Gastritis
Overview
Gastritis is a medical condition characterized by inflammation of the gastric mucosa, the lining of the stomach. This inflammation can be acute or chronic, and it may result from various etiological factors, including infection, prolonged use of nonsteroidal anti-inflammatory drugs (NSAIDs), excessive alcohol consumption, and autoimmune disorders. Gastritis can lead to a range of symptoms, from mild discomfort to severe pain, and may increase the risk of developing gastric ulcers or even gastric cancer.
Etiology
The causes of gastritis are multifactorial and can be broadly categorized into infectious, chemical, and autoimmune origins.
Infectious Causes
The most common infectious cause of gastritis is the bacterium Helicobacter pylori. This gram-negative microorganism colonizes the gastric epithelium, leading to chronic inflammation. The presence of H. pylori is associated with an increased risk of peptic ulcer disease and gastric malignancies. Viral infections, such as those caused by cytomegalovirus (CMV) and Epstein-Barr virus (EBV), can also contribute to gastritis, particularly in immunocompromised individuals.
Chemical Causes
NSAIDs, such as ibuprofen and aspirin, are frequently implicated in the development of gastritis. These medications inhibit cyclooxygenase enzymes, reducing the production of protective prostaglandins in the gastric mucosa. This reduction compromises the mucosal barrier, making it susceptible to damage by gastric acid. Excessive alcohol consumption can also irritate and erode the gastric lining, leading to inflammation.
Autoimmune Causes
Autoimmune gastritis is a chronic condition in which the body's immune system mistakenly attacks the parietal cells of the stomach lining. This attack leads to a decrease in gastric acid production and intrinsic factor, a protein necessary for vitamin B12 absorption. Over time, this can result in pernicious anemia and an increased risk of gastric carcinoma.
Pathophysiology
The pathophysiology of gastritis involves a complex interplay between host factors and environmental triggers. The gastric mucosa is protected by a layer of mucus, bicarbonate secretion, and tight junctions between epithelial cells. Disruption of these protective mechanisms, whether by infectious agents, chemical irritants, or autoimmune processes, leads to mucosal damage and inflammation.
In acute gastritis, the inflammatory response is typically dominated by neutrophils, whereas chronic gastritis is characterized by the infiltration of lymphocytes and plasma cells. Chronic inflammation can lead to atrophic changes in the gastric mucosa, with loss of glandular structures and intestinal metaplasia, a precursor to dysplasia and gastric cancer.
Clinical Manifestations
Gastritis can present with a wide range of symptoms, which may vary depending on the underlying cause and severity of the inflammation. Common symptoms include:
- Epigastric pain or discomfort
- Nausea and vomiting
- Bloating and belching
- Loss of appetite
- Hematemesis (vomiting blood) or melena (black, tarry stools) in severe cases
In some individuals, particularly those with chronic gastritis, symptoms may be absent or nonspecific, making diagnosis challenging.
Diagnosis
The diagnosis of gastritis is typically based on a combination of clinical evaluation, laboratory tests, and endoscopic examination.
Laboratory Tests
Blood tests may reveal anemia, particularly in cases of autoimmune gastritis. Serological tests can detect antibodies against H. pylori or intrinsic factor. A urea breath test or stool antigen test can also be used to identify H. pylori infection.
Endoscopy
Upper gastrointestinal endoscopy is the gold standard for diagnosing gastritis. During the procedure, a flexible tube with a camera is inserted through the mouth to visualize the stomach lining. Biopsies may be taken to assess the extent of inflammation and to test for H. pylori.
Treatment
The treatment of gastritis depends on the underlying cause and severity of the condition.
Eradication of H. pylori
For patients with H. pylori-associated gastritis, a combination of antibiotics and proton pump inhibitors (PPIs) is used to eradicate the infection and promote healing of the gastric mucosa.
Medication Adjustment
In cases where NSAIDs or other medications are implicated, discontinuation or substitution with alternative therapies may be necessary. The use of PPIs or H2-receptor antagonists can help reduce gastric acid secretion and alleviate symptoms.
Lifestyle Modifications
Patients are advised to avoid alcohol, smoking, and foods that exacerbate symptoms. Dietary modifications, such as eating smaller, more frequent meals and avoiding spicy or acidic foods, may also be beneficial.
Complications
If left untreated, gastritis can lead to several complications, including:
- Peptic ulcers: Erosion of the gastric or duodenal lining, leading to ulcer formation.
- Gastric bleeding: Resulting from erosions or ulcers.
- Gastric cancer: Chronic inflammation and atrophic changes increase the risk of malignancy.
- Pernicious anemia: Due to vitamin B12 deficiency in autoimmune gastritis.
Prognosis
The prognosis for gastritis varies depending on the cause and the patient's response to treatment. Acute gastritis often resolves with appropriate management, while chronic gastritis may require long-term monitoring and intervention to prevent complications.