Atrophic Gastritis (AG) is a chronic condition characterized by long-term inflammation of the stomach lining, which gradually leads to the loss of specialized glandular cells. This cellular loss causes the stomach lining to become thinner, a process called atrophy. The primary consequence of atrophy is a significant reduction in the stomach’s ability to produce hydrochloric acid and intrinsic factor.
The reduced production of these substances impairs food digestion and the absorption of specific micronutrients. AG is categorized into two main forms based on the underlying cause. Environmental Metaplastic Atrophic Gastritis (EMAG) is most often caused by a persistent Helicobacter pylori (H. pylori) infection. Autoimmune Metaplastic Atrophic Gastritis (AMAG) occurs when the immune system mistakenly attacks its own stomach cells, specifically the parietal cells that produce acid and intrinsic factor.
Identifying the Cause and Confirming Diagnosis
The definitive diagnosis of Atrophic Gastritis relies on histological examination. This procedure requires an upper endoscopy, where a flexible tube with a camera is passed into the stomach. The endoscopist takes multiple tissue samples from different areas of the stomach.
Multiple biopsies are essential, typically taken from the stomach’s body, antrum, and incisura, to determine the extent and pattern of atrophy. Microscopic analysis confirms the loss of gastric glands and often reveals Intestinal Metaplasia, where stomach cells resemble intestinal cells. This histological confirmation is the standard for diagnosis.
Blood tests are used alongside endoscopy to help identify the specific cause of AG. Testing for H. pylori antibodies confirms the presence of the environmental form (EMAG), the most common cause globally. For Autoimmune AG (AMAG), blood tests look for antibodies that target the parietal cells or intrinsic factor, confirming immune system involvement.
Blood markers, including pepsinogen I, pepsinogen II, and gastrin-17, indicate the functional state of the stomach lining. Low levels of pepsinogen I, especially when the ratio of pepsinogen I to pepsinogen II is low, suggest atrophy in the stomach body. Elevated gastrin levels indicate the body is attempting to compensate for low stomach acid, which points toward atrophy.
Targeted Medical Treatment Approaches
Treatment for Atrophic Gastritis depends on the cause and focuses on eliminating the trigger and managing nutritional deficiencies. For patients with H. pylori-associated AG, antibiotic eradication requires intervention. This treatment involves a combination of two or three antibiotics and an acid-suppressing medication, such as a proton pump inhibitor, for 10 to 14 days.
Successful eradication of H. pylori is confirmed with a follow-up test, such as a urea breath test or stool antigen test, at least four weeks after treatment. While eliminating the bacteria does not reverse pre-existing atrophy, it halts the progression of chronic inflammation and may reduce the long-term risk of gastric cancer.
Managing nutritional deficiencies is a significant part of the treatment plan, regardless of the cause. The loss of parietal cells reduces intrinsic factor, which is necessary for Vitamin B12 absorption, often leading to pernicious anemia. To bypass the lack of intrinsic factor, patients with confirmed B12 deficiency require intramuscular B12 injections, typically given monthly for life.
High-dose oral B12 supplements may be an option for patients with milder deficiency, as some B12 can be absorbed without intrinsic factor. The low stomach acid environment also impairs iron absorption, leading to iron deficiency anemia. Iron supplementation, often high-dose oral tablets or intravenous infusions, is necessary to restore iron levels.
Daily Strategies for Symptom Management
Managing the symptoms of Atrophic Gastritis involves dietary and lifestyle adjustments aimed at reducing irritation and aiding digestion. A core strategy is shifting from three large meals to five or six smaller, more frequent meals. This approach prevents the stomach from becoming overly full, minimizing common complaints like bloating and early satiety.
Patients should focus on consuming easily digestible foods, such as lean proteins, cooked vegetables, and refined whole grains. Highly fibrous or tough foods should be introduced cautiously, as the low acid environment makes them difficult to break down, leading to discomfort. Paying attention to individual food triggers is important, as tolerance varies.
Limiting or avoiding known gastric irritants reduces inflammation and discomfort. These irritants include:
- Highly acidic foods like tomatoes and citrus juices.
- Spicy, fatty, or fried foods.
- Beverages such as alcohol, carbonated drinks, and high-caffeine coffee and tea.
Lifestyle factors, particularly stress reduction, play a role in symptom management. Avoiding smoking is strongly advised, as tobacco use is a significant irritant to the stomach lining. Probiotic supplements, including those found in fermented foods like yogurt or kefir, may also be beneficial by helping to balance the gut flora in a low-acid environment.
The Importance of Long-Term Monitoring
Atrophic Gastritis requires continuous, long-term monitoring due to its association with the risk of developing gastric cancer. The progression to Intestinal Metaplasia is a precancerous sequence, making regular surveillance necessary. The surveillance protocol is tailored based on the extent and severity of the atrophy.
For individuals with advanced or extensive AG, including Intestinal Metaplasia, periodic follow-up endoscopies are recommended. An endoscopic check-up every three years is suggested for high-risk patients to screen for early signs of cancer or dysplasia. During these procedures, multiple biopsies are taken to assess changes in the stomach lining.
Continuous blood monitoring for nutritional status is a lifelong necessity, especially for those with Autoimmune AG. Serum levels of Vitamin B12 and iron must be checked regularly to ensure replacement therapy is effective. Low levels of these micronutrients indicate a need to adjust the supplementation regimen.
Patients with Autoimmune AG must also be screened for Type 1 gastric neuroendocrine tumors (NETs), which develop due to hormonal changes caused by low stomach acid. Small NETs can be removed endoscopically, requiring more frequent surveillance, sometimes every one to two years. Patients should seek immediate medical attention if they experience sudden, unexplained weight loss, persistent vomiting, or severe abdominal pain.