History
Atrophic gastritis represents the end stage of chronic gastritis, both infectious and autoimmune. In both cases, the clinical manifestations of atrophic gastritis are those of chronic gastritis, but pernicious anemia is observed specifically in patients with autoimmune gastritis and not in those with H pylori–associated atrophic gastritis.
H pylori-associated atrophic gastritis
Acute H pylori infection usually is not detected clinically, but experimental infection results in a clinical syndrome characterized by epigastric pain, fullness, nausea, vomiting, flatulence, malaise, and, sometimes, fever. The symptoms resolve in approximately a week, regardless of whether or not H pylori organisms are eliminated.
Persistence of the organism causes H pylori chronic gastritis, which usually is asymptomatic or may manifest as epigastric pain and, rarely, nausea, vomiting, anorexia, or significant weight loss. Symptoms associated with complications of chronic H pylori–associated atrophic gastritis may develop, including gastric ulcers and gastric adenocarcinoma.
Autoimmune atrophic gastritis
The clinical manifestations of autoimmune atrophic gastritis primarily are related to the deficiency of cobalamin, which is not absorbed adequately because of IF deficiency resulting from severe gastric parietal cell atrophy. The disease has an insidious onset and progresses slowly. Cobalamin deficiency affects the hematological, GI, and neurologic systems.
Hematologic manifestations
The most significant manifestation is megaloblastic anemia, but, rarely, purpura due to thrombocytopenia may develop. Symptoms of anemia include weakness, light-headedness, vertigo and tinnitus, palpitations, angina, and symptoms of congestive heart failure.
GI manifestations
The lack of cobalamin is associated with megaloblastosis of the GI tract epithelium. Patients sometimes complain of a sore tongue. Anorexia with moderate weight loss, occasionally associated with diarrhea may result from the malabsorption associated with megaloblastic changes in the epithelium of the small intestine.
Neurologic manifestations
These result from demyelination, followed by axonal degeneration and neuronal death. The affected sites include peripheral nerves, posterior and lateral columns of the spinal cord, and the cerebrum. Signs and symptoms include numbness and paresthesias in the extremities, weakness, and ataxia. Sphincter disturbances may be present. Mental function disturbances vary from mild irritability to severe dementia or psychosis. Neurologic disease may occur in patients with normal hematocrit and normal red cell parameters.
Anemia
Patients with pernicious anemia have an increased frequency of gastric polyps and have a 2.9-fold increase in gastric cancer.
Additionally, patients with autoimmune atrophic gastritis and H pylori infection may manifest iron deficient anemia that may be refractory to oral iron treatment. H pylori eradication in combination with continued oral iron therapy has been shown to result in a significant increase in hemoglobin levels.
Primary hyperparathyroidism
Massironi et al found evidence of a noncausal association between chronic autoimmune atrophic gastritis (CAAG) and primary hyperparathyroidism (PHPT). In a prospective study, they evaluated the prevalence of PHPT in 107 patients with CAAG and the prevalence of CAAG in 149 patients with sporadic PHPT. The results indicate that PHPT is about three-fold more prevalent in patients with CAAG than in the general population and that CAAG is about four-fold more prevalent in patients with PHPT than in the general population. [17]
Physical Examination
Physical examination is of little contributory value in atrophic gastritis; however, some findings are associated specifically with the complications of H pylori–associated atrophic gastritis and autoimmune atrophic gastritis.
In uncomplicated H pylori–associated atrophic gastritis, clinical findings are few and nonspecific. Epigastric tenderness may be present. If gastric ulcers coexist, guaiac-positive stool may result from occult blood loss.
Findings in a patient with autoimmune atrophic gastritis result from the development of pernicious anemia and neurologic complications.
With severe cobalamin deficiency, the patient is pale and has slightly icteric skin and eyes. The pulse is rapid, and the heart may be enlarged. Auscultation usually reveals a systolic flow murmur.
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Atrophic gastritis. Schematic representation of Helicobacter pylori–associated patterns of gastritis. Involvement of the corpus, fundus, and gastric antrum, with progressive development of gastric atrophy as a result of the loss of gastric glands and partial replacement of gastric glands by intestinal-type epithelium, or intestinal metaplasia (represented by the blue areas in the diagram) characterize multifocal atrophic gastritis. Individuals who develop gastric carcinoma and gastric ulcers usually present with this pattern of gastritis. Inflammation mostly limited to the antrum characterizes antral-predominant gastritis. Individuals with peptic ulcers usually develop this pattern of gastritis, and it is the most frequent pattern in the Western countries.
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Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.
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Atrophic gastritis. Helicobacter pylori–associated chronic active gastritis (Genta stain, 20x). Multiple organisms (brown) are observed adhering to gastric surface epithelial cells. A mononuclear lymphoplasmacytic and polymorphonuclear cell infiltrate is observed in the mucosa.
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Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20x). Intestinal-type epithelium with numerous goblet cells (stained blue with the Alcian blue stain) replace the gastric mucosa and represent gastric atrophy. Mild chronic inflammation is observed in the lamina propria. This pattern of atrophy is observed both in Helicobacter pylori–associated atrophic gastritis and autoimmune gastritis.
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Marked gastric atrophy of the stomach body.
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Severe gastric atrophy of the stomach antrum.
