Complications
Your Organizational Guidance
ebpracticenet urges you to prioritize the following organizational guidance:
MaagklachtenPublished by: NHGLast published: 2025Patients infected with Helicobacter pylori have a two- to sixfold increased risk of developing gastric cancer and mucosal associated-lymphoid-type lymphoma compared with their uninfected counterparts.[22] One large retrospective cohort study from the US found that the risk of gastric cancer was especially higher among racial and ethnic minorities and smokers who were infected with H pylori.[63] 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.[70][106]
Suspicious features suggestive of upper gastrointestinal malignancy include bleeding, anemia, early satiety, unexplained weight loss (>10% body weight), progressive dysphagia, odynophagia, or persistent vomiting.[40]
Patients with autoimmune gastritis may also be at higher risk for developing gastric neuroendocrine tumors and gastric adenocarcinoma.[57]
Endoscopy confirms presence of gastric carcinoma.
Treatment with total/subtotal gastrectomy and/or chemotherapy is required.
Patients with atrophic gastritis, in particular if pernicious anemia is present, are at risk of gastric carcinoids.[103][104]
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.
Patients infected with Helicobacter pylori have a two- to sixfold increased risk of developing gastric cancer and mucosal associated-lymphoid-type lymphoma compared with their uninfected counterparts.[22]
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.[31]
Atrophic or autoimmune gastritis, chronic Helicobacter pylori infection, achlorhydria, and impaired metabolism secondary to H2 antagonists/proton-pump inhibitors (PPIs) 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.
Use of this content is subject to our disclaimer