Dr. Stanley is a pathologist in private practice in Nobleboro, Maine, and an editor for DynaMed. Dr. Brown is a neurologist and deputy editor for DynaMed (www.dynamicmedical.com), a database of comprehensive updated summaries covering nearly 3,000 clinical topics.
- Chronic inflammation of stomach
- Clinical, radiologic, and pathologic classifications are controversial, numerous, and inconsistent.
- Pathologic findings may include inflammation, atrophy, and/or metaplasia.
- Clinical concerns are predisposition to cancer and chronic symptoms.
- 535.1 Atrophic gastritis
- 535.2 Gastric mucosal hypertrophy
- 535.3 Alcoholic gastritis
- 535.4 Other specified gastritis
- 535.5 Unspecified gastritis and gastroduodenitis
- All codes have subcategories to indicate the presence or absence of hemorrhage.
- Increases with age and may be higher in certain populations (Japanese, Italians)
- Up to 25% incidence reported in endoscopic screening studies
- Up to 63% incidence reported in symptomatic patients having endoscopy
Types and causes
- Nonatrophic gastritis (also called superficial gastritis, diffuse antral gastritis, chronic antral gastritis, Type B gastritis, interstitial-follicular gastritis, hypersecretory gastritis)—may be caused by Helicobacter pylori or other factors
- Atrophic gastritis (also called Type A gastritis, Type AB gastritis, diffuse corporal gastritis, pernicious anemia-associated gastritis, metaplastic gastritis, environmental gastritis)—may be caused by autoimmunity, H. pylori, dietary or possibly environmental factors
- H. pylori—lives in mucus, is noninvasive
- Treatment with omeprazole (Prilosec, others) may be associated with development of atrophic gastritis in H. pylori-positive patients.
- Special types of chronic gastritis:
- Chemical (also called reactive gastritis, reflux gastritis, NSAID gastritis, Type C gastritis): bile, alcohol, nonsteroidal anti-inflammatory drugs (NSAIDs)
- Radiation injury-induced
- Lymphocytic (also called varioliform gastritis, celiac disease-associated gastritis): gluten, celiac disease, drugs (ticlopidine)
- Noninfectious granulomatous: Possible causes are autoimmune diseases, such as Crohn’s disease, sarcoidosis, Wegener’s granulomatosis, and other vasculitides
- Eosinophilic or allergic gastritis
- Increased (but low) risk of gastric malignancies
- Little to no risk in patients with simple nonatrophic
- H. pylori gastritis, except possibly in direct relatives of patients with gastric cancer
- Risk in patients with atrophic gastritis appears related to extent and distribution of atrophic areas.
- Impaired vitamin B12 absorption
- Associated conditions:
- Autoimmune disorders
- Gastric polyps
- Gastric atrophy
- Gastric or duodenal ulcer
- Often asymptomatic
- Symptoms may include abdominal pain, bloating, reflux, nausea, vomiting.
- Ask about prior H. pylori infection, alcohol use, NSAIDs, steroids, chemotherapeutic agents.
Making the diagnosis
- Based on five or six endoscopic biopsies from corpus, antrum, and incisura, as the inflammatory and atrophic processes have different phenotypic expression in different regions of stomach.
- Gastric peptic ulcer disease
- Gastric carcinoma
- Gastric lymphoma
- Pernicious anemia (B12 deficiency)
- Ischemic gastritis
Testing to consider
- For diagnosis of H. pylori infection:
- Noninvasive tests
- Serum and urine antibody testing
- Urea breath test
- Stool antigen:
- Invasive tests on biopsy specimen
- Rapid urease test
- Tests for pernicious anemia (e.g., atrophic gastritis)
- Complete blood count, B12 level, folate level (B12 may be falsely low if severe folate deficiency)
- Anti-intrinsic factor antibody
- Anti-gastric parietal cell antibody
- Serum gastrin level:
- Biopsy at time of endoscopy
- Two antral biopsies
- Two corpus biopsies
- One or more additional biopsies from incisura
- Additional biopsies from any visible lesion or to determine extent or distribution of dysplasia
- Discontinue causative or exacerbating factors
- H. pylori eradication:
- Established drug regimen, e.g., with proton-pump inhibitor (lansoprazole 30 mg b.i.d.), amoxicillin 1 g b.i.d., and clarithromycin 500 mg b.i.d. for 7-14 days
- May decrease symptoms in patients with nonulcer dyspepsia
- Inconsistent evidence of effect on intestinal metaplasia
- May decrease gastritis in multiple clinical settings
- Medications for chronic gastritis:
- Bismuth compounds have limited evidence for histologic improvement of gastritis and inconsistent evidence for symptomatic improvement.
- Limited evidence for acid-suppression therapy in duodenal ulcer-associated chronic gastritis
- Sucralfate (Carafate) has limited inconsistent evidence
- Misoprostol (Cytotec) 200 mg p.o. b.i.d. may decrease symptoms of gastritis
- Ursodeoxycholic acid (Actigall) 1,000 mg daily may decrease symptoms of bile reflux gastritis
- Various antioxidants and Chinese herbs reported to be beneficial in patients with chronic gastritis
- Avoid causative agent (NSAIDs, alcohol, tobacco).
For references, see www.dynamicmedical.com.