Complications
Untreated or treatment-refractory gastritis associated with Helicobacter pylori infection may predispose to gastric and duodenal ulcers, as well as gastric adenocarcinoma.[4] In populations at high risk of gastric cancer, H pylori screening and treatment is a recommended gastric cancer risk reduction strategy. These may be identified with a family history of gastric cancer and/or low serum pepsinogens reflecting gastric atrophy.[62][92]
One systematic review and meta-analysis demonstrated that eradication of H pylori infection was associated with a reduced incidence of gastric cancer.[93] Another randomized controlled trial found that H pylori treatment in patients with early gastric cancer resulted in lower rates of metachronous gastric cancer and greater improvement in gastric corpus atrophy than in patients who received placebo.[94] Suspicious features suggestive of upper gastrointestinal malignancy include bleeding, anemia, early satiety, unexplained weight loss (>10% body weight), progressive dysphagia, odynophagia, or persistent vomiting.[33]
Endoscopy confirms presence of gastric carcinoma.
Treatment with total/subtotal gastrectomy and/or chemotherapy is required.
Eradication rates did not differ between gastric cancer patients with H pylori infection (n = 150) who were randomized to standard triple therapy preoperatively or postoperatively (68.6% versus 69.4%; p = 1.00).[95]
Patients with atrophic gastritis, in particular if pernicious anemia is present, are at risk of gastric carcinoids.[89][90]
Tumors are generally asymptomatic but may present with abdominal pain and bleeding.
Endoscopy may show small localized multiple polypoid tumors. Treatment is endoscopic surgical excision.
Untreated or treatment-refractory gastritis associated with Helicobacter pylori infection may predispose to gastric mucosa-associated lymphoid tissue (MALT) lymphoma.[4]
Tumors may present with increasing epigastric pain, weight loss, and occult or overt gastrointestinal bleeding.
Treatment is eradication of H pylori infection, radiation therapy, and chemotherapy.
Atrophic gastritis as a consequence of Helicobacter pylori infection, longstanding gastric mucosal inflammation, and autoimmune gastritis may cause achlorhydria (decreased/absent production of hydrochloric acid) and decreased intrinsic factor production due to a decrease in the parietal cell mass. Consequently, impaired absorption of vitamin B₁₂, iron, and calcium may occur.
Clinical presentation may include lethargy, weakness, and pallor as a consequence of vitamin B₁₂ deficiency or iron deficiency.
Replacement therapy with cyanocobalamin, iron, calcium, and vitamins C and D may be required.[25]
Atrophic or autoimmune gastritis, chronic Helicobacter pylori infection, achlorhydria, and impaired metabolism secondary to H₂ antagonists/proton-pump inhibitors reduce vitamin B₁₂ absorption and may also result in overt vitamin B₁₂ deficiency.
Clinical presentation may include altered reflexes or sensory deficits, cognitive impairment, and angular cheilitis or atrophic glossitis.
Replacement therapy with cyanocobalamin is required.
Untreated or treatment-refractory gastritis associated with Helicobacter pylori infection and/or nonsteroidal anti-inflammatory drug (NSAID) use may progress to peptic ulcer disease. Factors that have been identified as placing patients at increased risk for NSAID-related gastrointestinal (GI) complications include prior history of a GI event (ulcer, hemorrhage), age >60 years, high dosage of NSAID, and concurrent use of corticosteroids or anticoagulants.
Patients may develop occult or overt GI bleeding. Perforation may occur presenting with clinical features of shock and/or peritonitis.
Endoscopic ligation of bleeding ulcer may be necessary.
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