Atrophic gastritis is a chronic inflammatory condition affecting the stomach’s inner lining. This leads to a gradual thinning of the gastric mucosa. As the lining thins, specialized glandular cells are lost and replaced by fibrous tissue or intestinal-like cells. This alteration can impair the stomach’s ability to function properly.
Understanding Atrophic Gastritis
In atrophic gastritis, gastric glandular cells are lost. These cells are replaced by intestinal-type cells (metaplasia) or by fibrous tissues. This cellular transformation impairs the stomach’s capacity to secrete essential substances like hydrochloric acid, pepsin, and intrinsic factor, which are important for digestion and nutrient absorption.
Atrophic gastritis primarily stems from two main causes: Helicobacter pylori (H. pylori) infection and autoimmune atrophic gastritis. H. pylori is a bacterium that infects the stomach lining, disrupting its protective mucus barrier, leading to chronic inflammation and cell destruction. Autoimmune atrophic gastritis occurs when the body’s immune system mistakenly attacks healthy stomach cells, especially those producing stomach acid and intrinsic factor.
Symptoms include indigestion, abdominal pain, nausea, vomiting, loss of appetite, or unexplained weight loss. Individuals may also experience nutrient deficiency symptoms, such as fatigue and brittle nails from iron deficiency, or neurological issues and palpitations from vitamin B12 deficiency. These symptoms arise because the impaired stomach lining struggles to absorb nutrients effectively.
The Question of Reversibility
Complete reversal of true glandular atrophy is not expected. However, the progression of atrophic gastritis can often be halted. Associated inflammation or earlier changes like intestinal metaplasia may be managed or prevented from worsening, especially when the underlying cause is addressed.
For atrophic gastritis caused by H. pylori infection, eradicating the bacteria can stop the disease’s progression. In some instances, particularly in earlier stages, treating the infection can lead to a regression of inflammation and even partial restoration of glandular function. While the stomach lining might not return to its original state, its deterioration can be slowed or arrested.
In contrast, for autoimmune atrophic gastritis, the atrophy of the stomach glands is not reversible, as it results from the body’s immune system attacking its own cells. Management focuses on addressing complications and preventing further damage rather than reversing the atrophy itself. This underscores the distinct management strategies needed for different causes.
Management and Treatment Strategies
Once atrophic gastritis is diagnosed, treatment focuses on addressing underlying causes and managing resulting complications. For H. pylori-induced atrophic gastritis, eradication therapy is prescribed, involving a combination of antibiotics and proton pump inhibitors (PPIs). These medications eliminate the bacterial infection and reduce stomach acid, promoting stomach lining healing. Treatment regimens often last between 10 to 14 days.
For autoimmune atrophic gastritis, management centers on addressing complications like vitamin B12 deficiency, which can lead to pernicious anemia. This often involves lifelong vitamin B12 supplementation, usually through injections, as oral absorption may be impaired due to the lack of intrinsic factor. Iron supplementation may also be needed for iron deficiency anemia, which can occur due to reduced stomach acid affecting iron absorption.
Lifestyle adjustments can help manage symptoms and support stomach health. Avoiding irritants like excessive alcohol, nonsteroidal anti-inflammatory drugs (NSAIDs), and spicy or fried foods can reduce irritation to the stomach lining. Adopting a balanced diet rich in fruits, vegetables, whole grains, and lean proteins, and eating smaller, more frequent meals, can help minimize symptoms and promote healing.
Monitoring and Long-Term Outlook
Regular follow-up is important for individuals with atrophic gastritis due to an increased risk of gastric cancer, especially when intestinal metaplasia or dysplasia is present. Endoscopic surveillance with biopsies is a recommended monitoring method, involving visual examination of the stomach lining and collection of tissue samples for microscopic analysis to detect concerning changes.
The frequency of endoscopic surveillance varies based on individual risk factors, such as the extent of atrophy, the presence of intestinal metaplasia, family history of gastric cancer, and ethnicity. For advanced atrophic gastritis, endoscopy every three years is often recommended. For those with intestinal metaplasia, annual endoscopic follow-up is a common recommendation.
While the atrophy itself might be permanent, effective management can prevent complications and improve quality of life. Early detection and treatment of any underlying H. pylori infection can significantly reduce the risk of gastric cancer progression. Ongoing monitoring for nutrient deficiencies and endoscopic surveillance contribute to a better long-term outlook by allowing for timely intervention if precancerous changes develop.