1 Causes and Treatment
1.2.2 Helicobacter pylori
5 See also
Gastritis is an inflammation of the lining of the stomach, and has many possible causes. The main acute causes are excessive alcohol consumption or prolonged use of nonsteroidal anti-inflammatory drugs (also known as NSAIDs) such as aspirin or ibuprofen. Sometimes gastritis develops after major surgery, traumatic injury, burns, 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. Certain diseases, such as pernicious anemia, chronic bile reflux, and 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. Some may have a feeling of fullness or burning in the upper abdomen. A gastroscopy, 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, or avoiding hot or spicy foods. For those with pernicious anemia, B12 injections are given.
Erosive gastritis is gastric mucosal erosion caused by damage to mucosal defenses. 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. 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 to form. Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called prostaglandin. These drugs used in a short period of time are not typically dangerous. However, regular use can lead to gastritis.
If the cardiac sphincter fails to do its job properly, some stomach acid can escape up the esophagus. This causes very painful "heartburn" or "gastritis" in the chest as the esophageal walls are eroded by the hydrochloric acid. Chronic gastritis refers to a wide range of problems of the gastric tissues that are mainly the result of H. pylori infection. The immune system makes proteins and antibodies that fight infections in the body to maintain a homeostatic condition. In some disorders, the body accidentally targets the stomach, believing it is a foreign protein or pathogen. It makes antibodies against, severely damages, and may even destroy the stomach and/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, because it had been removed during surgery or may not work properly. This also leads to gastritis. Gastritis may also be caused by other medical conditions, including HIV/AIDS, Crohn's disease, certain connective tissue disorders, or liver/kidney failure.
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), which 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.
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 all infected individuals and in a subset of patients chronic gastritis progresses to complications (i.e. ulcer disease, gastric neoplasias, some distinct extra gastric disorders). However, gastritis has no adverse consequences for most hosts and emerging evidence suggests that H. pylori prevalence is inversely related to gastroesophageal reflux disease and allergic disorders. These observations indicate that eradication may not be appropriate for certain populations due to the potentially beneficial effects conferred by persistent gastric inflammation.
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 don't provide enough relief, medications such as cimetidine, ranitidine, nizatidine or famotidine that helps 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 your 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. 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 regiment. 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.
Severe gastritis is possible when the stomach is viewed without symptoms being present and may be present despite only minor changes in the stomach lining. Seniors have a higher likelihood of developing painless stomach damage. They may have no symptoms at all, such as an absence of vomiting or pain, until they are suddenly taken ill with internal bleeding. Pain in the upper abdomen is the most common symptom. The pain is usually in the upper central portion of the abdomen, the "pit" of the stomach. Gastritis pain can occur in the left upper portion of the abdomen and in the back. The pain seems to travel from the belly to the back. The pain is typically vague, but can be a sharp pain. Belching either doesn't relieve pain or only relieves it for a moment. The vomit is either clear, green or yellow, has a bloody streak in it, or is completely bloody, depending on the severity of inflammation. Bloating and a feeling of fullness or burning in the upper abdomen are also signs of moderate gastritis. Severe gastritis presents pallor, sweating, rapid heart beat, feeling faint or short of breath, severe chest or stomach pain, vomiting large amounts of blood, or bloody or dark, sticky, foul-smelling bowel movements.
Typically, a diagnosis is made based on the patients description of his or her symptoms. If a diagnosis is not possible based on these symptoms, however, other methods are used. Tests for blood cell count, H. pylori, and pregnancy; and liver, kidney, gallbladder, and pancreas functions, may be ordered. Urinalysis may be used, or a stool sample taken, to look for blood in the stool. X-rays may be ordered, as well as ECGs. If none of these tests are able to be used for diagnosis, the patient may be recommended to a gastroenterologist. An endoscopy may be performed, where a flexible probe with a camera on the end is sent into the stomach to check for stomach lining inflammation and mucous erosion. At the same time, a stomach biopsy may be taken to test for gastritis and a variety of other conditions.
"Gastritis". University of Maryland Medical Center (University of Maryland Medical System). 2002-12-01. Retrieved on 2008-10-07.
a b c d "Gastritis". Merck. January 2007. Retrieved on 2009-01-11.
"Gastritis". National Digestive Diseases Information Clearinghouse (National Institute of Diabetes and Digestive and Kidney Diseases). December 2004. Retrieved on 2008-10-06.
"Gastritis: Diagnostic Tests for Gastritis". Wrong Diagnosis. December 30 2008. Retrieved on 2009-01-11.
"What is Gastritis?". Cleveland Clinic (WebMD). Retrieved on 2009-01-11.
Wolff G (1989). "[Effect of alcohol on the stomach]" (in German). Gastroenterol J 49 (2): 45–9. PMID 2679657.
Dajani EZ, Islam K (August 2008). "Cardiovascular and gastrointestinal toxicity of selective cyclo-oxygenase-2 inhibitors in man" (PDF). J Physiol Pharmacol. 59 Suppl 2: 117–33. PMID 18812633.
a b Siegelbaum, Jackson (2006). "Gastritis". Jackson Siegelbaum Gastroenterolgoy. Retrieved on 2008-11-18.
"Gastritis". MayoClinic. April 13, 2007. Retrieved on 2008-11-18.
"Helicobacter pylori infection: a clinical overview.". Dig Liver Dis.. August 2008. PMID 18396114. Retrieved on 2009-01-12.
Peek, RM (July 2008). "Helicobacter pylori infection and disease: from humans to animal models.". Dis Model Mech.. PMID 19048053. Retrieved on 2009-01-12.