Prevention involves avoidance of things which irritate the gut and which trigger symptoms, including alcohol, nonsteroidal anti-inflammatory drugs (NSAIDs), tobacco, and certain foods.[4][examples needed] It is also recommended to treat for any underlyingH. pylori infection before starting NSAID treatment in order to prevent irritation and gastroduodenal ulcers.[7] Treatment includes medications such asantacids,H2 blockers, andproton pump inhibitors.[1] During an acute flare-up, drinkingviscous lidocaine may help.[8] If gastritis is caused by NSAID use (e.g. aspirin, ibuprofen, naproxen), usage may be ceased.[1] IfH. pylori is present, it may be treated with a combination ofantibiotics such asamoxicillin andclarithromycin.[1] For those with pernicious anemia, vitamin B12 supplements are recommended by injection.[3]
Gastritis is believed to be present in 30% to 50% of people worldwide, but most cases are asymptomatic.[4] In 2013 there were approximately 90 million new cases of the condition.[9] The risk of developing gastritis increases as one ages.[4] Gastritis, along with a similar condition in the first part of theintestines calledduodenitis, resulted in 50,000 deaths in 2015.[5]H. pylori was first discovered in 1981 byBarry Marshall andRobin Warren.[10]
Updated Sydney System (USS) for classification of gastritis based on morphological features.
There are multiple classification systems which may be used to categorise gastritis cases. The Updated Sydney System (USS) of 1994 is commonly used for classification, based primarily on the morphological features of the disease seen in endoscopic biopsies. The Kyoto system (from the 2015 Kyoto Consensus Conference) classifies gastritis based primarily on the cause and duration of symptoms, resulting in the 3 types acute, chronic, and special.[11] Gastritis may also be classified based on the kind of mucosal injury, resulting in the 2 types erosive and non-erosive.[12][13]
The Operative Link for Gastritis Assessment (OLGA) staging system may also be used to classify cases of gastritis.[14] The OLGA system was devised in an attempt to evaluate complication risk, in particular the development of gastritis intointestinal metaplasia orgastric cancer. The degree of atrophy and metaplasia at two main sites is scored on a four-tiered scale.[15]
A peptic ulcer, which may accompany gastritis, seen via endoscopy.
Many people with gastritis experience no symptoms at all. However, upper centralabdominal pain is the most common symptom; the pain may be dull, vague, burning, aching, gnawing, sore, or sharp.[16] Pain is usually located in the upper central portion of theabdomen, but it may occur anywhere from the upper left portion of the abdomen around to the back.[17]
Other signs and symptoms may include the following:[16]
Helicobacter pylori infection is the most common cause of gastritis; when contracted this way, it may be termedH. pylori gastritis.[18][19]H. pylori is a kind of bacteria which colonizes the gut of more than half of the world's population. While the bacteria is present in over half of the world's population, infection does not necessarily cause symptoms and thus most cases are asymptomatic.[20] It has been suggested thatH. pylori plays an important role in the natural stomach ecology.[21]
Gastritis can result from usage of some drugs, the most common being usage of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen. Other drugs includecocaine,iron,colchicine when administered at toxic levels,kayexalate (a kind of polystyrene sulfonate),ticlopidine, and those associated withchemotherapy andimmunotherapy for cancer.[7][18] Drugs used for COVID-19 treatment have also been found to cause gastritis;tocilizumab andsarilumab are associated with chronic gastritis, whilelopinavir/ritonavir is associated with the acute form.[7]
Gastritis is also associated withbile reflux, in which bile and/or pancreatic enzymes flow up into the stomach; when bile travels further upwards into the esophagus, it is calledgastric reflux. Excessive refluxed bile in the stomach causes irritation and inflammation to the stomach lining, leading to the development ofgastric ulcers and/or gastritis; when contracted this way, it may be termed bile reflux gastritis.[22][23]
Evidence does not support a role for specific foods, including spicy foods and coffee, in the development ofpeptic ulcers.[27] People are, however, usually advised to avoid foods that trigger symptoms.[28] There is little specific advice on diet published by authoritative sources. TheNational Health Service of theUnited Kingdom advises avoiding spicy, acidic or fried foods which may irritate the stomach.[29]
It is generally advised to avoid alcohol consumption for the prevention and mitigation of gastrointestinal injury.[4][7] Some sources describe alcohol as a potential cause of gastritis,[1][4][13] while others describe it instead as a potential contributor to the erosion of the stomach's mucosal lining when ingested in large doses.[30][31]
Gastritis should be investigated when a patient reports abdominal discomfort, pain, and/or nausea.[13] Diagnosis relies primarily on the findings of anupper endoscopy withbiopsy, but also involves taking a comprehensive patient history.[4][11] While history and other tests can help provide insights, histopathological examination of gastric biopsies are the gold standard, and allow one to identify the distribution, severity, and etiology of the disease.[11]
Other tests which may be ordered to diagnose or rule out gastritis include:
H. pylori testing by urea breath test, stool antigen test, endoscopic biopsy, or specific antibody test[4]
Antacids are a common treatment for mild to medium gastritis.[32] When antacids do not provide enough relief, medications such asH2 blockers andproton-pump inhibitors that help reduce the amount of acid are often prescribed.[32][33]
Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine.[34] They include the medicationssucralfate andmisoprostol. IfNSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent isbismuth subsalicylate.[35]
Several regimens are used to treatH. pylori infection. Most use a combination of twoantibiotics and a proton pump inhibitor. Sometimes bismuth is added to the regimen.[citation needed]
Gastric cancer was first described in 1000 A.D. by Persian physicianAvicenna. In 1728, German physicianGeorg Ernst Stahl coined the term "gastritis". Italian anatomical pathologistGiovanni Battista Morgagni further described the characteristics of gastric inflammation, including the characteristics of erosive or ulcerative gastritis and erosive gastritis. Between 1808 and 1831, French physicianFrançois-Joseph-Victor Broussais gathered information from autopsies of dead French soldiers. He described chronic gastritis as "gastritide" and erroneously believed that gastritis was the cause ofascites,typhoid fever, andmeningitis. In 1854,Charles Handfield Jones andWilson Fox described the microscopic changes of the stomach's inner lining in gastritis. In 1855,Baron Carl von Rokitansky first described hypertrophic gastritis. In 1859, British physicianWilliam Brinton first described acute, subacute, and chronic gastritis. In 1870, Samuel Fenwick noted thatpernicious anemia causes glandularatrophy in gastritis. German surgeon Georg Ernst Konjetzny noticed that both gastric ulcers and gastric cancer are the results of gastric inflammation.Shields Warren and Willam A. Meissner described theintestinal metaplasia of the stomach as a feature of chronic gastritis.[36]
Early acute superficial gastritis. Marked neutrophilic infiltrates appear in the mucous neck region and lamina with a pit microabscess. This case was caused byHelicobacter pylori.
Acute erosive gastritis typically involves discrete foci of surface necrosis due to damage to mucosal defenses.[37] NSAIDs inhibitcyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis ofeicosanoids in the stomach, increasing the likelihood ofpeptic ulcers forming.[38][39][40] NSAIDs also inhibitprostaglandin synthesis, a hormone with a protective effect on the stomach's mucosal lining. While short-term NSAID use causes no problems, long-term use can lead to gastritis or other complications.[41][30]
Metaplasia is the transformation of differentiated cells from one type into another type.Mucous gland metaplasia can occur after severe damage to the gastric glands causes them to waste away (atrophic gastritis) and be progressively replaced by mucous glands. Gastric ulcers may develop; it is unclear if they are the causes or the consequences.[37]
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. In the complete type, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In the incomplete type, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibitsdysplasia.[37]
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