|Classification and external resources|
Gastritis is inflammation of the lining of the stomach and has many possible causes. Common causes of gastritis are excessive alcohol consumption or prolonged use of nonsteroidal anti-inflammatory drugs (also known as NSAIDs) such as aspirin or ibuprofen. Gastritis may also develop after major surgery or traumatic injury ("Cushing ulcer"), burns ("Curling ulcer"), or severe infections. Gastritis may also occur in those who have had weight loss surgery resulting in the banding or reconstruction of the digestive tract.
Chronic causes are infection with bacteria, primarily Helicobacter pylori, chronic bile reflux, and stress; certain autoimmune disorders can cause gastritis as well. The most common symptom is abdominal upset or pain. Other symptoms are indigestion, abdominal bloating, nausea, and vomiting and pernicious anemia. Some may have a feeling of fullness or burning in the upper abdomen. An esophagogastroduodenoscopy, blood test, complete blood count test, or a stool test may be used to diagnose gastritis. Treatment includes taking antacids or other medicines, such as proton pump inhibitors or antibiotics, and avoiding hot or spicy foods. For those with pernicious anemia, B12 injections are given, but more often oral B12 supplements are recommended.
Signs and symptoms
Many people with gastritis experience no symptoms at all. However, upper central abdominal pain is the most common symptom; the pain may be dull, vague, burning, aching, gnawing, sore, or sharp. Pain is usually located in the upper central portion of the abdomen, but it may occur anywhere from the upper left portion of the abdomen around to the back.
Other signs and symptoms may include:
- Vomiting (if present, may be clear, green or yellow, blood-streaked, or completely bloody, depending on the severity of the stomach inflammation)
- Belching (if present, usually does not relieve the pain much)
- Early satiety
- Loss of appetite
- Unexplained weight loss
Acute erosive gastritis typically involves discrete foci of surface necrosis due to damage to mucosal defenses. NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis of eicosanoids in the stomach, which increases the possibility of peptic ulcers forming. Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called prostaglandin. These drugs used in a short period are not typically dangerous. However, regular use can lead to gastritis. Additionally, severe physiologic stress ("stress ulcers") from sepsis, hypoxia, trauma, or surgery, is also a common etiology for acute erosive gastritis. This form of gastritis can occur in more than 5% of hospitalized patients.
Also, note that alcohol consumption does not cause chronic gastritis. It does, however, erode the mucosal lining of the stomach; low doses of alcohol stimulate hydrochloric acid secretion. High doses of alcohol do not stimulate secretion of acid.
Chronic gastritis refers to a wide range of problems of the gastric tissues. The immune system makes proteins and antibodies that fight infections in the body to maintain a homeostatic condition. In some disorders the body targets the stomach as if it were a foreign protein or pathogen; it makes antibodies against, severely damages, and may even destroy the stomach or its lining. In some cases bile, normally used to aid digestion in the small intestine, will enter through the pyloric valve of the stomach if it has been removed during surgery or does not work properly, also leading to gastritis. Gastritis may also be caused by other medical conditions, including HIV/AIDS, Crohn's disease, certain connective tissue disorders, and liver or kidney failure. Since 1992, chronic gastritis lesions are classified according to the Sydney system.
Mucous gland metaplasia, the reversible replacement of differentiated cells, occurs in the setting of severe damage of the gastric glands, which then waste away (atrophic gastritis) and are progressively replaced by mucous glands. Gastric ulcers may develop; it is unclear if they are the causes or the consequences. Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum, and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics. Intestinal metaplasia is classified histologically as complete or incomplete. With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia.
Coffee can irritate and damage the lining of the gastrointestinal tract, increasing the risk of gastritis and ulcers. The consumption of coffee is not recommended for people with gastritis, colitis, or ulcers.
Helicobacter pylori colonizes the stomach of more than half of the world's population, and the infection continues to play a key role in the pathogenesis of a number of gastroduodenal diseases. Colonization of the gastric mucosa with Helicobacter pylori results in the development of chronic gastritis in infected individuals, and in a subset of patients chronic gastritis progresses to complications (e.g., ulcer disease, gastric neoplasias, some distinct extragastric disorders). However, over 80 percent of individuals infected with the bacterium are asymptomatic and it has been postulated that it may play an important role in the natural stomach ecology.
Often, a diagnosis can be made based on the patient's description of their symptoms, but other methods which may be used to verify gastritis include:
- Blood tests:
- Blood cell count
- Presence of H. pylori
- Liver, kidney, gallbladder, or pancreas functions
- Stool sample, to look for blood in the stool
- Endoscopy, to check for stomach lining inflammation and mucous erosion
- Stomach biopsy, to test for gastritis and other conditions
Over-the-counter antacids in liquid or tablet form are a common treatment for mild gastritis. Antacids neutralize stomach acid and can provide fast pain relief. When antacids do not provide enough relief, medications such as cimetidine, ranitidine, nizatidine or famotidine that help reduce the amount of acid the stomach produces are often prescribed. An even more effective way to limit stomach acid production is to shut down the acid "pumps" within acid-secreting stomach cells. Proton pump inhibitors reduce acid by blocking the action of these small pumps. This class of medications includes omeprazole, lansoprazole, rabeprazole, and esomeprazole. Proton pump inhibitors also appear to inhibit H. pylori activity. Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. They include the medications sucralfate and misoprostol. If NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate. Many people also drink milk to relieve symptoms, however the high calcium levels actually stimulate release of gastric acid from parietal cells, ultimately worsening symptoms. In addition to protecting the lining of stomach and intestines, bismuth preparations appear to inhibit H. pylori activity as well. Several regimens are used to treat H. pylori infection. Most use a combination of two antibiotics and a proton pump inhibitor. Sometimes bismuth is also added to the regimen. The antibiotic aids in destroying the bacteria, and the acid blocker or proton pump inhibitor relieves pain and nausea, heals inflammation, and may increase the antibiotic's effectiveness.
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