Chronic gastritis

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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.

Description

  • 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.

ICD-9 codes

  • 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.

Incidence

  • 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

Complications

  • 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

Presentation

  • 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.

Rule out

  • 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
  • Histology
  • Culture
  • 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

Treatment

  • 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

Prevention

  • Avoid causative agent (NSAIDs, alcohol, tobacco).

For references, see www.dynamicmedical.com.

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