Gastritis is the general term for inflammation of the stomach lining, which can arise from various causes, including infection or injury. When the immune system mistakenly targets the body’s own tissues, it causes autoimmune gastritis (AIG). This process involves the body’s defenses attacking healthy cells within the stomach. Understanding this immune system misdirection helps recognize the specific diseases that lead to this chronic form of stomach inflammation.
Autoimmune Gastritis: The Primary Mechanism
Autoimmune Gastritis (AIG) is a chronic inflammatory condition of the stomach’s inner lining. The immune system attacks the parietal cells, specialized cells located in the stomach’s corpus and fundus. These cells produce hydrochloric acid and intrinsic factor (IF). The immune attack often targets the gastric proton pump (H+/K+-ATPase) found on the parietal cells.
The progressive destruction of parietal cells leads to a loss of both acid and intrinsic factor production. This loss of function has biological consequences. Hydrochloric acid is necessary for nutrient absorption, and its absence can cause malabsorption of inorganic iron.
Intrinsic factor is necessary for the body to absorb Vitamin B12 in the small intestine. When the immune system destroys the parietal cells and intrinsic factor, the body cannot absorb B12 from the diet, leading to a deficiency. This specific B12 deficiency is known as pernicious anemia, a common, late-stage outcome of AIG. Autoantibodies also directly target the intrinsic factor, further blocking B12 absorption.
Related Systemic Autoimmune Conditions
While AIG is the direct cause, it rarely occurs in isolation, as autoimmune conditions often cluster together. Several systemic autoimmune conditions share a genetic or immune predisposition with AIG, increasing the likelihood of co-occurrence. The most frequent co-occurring condition is autoimmune thyroid disease, especially Hashimoto’s thyroiditis. Studies show AIG is present in up to 40% of patients with this thyroid disorder.
Type 1 Diabetes Mellitus also has a documented association with AIG, suggesting a common immune vulnerability across different organs. Other systemic conditions linked to AIG include Addison’s disease, myasthenia gravis, vitiligo, and Sjögren’s syndrome. While these conditions do not directly cause stomach inflammation, their presence signals that the immune system is prone to attacking its own tissues, making AIG screening important.
While Celiac Disease is an autoimmune condition affecting the gut, some research suggests it may not increase the risk of AIG. The clustering of autoimmune diseases emphasizes the need for comprehensive screening once any single autoimmune disorder is diagnosed.
Symptoms and Diagnostic Procedures
The symptoms of AIG are often non-specific and can be mistaken for other common digestive issues. Early symptoms include upper abdominal pain, bloating, or a feeling of fullness after eating. As the disease progresses and leads to Vitamin B12 deficiency, the symptoms become systemic and related to pernicious anemia.
Symptoms related to B12 deficiency include fatigue, weakness, paleness, and shortness of breath due to anemia. Neurological issues can also develop, such as sensory changes, tingling or numbness in the hands and feet (paresthesia), balance problems, and difficulty with thinking. The tongue may also become sore and inflamed (glossitis).
Diagnosis relies on a combination of blood tests and procedural examination. Blood tests check for low Vitamin B12 levels and high levels of gastrin, a hormone produced in excess to stimulate acid production. Blood work screens for specific autoantibodies, including anti-parietal cell antibodies (APCA) and anti-intrinsic factor antibodies (IFA), which confirm the autoimmune nature of AIG. The most definitive procedure is an endoscopy with a biopsy, where a tissue sample is taken from the stomach lining to confirm chronic inflammation and atrophy of the corpus and fundus.
Long-Term Management and Monitoring
Since the damage to the acid- and intrinsic factor-producing parietal cells is typically permanent, AIG management focuses on correcting nutritional deficiencies. The primary treatment is lifelong Vitamin B12 supplementation, often administered through regular injections to bypass the damaged absorption mechanism. High-dose oral B12 supplements may be used in some cases, but injections are frequently required for adequate absorption.
Monitoring tracks B12 levels and other complications, particularly iron deficiency, which is common due to the lack of stomach acid. Patients often require iron supplementation to prevent or treat iron deficiency anemia. A long-term concern with AIG is the increased, albeit low, risk of developing gastric carcinoid tumors or gastric adenocarcinoma (a type of stomach cancer). Ongoing endoscopic surveillance is generally recommended to monitor the atrophic stomach lining and detect precancerous changes or early malignancies.