1. Phlegmonous gastritis is an uncommon form of gastritis caused by numerous bacterial agents, including streptococci, staphylococci, Proteus species, Clostridium species, and Escherichia coli.2. Acute necrotizing hemorrhagic gastritis (a rare variant of phlegmonous gastritis) is mostly related to bacterial infection, which could progress to gastric gangrene.
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]
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.[11] Pain is usually located in the upper central portion of theabdomen,[12] but it may occur anywhere from the upper left portion of the abdomen around to the back.
Other signs and symptoms may include the following:[11]
Helicobacter pylori infection is the most common cause of gastritis; when contracted this way, it may be termedH. pylori gastritis.[13][14]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.[15] It has been suggested thatH. pylori plays an important role in the natural stomach ecology.[16]
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][13] 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.[18][19]
Evidence does not support a role for specific foods, including spicy foods and coffee, in the development ofpeptic ulcers.[23] People are, however, usually advised to avoid foods that trigger symptoms and alcoholic beverages.[24][4][7] 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.[25]
There are multiple classification systems which may be used to categorise gastritis cases. The Sydney system introduced in 1990 is commonly used for classification based primarily on the morphological features of the disease as seen in endoscopic biopsies. The Kyoto system (which resulted from the 2015 Kyoto Consensus Conference) classifies gastritis based primarily on the cause and duration of symptoms, resulting in 3 subtypes; acute, chronic, and special.[17] It may also be classified based on mucosal injury, resulting in the 2 types erosive and non-erosive.[26][27]
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.[28] NSAIDs inhibitcyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis ofeicosanoids in the stomach, which increases the possibility ofpeptic ulcers forming.[29][30][31] Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach calledprostaglandin. These drugs used in a short period are not typically dangerous. However, regular use can lead to gastritis.[32] Additionally, severe physiologic stress from sepsis, hypoxia, trauma, or surgery is also a common etiology for acute erosive gastritis, resulting in "stress ulcers". This form of gastritis can occur in more than 5% of hospitalized patients.[citation needed]
Also, alcohol consumption does not cause chronic gastritis. It does, however, erode the mucosal lining of the stomach; low doses of alcohol stimulatehydrochloric acid secretion. High doses of alcohol do not stimulate secretion of acid.[33]
Chronic gastritis refers to a wide range of gastric issues.[28] In some cases, chronic gastritis results when the immune system targets the stomach as if it were a foreign body, causing damage to the stomach or its lining.[32] In other cases, it may result from bile entering the stomach through thepyloric valve due to surgical removal or a defect. Gastritis may also be caused by other medical conditions, includingHIV/AIDS,Crohn's disease, certainconnective tissue disorders, andliver orkidney failure.[34]
Mucous glandmetaplasia, 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 exhibitsdysplasia.[28]
Endoscopy, to check for stomach lining inflammation and mucous erosion
Stomach biopsy, to test for gastritis and other conditions[35]
The OLGA staging frame of chronic gastritis on histopathology. Atrophy is scored as the percentage of atrophic glands and scored on a four-tiered scale. No atrophy (0%) = score 0; mild atrophy (1–30%) = score 1; moderate atrophy (31–60%) = score 2; severe atrophy (>60%) = score 3. These scores (0–3) are used in the OLGA staging assessment in each 10 compartment:[36]
Antacids are a common treatment for mild to medium gastritis.[37] When antacids do not provide enough relief, medications such asH2 blockers andproton-pump inhibitors that help reduce the amount of acid are often prescribed.[37][38]
Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine.[39] 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.[40]
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.
In 1,000 A.D,Avicenna first gave the description of stomach cancer. In 1728, German physicianGeorg Ernst Stahl first coined the term "gastritis". Italian anatomical pathologistGiovanni Battista Morgagni further described the characteristics of gastric inflammation. He described the characteristics of erosive or ulcerative gastritis and erosive gastritis. Between 1808 and 1831, French physicianFrançois-Joseph-Victor Broussais gathered information from the 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 stomach inner lining in gastritis which existed in diffuse and segmental forms. In 1855,Baron Carl von Rokitansky first describedhypertrophic gastritis. In 1859, British physician,William Brinton first described aboutacute,subacute, andchronic gastritis. In 1870, Samuel Fenwick noted thatpernicious anemia causes glandularatrophy in gastritis. German surgeon Georg Ernst Konjetzny noticed that both gastric ulcer 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.[41]
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