Chronic Gastritis Clinical Presentation

H pyloriinfection

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 about 1 week, regardless of whether the organism is eliminated.

Persistence of the organism causes H pylori chronic gastritis, which is usually asymptomatic but may manifest as gastric pain or, rarely, with nausea, vomiting, anorexia, or significant weight loss. Symptoms may occur with the development of complications of chronic H pylori gastritis, which include peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma.

Autoimmune gastritis

The clinical manifestations of autoimmune gastritis are primarily related to the deficiency in cobalamin, which is not adequately absorbed because of intrinsic factor (IF) deficiency resulting from severe gastric parietal cell atrophy. The disease has an insidious onset and progresses slowly. Cobalamin deficiency affects the hematologic, gastrointestinal (GI), and neurologic systems.

The most significant hematologic manifestation is megaloblastic anemia, but on rare occasions, purpura due to thrombocytopenia may develop. Symptoms of anemia include weakness, light-headedness, vertigo and tinnitus, palpitations, angina, and symptoms of congestive failure.

The main GI manifestation is megaloblastosis of the GI tract epithelium, which is associated with the lack of cobalamin. Patients sometimes report having a sore tongue. Anorexia with moderate weight loss that is occasionally associated with diarrhea may result from malabsorption associated with megaloblastic changes of the small intestinal epithelial cells.

Neurologic manifestations result from demyelination, followed by axonal degeneration and neuronal death. Affected sites include the peripheral nerves, posterior and lateral columns of the spinal cord, and cerebrum. Signs and symptoms include numbness and paresthesias in the extremities, weakness, and ataxia. Sphincter disturbances may occur. Mental function disturbances range from mild irritability to severe dementia or psychosis. Neurologic disease may occur in a patient with hematocrit and red cell parameters within the reference range.

Patients with pernicious anemia have an increased frequency of gastric polyps and gastric carcinoid and a 2.9-fold increase in the frequency of gastric cancer.

Granulomatous gastritis

In multisystemic diseases, specific symptoms related to gastric involvement may be minor. Caseating granulomas secondary to tuberculosis may be found in the absence of lung disease in patients who are malnourished, immunosuppressed, or alcoholic.

Patients with Crohn disease and gastric involvement may report gastric pain, nausea, and vomiting. Gastric involvement in Crohn disease is almost invariably associated with intestinal disease, and intestinal manifestations predominate.

Sarcoidosis of the stomach is usually associated with granulomatous inflammation in other locations, especially the lungs, hilar nodes, or salivary glands. About 10% of patients with sarcoid involvement in the stomach are asymptomatic. Patients who are symptomatic present with gastric ulcers, hemorrhage, pyloric stricture, and gastric outlet obstruction.

Idiopathic isolated granulomatous gastritis

The diagnosis of idiopathic isolated granulomatous gastritis is established only when known entities associated with granulomas are excluded. Patients who are symptomatic usually are older than 40 years at presentation and have epigastric pain, weight loss, and vomiting secondary to pyloric obstruction.

Lymphocytic gastritis

Lymphocytic gastritis mostly affects middle-aged or elderly patients. It may be associated with chronic H pylori infection, gluten-sensitive enteropathy, and Menetrier disease. It may represent a hypersensitivity reaction involving the gastric body. Lymphocytic gastritis has been described as complicating MALT lymphoma and gastric carcinoma.

Eosinophilic gastroenteritis

Some patients with eosinophilic gastroenteritis have underlying connective tissue disorders. Those with predominant mucosal involvement may report nausea, vomiting, and abdominal pain related to ingestion of specific foods. Those with involvement of the muscularis propria and resulting thickening and rigidity may present with outlet obstruction symptoms. Many patients have a history of allergy, peripheral eosinophilia, asthma, eczema, or food sensitivity. Some respond to removal of these items from the diet, and steroid treatment is often helpful.

Gastritis in graft versus host disease

Graft versus host disease (GVHD) follows allogeneic bone marrow transplantation or transfusions, especially in patients who are immunocompromised. Patients with isolated gastric GVHD have symptoms of nausea, vomiting, and upper abdominal pain without diarrhea.^[20]

The physical examination contributes relatively little to the assessment and management of chronic gastritis. However, some findings are specifically associated with the particular complications of H pylori– associated gastritis and autoimmune gastritis.

In uncomplicated H pylori– associated atrophic gastritis, clinical findings are few and nonspecific. Epigastric tenderness may exist. If gastric ulcers coexist, guaiac-positive stool may result from occult blood loss. Bad breath (ie, halitosis) and abdominal pain or discomfort may occur, with bloating associated with bacterial overgrowth syndrome.

Physical findings may result from the development of pernicious anemia and neurologic complications in patients with autoimmune atrophic gastritis. 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.