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Prevention is by avoiding things that cause the disease. Gastritis is believed to affect about half of people worldwide. 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.
Less common causes include alcohol , cocaine , severe illness and Crohn disease , among others. Helicobacter pylori colonizes the stomachs 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. 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.
Evidence does not support a role for specific foods including spicy foods and coffee in the development of peptic ulcers. Acute erosive gastritis typically involves discrete foci of surface necrosis due to damage to mucosal defenses. These drugs used in a short period are not typically dangerous. However, regular use can lead to gastritis. 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. 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. Since , 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. 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:. Antacids are a common treatment for mild to medium gastritis.
Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. If NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate [ citation needed ]. Several regimens are used to treat H. Most use a combination of two antibiotics and a proton pump inhibitor.
Sometimes bismuth is added to the regimen. D, Avicenna first gave the description of stomach cancer. In , German physician Georg Ernst Stahl first coined the term "gastritis". Italian anatomical pathologist Giovanni Battista Morgagni further described the characteristics of gastric inflammation. He described the characteristics of erosive or ulcerative gastritis and erosive gastritis. Between and , French physician François-Joseph-Victor Broussais gathered information from the autopsy of the dead French soldiers.
He described chronic gastritis as "Gastritide" and erroneously believed that gastritis was the cause of ascites , typhoid fever , and meningitis. In , Charles Handfield Jones and Wilson Fox described the microscopic changes of stomach inner lining in gastritis which existed in diffuse and segmental forms. In , Baron Carl von Rokitansky first described hypetrophic gastritis. In , British physician, William Brinton first described about acute , subacute , and chronic gastritis.
In , Samuel Fenwick noted that pernicious anemia causes glandular atrophy in gastritis. German surgeon, Georg Ernst Konjetzny noticed that gastric ulcer and gastric cancer are the result of gastric inflammation. Shields Warren and Willam A. Meissner described the intestinal metaplasia of the stomach as a feature of chronic gastritis.
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