Gastritis, Atrophic Clinical Presentation

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.

• 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 H pylori organisms are eliminated.
• Persistence of the organism causes H pylori chronic gastritis, which usually is asymptomatic or may manifest as gastric 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 clinical manifestations primarily are related to deficiency in 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 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 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.
  • Pernicious 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 was shown to result in a significant increase in hemoglobin levels.

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.

Atrophic gastritis usually is associated with either chronic H pylori infection or with autoimmune gastritis. The environmental subtype of atrophic gastritis corresponds mostly with H pylori– associated atrophic gastritis, although other unidentified environmental factors may play a role in the development of gastric atrophy.

• Chronic gastritis caused by H pylori infection of the stomach

  • H pylori infection of the stomach is by far the most common cause of chronic atrophic gastritis.
  • Whether H pylori infection follows the multifocal atrophic gastritis pathway or the nonatrophic antral gastritis pathway may be related to genetic susceptibility factors, environmental factors that modulate the host-bacterial interaction, or bacterial strains.
  • Although H pylori possessing the cag (cytotoxin-associated gene) pathogenicity island have been shown to have increased virulence, to cause higher levels of mucosal inflammation, and to be present more frequently in individuals infected with H pylori who develop gastric cancer, no specific virulence factors have been identified that might be useful to predict specific H pylori disease outcome.
  • Host factors or the effects of other environmental agents are likely to be the determinant elements modulating patterns of disease progression. For example, family relatives of individuals with gastric cancer develop pangastritis more frequently in response to H pylori infection and they also develop multifocal intestinal metaplasia more often, a preneoplastic lesion of the stomach and a component of H pylori– associated atrophic gastritis.
• Autoimmune atrophic gastritis

  • Autoimmune atrophic gastritis is a type of chronic atrophic gastritis limited to corpus-fundus mucosa and characterized by marked diffuse atrophy of parietal and chief cells.
  • Autoimmune gastritis is associated with serum antiparietal and anti-IF antibodies that cause IF deficiency, which, in turn, causes decreased availability of cobalamin and, eventually, pernicious anemia in some patients.
  • In some families, the disease appears to be transmitted with an autosomal dominant pattern of inheritance.