What are the clinical findings and treatment options for acute and chronic gastritis in patients with a history of Helicobacter pylori (H. pylori) infection, Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) use, or alcohol use?

Clinical Findings in Acute and Chronic Gastritis

Acute Gastritis Clinical Presentation

Acute gastritis typically presents with sudden onset epigastric pain, nausea, vomiting, and may be associated with hematemesis or melena in severe erosive cases. 1 The condition is often triggered by NSAIDs, alcohol, or stress, and symptoms develop rapidly over hours to days.

Key Clinical Features:

• Epigastric pain or discomfort that is typically burning in nature and may worsen with eating 1
• Nausea and vomiting, which may contain blood in erosive gastritis 1
• Loss of appetite and early satiety 1
• Upper gastrointestinal bleeding manifesting as hematemesis or melena in severe erosive cases 1

Etiologic Associations:

• NSAID use is a major cause, with up to 25% of chronic NSAID users experiencing upper gastrointestinal adverse effects 2
• Alcohol consumption can cause acute gastric injury, though it does not typically induce inflammatory cell infiltrate without concurrent H. pylori infection 3
• H. pylori infection is found in approximately 70% of patients with dyspepsia and gastritis in European populations 2

Chronic Gastritis Clinical Presentation

Chronic gastritis is often asymptomatic or presents with vague, persistent dyspeptic symptoms including epigastric discomfort, bloating, and early satiety that persist for weeks to months. 2 The condition is characterized by histologic inflammation and may progress to atrophic gastritis and intestinal metaplasia.

Key Clinical Features:

• Persistent dyspepsia with epigastric discomfort, bloating, and postprandial fullness 2
• Often asymptomatic until complications develop, particularly in H. pylori-associated chronic gastritis 2
• Symptoms may be minimal despite significant histologic changes on endoscopy 4

Histologic Patterns and Disease Associations:

• Antral-predominant gastritis is associated with duodenal ulcer diathesis 2
• Corpus-predominant gastritis, especially with multifocal atrophy, increases risk of gastric ulcer and carcinoma 2
• Chronic atrophic gastritis accelerates with long-term PPI use in H. pylori-positive patients, progressing to corpus-predominant pattern 2

H. pylori-Associated Gastritis

H. pylori infection is present in at least 70% of gastritis cases in European populations and is the primary cause of chronic active gastritis. 2 The infection causes characteristic acute-on-chronic inflammation with specific histologic patterns.

Clinical Significance:

• CagA-positive strains (present in 70% of European H. pylori infections) are associated with increased risk for peptic ulcer disease, atrophic gastritis, and gastric cancer 2
• Lifetime risk of peptic ulcer is approximately 17% (1 in 6) among those with H. pylori infection 2
• Gastric cancer risk varies from 0.6% to 22% lifetime risk depending on geographic location and strain virulence 2

Diagnostic Findings:

• Histology reveals acute-on-chronic inflammation with organisms easily detected using immunohistochemistry 2
• Non-invasive testing with urea breath test or monoclonal stool antigen test is preferred for diagnosis 2, 4
• Serology is no longer recommended as it remains positive after eradication and cannot confirm treatment success 5

NSAID-Associated Gastritis

NSAID use increases the risk of both uncomplicated and complicated gastroduodenal ulcers, with H. pylori infection providing an additive two- to fourfold increased risk. 2

Clinical Features:

• Gross gastric injury occurs with NSAIDs but without inducing inflammatory cell infiltrate unless H. pylori is present 3
• Gastric ulcers are more common than duodenal ulcers with NSAID use 3
• Risk factors include prior ulcer history (strongest predictor), age >60 years, cardiovascular disease, and concomitant use of aspirin, steroids, or anticoagulants 2

Risk Stratification:

• Low risk (no risk factors): 0.8% annual incidence of complications 2
• Moderate risk (1-2 risk factors): 2% annual incidence 2
• High risk (3+ risk factors): 7.6-8.6% annual incidence 2
• Very high risk (prior ulcer complications): 18% annual incidence 2

Alcohol-Associated Gastritis

Alcohol itself does not cause chronic gastritis; rather, gastritis in alcoholics is primarily due to concurrent H. pylori infection. 6, 7 H. pylori is found in 14 of 18 (78%) alcoholics with dyspepsia and chronic antral gastritis. 6

Key Findings:

• Controlled abstinence for 3-4 weeks does not change histologic findings, indicating alcohol is not the primary causative agent 6
• H. pylori eradication results in almost complete normalization of histology and significant symptom improvement 6
• Gastric alcohol metabolism produces acetaldehyde, a toxic metabolite, while H. pylori breaks down urea to ammonia, another toxic product 7
• Paradoxically, daily alcohol consumption (4-60g pure ethanol) appears to improve H. pylori eradication rates compared to abstinence (100% vs 70.1%), though the mechanism is unclear 8

Autoimmune Gastritis

Autoimmune gastritis presents with corpus-predominant atrophic gastritis and is associated with vitamin B12 and iron deficiencies. 1, 4

Diagnostic Features:

• Antiparietal cell antibodies and anti-intrinsic factor antibodies are present 1, 4
• Vitamin B12 deficiency and iron deficiency anemia are common complications 1, 4
• Associated autoimmune disorders, particularly autoimmune thyroid disease, should be screened 1
• Surveillance endoscopy every 3 years is recommended for advanced atrophic gastritis due to increased gastric cancer risk 1, 4

Critical Diagnostic Pitfalls to Avoid

• Testing for H. pylori while on PPIs causes false-negative results; patients must be off PPIs for at least 2 weeks before testing 4, 5
• Relying on serology alone is inadequate as it remains positive after eradication 5
• Assuming alcohol causes chronic gastritis when H. pylori is the actual culprit in most cases 6, 3
• Failing to assess vitamin B12 and iron status in patients with atrophic gastritis leads to inadequate management 1
• Not screening first-degree relatives of gastric cancer patients, who have 2-3 times increased risk 4, 5