- Gastritis refers to inflammation of the stomach lining, or gastric mucosa. It encompasses a spectrum of conditions ranging from acute irritation to chronic inflammation, which can result in mucosal atrophy, metaplasia, or even progression to gastric cancer.
- Gastritis may be either acute or chronic, and it can arise from various causes including infection, autoimmune processes, chemical irritants, and systemic diseases. The condition is frequently underdiagnosed due to its often subtle or nonspecific clinical presentation.
- Gastritis can be classified based on its duration, histological features, and anatomical distribution.
- Acute gastritis is characterized by the sudden onset of mucosal inflammation and is typically reversible.
- Chronic gastritis, in contrast, involves long-standing inflammation that can lead to significant structural and functional changes in the stomach lining.
- Histologically, gastritis is subdivided into non-atrophic, atrophic, and special forms such as reactive, eosinophilic, and lymphocytic gastritis.
- Anatomically, gastritis may be antral-predominant, corpus-predominant, or involve the entire stomach (pangastritis), with the pattern often reflecting the underlying etiology.
- The most common cause of gastritis worldwide is infection with Helicobacter pylori, a bacterium that colonizes the gastric epithelium and triggers a persistent inflammatory response. Other infectious agents such as cytomegalovirus (CMV) or fungi may also cause gastritis, particularly in immunocompromised individuals.
- Autoimmune gastritis is caused by immune-mediated destruction of parietal cells and intrinsic factor, leading to vitamin B12 deficiency and increased risk of gastric neoplasia.
- Chemical or reactive gastritis results from irritation by nonsteroidal anti-inflammatory drugs (NSAIDs), alcohol, or bile reflux.
- In critically ill patients, stress-related mucosal injury due to hypoperfusion and reduced protective mechanisms may also lead to gastritis.
- Less common causes include radiation therapy, Crohn’s disease, sarcoidosis, and eosinophilic or lymphocytic infiltration in the setting of allergic or immune-mediated disorders.
- The development of gastritis involves a breakdown in the balance between mucosal defense mechanisms and injurious factors.
- The stomach’s defense includes mucus and bicarbonate secretion, epithelial cell regeneration, and adequate blood flow. When these defenses are compromised or overwhelmed—whether by H. pylori toxins, chemical irritants, or immune dysregulation—inflammation and mucosal damage ensue.
- In H. pylori gastritis, virulence factors such as CagA and VacA promote epithelial injury and immune activation. In autoimmune gastritis, CD4+ T cells target gastric parietal cells, resulting in hypochlorhydria, hypergastrinemia, and loss of intrinsic factor production.
- Gastritis may be asymptomatic or present with vague, nonspecific symptoms such as upper abdominal discomfort, nausea, bloating, early satiety, or loss of appetite.
- In erosive gastritis, mucosal bleeding may result in hematemesis or melena.
- Chronic atrophic gastritis often goes unnoticed until complications like iron or vitamin B12 deficiency, or even gastric cancer, develop. Because of this variability, diagnosis often relies on endoscopic evaluation and histological confirmation.
- Endoscopy remains the cornerstone of gastritis diagnosis, allowing direct visualization of the gastric mucosa and biopsy sampling. Findings may include erythema, erosions, atrophy, or intestinal metaplasia.
- Histopathologic analysis is used to assess the type and severity of inflammation and detect features such as atrophy, metaplasia, or dysplasia.
- Detection of H. pylori can be achieved through biopsy-based methods (histology, rapid urease test) or non-invasive tests like the urea breath test, stool antigen test, or serologic assays.
- In autoimmune gastritis, laboratory findings may include anemia, low vitamin B12 levels, and elevated serum gastrin. Anti-parietal cell or intrinsic factor antibodies may also be present.
- Treatment of gastritis depends on the underlying cause.
- In H. pylori-associated gastritis, eradication with a combination of antibiotics and a proton pump inhibitor (PPI) is the standard approach.
- For reactive or NSAID-induced gastritis, discontinuation of the offending agent and acid suppression with PPIs or H2-receptor antagonists are effective.
- Autoimmune gastritis management includes monitoring for pernicious anemia and supplementation with vitamin B12.
- In all cases, addressing modifiable risk factors—such as alcohol use or stress in critically ill patients—is essential. Patients with premalignant changes like atrophy or metaplasia may require endoscopic surveillance to monitor for progression to dysplasia or cancer.
- Untreated or persistent gastritis may lead to several complications.
- Peptic ulcer disease is a common consequence of H. pylori-related or NSAID-induced gastritis.
- Chronic inflammation, especially in the setting of H. pylori or autoimmunity, may lead to gastric atrophy, intestinal metaplasia, and an increased risk of gastric adenocarcinoma.
- Autoimmune gastritis is also associated with pernicious anemia due to vitamin B12 malabsorption and, less commonly, with gastric carcinoid tumors.
- Early detection and treatment can prevent these complications in many cases.
- Gastritis represents a multifaceted condition with diverse etiologies and clinical outcomes. While often asymptomatic, it can lead to significant morbidity when chronic or complicated by ulceration, anemia, or malignancy. A thorough understanding of its types, pathogenesis, and diagnostic criteria is vital for clinicians to manage gastritis effectively.
- Eradication of H. pylori, avoidance of irritants, and appropriate monitoring of high-risk patients are key strategies in reducing the burden of this common gastrointestinal disorder.
