa is endoscopically normal in the majority of cases. Polyps become common in the advanced stages of the disease; therefore, atrophic gastritis must be ruled out in patients in whom multiple hyperplastic gastric polyps are detected at endoscopy.

Histopathology

The main histopathological features of autoimmune gastritis are diffuse corpus-restricted chronic atrophic gastritis with mild to moderate intestinal metaplasia and, in the absence of concurrent H.pylori infection, a normal gastric antrum. This pattern is characteristic of the advanced stage of the disease and is found in patients with pernicious anemia. Persons with parietal cell antibodies and no pernicious anemia show a broad spectrum of atrophic changes, from minimal oxyntic gland loss to severe and diffuse atrophy of the oxyntic mucosa. In the early phases, one sees diffuse or multifocal, dense mononuclear cell infiltration of the lamina propria and lymphocytic infiltration of individual oxyntic glands. Later, marked atrophy of the oxyntic glands with diffuse mononuclear cell infiltration of the lamina propria develops. Pyloric metaplasia is extensive, whereas intestinal metaplasia tends to be still limited to few foci. The end stage is characterized by a great reduction in corpus mucosal thickness, foveolar hyperplasia, and replacement of oxyntic glands by pyloric, pseudopyloric, or intestinal metaplasia. The inflammatory infiltrate is minimal, although scattered lymphoid aggregates and follicles may be found.

In the majority of patients, the antral mucosa is either normal or shows only focal areas of mild chronic inflammation with intestinal metaplasia, similar in degree and extension to what is observed in the general asymptomatic population. Hyperplasia of gastrin cells secondary to achlorhydria is often seen. Enterochromaffin-like cell carcinoids may arise during the florid phase, but they are found more commonly in association with an end-stage histopathological pattern.

Diagnosis

Autoimmune gastritis should be suspected in patients with megaloblastic anemia, with evidence of clinically significant cobalamin deficiency with values lower than 150 pg/mL, or with multiple gastric polyps. The diagnosis must be confirmed by the characteristic histopathological findings of corpus-restricted atrophic gastritis and by the presence of serum anti–intrinsic factor or anti–parietal cell antibodies.

Management

The management of patients with autoimmune gastritis should address two aspects of the condition: the gastric lesions and the manifestations related to the cobalamin deficiency. Gastric mucosal atrophy is irreversible. Patients with extensive intestinal metaplasia and those with multiple polyps may be at increased risk of gastric cancer. Although there are no accepted guidelines, a surveillance gastroscopy every 1 or 2 years may represent a sensible empiric approach.

With cobalamin replacement, most abnormalities resulting from cobalamin deficiency undergo complete and lifelong correction, except for the neurological manifestations. Their improvement depends on the extent that irreversible changes in the nervous system may have occurred before treatment.

Дата добавления: 2015-11-14