Chronic gastritis

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.