Overview
This lecture reviews autoimmune gastritis (AIG), focusing on its epidemiology, risk factors, clinical manifestations, diagnosis, complications, and management strategies, including connections to pernicious anemia.
Definition and Pathogenesis
- Autoimmune gastritis (AIG) is chronic inflammation triggered by immune destruction of gastric parietal cells.
- AIG leads to atrophy and metaplasia of the gastric oxyntic mucosa, impacting acid and intrinsic factor production.
- Genetic predisposition (HLA haplotypes) and environmental factors, possibly including H. pylori, contribute to pathogenesis.
- T-cell-mediated immunity targets parietal cells; autoantibodies (PCA, IF antibodies) may be present.
Epidemiology and Risk Factors
- Prevalence estimates are 0.1–12%, higher in women and older adults (>60 years).
- AIG is more common with other autoimmune diseases, especially autoimmune thyroiditis and type 1 diabetes mellitus (risk up to 35x general population).
Diagnosis
- Often delayed due to nonspecific or absent symptoms.
- Gold standard: upper endoscopy with gastric biopsies (Sydney protocol) and histology showing oxyntic atrophy.
- Endoscopic findings: loss of rugal folds, pale/thinned mucosa, visible vessels, possible polyps or tumors.
- Serology: PCA and IF antibodies are supportive but neither sensitive nor specific alone.
- Pepsinogen I/II ratio may indicate corpus atrophy but has variable usefulness.
Clinical Manifestations
- Frequently asymptomatic; most common complaint is dyspepsia (post-meal discomfort).
- Anemia is common (about 50%), may be microcytic, normocytic, or macrocytic (classic is macrocytic from B12 deficiency).
- Iron deficiency often precedes B12 deficiency due to loss of gastric acid.
- B12 deficiency can cause irreversible neurologic deficits, infertility, and recurrent miscarriages.
- Concomitant micronutrient deficiencies (vitamin D, folate) occur.
- Frequently associated with other autoimmune diseases (thyroiditis, type 1 diabetes, Addison’s, vitiligo).
Complications
- AIG/PA is a preneoplastic condition, increasing risks for gastric adenocarcinoma and type-1 neuroendocrine tumors (NETs).
- Advanced atrophy/metaplasia is associated with greatest neoplasia risk.
- Risk of cancer is highest within the first year after PA diagnosis, with continued elevated risk thereafter.
Clinical Management
- Endoscopic surveillance is recommended every 3–5 years, especially in high-risk patients, but the optimal interval is unclear.
- Baseline endoscopy with biopsies and NET screening should be performed after AIG or PA diagnosis.
- Management includes lifelong monitoring and parenteral vitamin B12 and iron supplementation as needed.
- Address and monitor for concomitant autoimmune conditions and other micronutrient deficiencies.
Key Terms & Definitions
- Autoimmune Gastritis (AIG) — Chronic inflammation where the immune system destroys stomach parietal cells.
- Parietal Cells — Stomach cells producing acid and intrinsic factor.
- Intrinsic Factor (IF) — A protein necessary for vitamin B12 absorption.
- Pernicious Anemia (PA) — Megaloblastic anemia due to vitamin B12 deficiency from lack of IF.
- Parietal Cell Antibodies (PCA) — Autoantibodies targeting parietal cells, often present in AIG.
- Neuroendocrine Tumor (NET) — Tumor arising from hormone-producing gastric cells.
- Oxyntic Mucosa — Acid-secreting lining of the stomach body/fundus.
Action Items / Next Steps
- Review and understand the Sydney protocol for gastric biopsy sampling.
- Be able to recognize clinical presentations and risk factors for AIG and PA.
- Know the recommended surveillance and nutritional monitoring strategies for AIG patients.
- Complete any assigned readings on guidelines for atrophic gastritis or autoimmune disease associations.