Celiac disease (CD) is a chronic, immune-mediated disorder of the small intestine triggered by gluten ingestion in genetically susceptible individuals. This condition causes an inflammatory response that damages the small intestinal lining, leading to malabsorption. Gastritis is defined as inflammation of the stomach lining, which can cause symptoms such as upper abdominal pain, nausea, and burning. Research confirms a recognized association between CD and gastritis, indicating that CD is a systemic condition, not solely a digestive one.
The Confirmed Link Between Celiac Disease and Gastritis
Celiac disease is correctly understood as a systemic autoimmune condition, which means the immune dysfunction extends beyond the small intestine to affect other organs. The inflammation triggered by gluten exposure can involve the entire gastrointestinal tract, including the stomach. This systemic nature provides the fundamental link to gastritis.
A shared genetic background and a generalized inflammatory environment contribute to the co-occurrence of these two conditions. Individuals with CD have a heightened risk of developing other autoimmune disorders, and gastritis often presents as one of these associated conditions. The presence of chronic inflammation in the body predisposes the gastric mucosa to damage through similar mechanisms that affect the small intestine.
Types of Gastritis Linked to Celiac Disease
The association between CD and gastritis most commonly manifests in two specific forms: Lymphocytic Gastritis (LG) and Autoimmune Gastritis (AIG). These conditions reflect the systemic nature of Celiac disease, where the immune response targets different parts of the digestive tract.
Lymphocytic Gastritis (LG)
Lymphocytic Gastritis (LG) is strongly associated with CD, often viewed as the gastric equivalent of the small intestine damage. LG is characterized by an abnormal increase in lymphocytes (a type of white blood cell) within the stomach lining. Diagnosis requires pathologists to find at least 25 lymphocytes per 100 epithelial cells. This immune-mediated response mirrors the damage pattern in the small intestine. LG often improves significantly once a patient adheres to a strict gluten-free diet (GFD), and its severity correlates with villous atrophy in the duodenal biopsy.
Autoimmune Gastritis (AIG)
Autoimmune Gastritis, sometimes referred to as Autoimmune Atrophic Gastritis, represents the body attacking its own stomach cells. Specifically, the immune system produces autoantibodies that target the parietal cells, which are responsible for producing stomach acid and intrinsic factor. The destruction of these cells leads to a decrease in stomach acid production and, critically, a deficiency in intrinsic factor. Intrinsic factor is necessary for the absorption of Vitamin B12, so its lack can result in pernicious anemia, a form of B12 deficiency.
While AIG is less frequently reported than LG in CD patients, it represents a more complex, long-term autoimmune issue. This form of gastritis does not typically improve with a GFD alone because the autoimmune attack is directed against the parietal cells, not immediately against gluten itself.
Diagnosing Gastritis in Celiac Patients
Identifying gastritis in a patient with Celiac disease often occurs if symptoms persist despite strict adherence to a GFD. The gold standard for confirming the diagnosis is an upper endoscopy with a biopsy of the stomach lining. This procedure allows the physician to visually inspect the gastric mucosa and take tissue samples for microscopic analysis.
The biopsy differentiates the specific type of gastritis, such as identifying the increased intraepithelial lymphocytes characteristic of LG. For suspected AIG, blood tests for specific autoantibodies, like anti-parietal cell antibodies, are ordered. Assessment of Vitamin B12 and iron levels is also performed, as deficiencies are common consequences of AIG-related malabsorption.
Treatment and Long-Term Management
The foundational treatment for any CD patient with co-occurring gastritis is lifelong, strict adherence to a Gluten-Free Diet (GFD). For patients with LG, the GFD alone is often sufficient to resolve the inflammation, as it calms the systemic immune response and allows the gastric mucosa to heal. For AIG, management focuses on addressing the consequences of parietal cell destruction, requiring regular B12 supplementation, usually via injection. Medications like Proton Pump Inhibitors (PPIs) may relieve persistent symptoms in non-AIG cases.
Because AIG causes chronic atrophy of the stomach lining, patients require long-term surveillance due to an elevated risk of complications. This monitoring involves periodic endoscopies to screen for the development of gastric carcinoid tumors or adenocarcinoma.