Gastritis

Template:Short description Template:Cs1 config Template:Infobox medical condition (new) Gastritis is the inflammation of the lining of the stomach.<ref name=NID2013/> It may occur as a short episode or may be of a long duration.<ref name=NID2013/> There may be no symptoms but, when symptoms are present, the most common is upper abdominal pain (see dyspepsia).<ref name=NID2013/> Other possible symptoms include nausea and vomiting, bloating, loss of appetite and heartburn.<ref name=NID2013/><ref name=Rosen2012>Template:Cite book</ref> Complications may include stomach bleeding, stomach ulcers, and stomach tumors.<ref name=NID2013/> When due to autoimmune problems, low red blood cells due to not enough vitamin B12 may occur, a condition known as pernicious anemia.<ref name=Var2014>Template:Cite journal</ref>

Common causes include infection with Helicobacter pylori and use of nonsteroidal anti-inflammatory drugs (NSAIDs).<ref name=NID2013/> When caused by H. pylori this is now termed Helicobacter pylori induced gastritis, and included as a listed disease in ICD11.<ref name="Maastricht 2022">Template:Cite journal</ref><ref name="ICD11">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Less common causes include alcohol, smoking, cocaine, severe illness, autoimmune problems, radiation therapy and Crohn's disease.<ref name=NID2013>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name=Mayo2014>Template:Cite book</ref> Endoscopy, a type of X-ray known as an upper gastrointestinal series, blood tests, and stool tests may help with diagnosis.<ref name=NID2013/> Other conditions with similar symptoms include inflammation of the pancreas, gallbladder problems, and peptic ulcer disease.<ref name=Rosen2012/>

Prevention is by avoiding things that cause the disease.<ref name=Ferri2013/>Template:Example needed Treatment includes medications such as antacids, H2 blockers, or proton pump inhibitors.<ref name=NID2013/> During an acute attack drinking viscous lidocaine may help.<ref>Template:Cite book</ref> If gastritis is due to NSAIDs these may be stopped.<ref name=NID2013/> If H. pylori is present it may be treated with a combination of antibiotics such as amoxicillin and clarithromycin.<ref name=NID2013/> For those with pernicious anemia, vitamin B12 supplements are recommended either by mouth or by injection.<ref name=Var2014/> People are usually advised to avoid foods that bother them.<ref name=Hold2012>Template:Cite book</ref>

Gastritis is believed to affect about half of people worldwide.<ref name=Ferri2013/> In 2013 there were approximately 90 million new cases of the condition.<ref>Template:Cite journal</ref> As people get older the disease becomes more common.<ref name=Ferri2013>Template:Cite book</ref> It, along with a similar condition in the first part of the intestines known as duodenitis, resulted in 50,000 deaths in 2015.<ref name=GBD2015De>Template:Cite journal</ref> H. pylori was first discovered in 1981 by Barry Marshall and Robin Warren.<ref>Template:Cite journal</ref> Template:TOC limit

Signs and symptoms

File:Deep gastric ulcer.png

A peptic ulcer may accompany gastritis. Endoscopic image.

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.<ref name="eMed">Template:Cite news</ref> Pain is usually located in the upper central portion of the abdomen,<ref name='NIH Publication No. 05–4764'>Template:Cite news</ref> 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:<ref name="eMed" />

• Nausea
• Vomiting (may be clear, green or yellow, blood-streaked or completely bloody depending on the severity of the stomach inflammation)
• Belching (does not usually relieve stomach pain if present)
• Bloating
• Early satiety
• Loss of appetite

Causes

There are two categories of gastritis depending on the cause of the disease. There is erosive gastritis, for which the common causes are stress, alcohol, some drugs, such as aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), and Crohn's disease. And, there is non-erosive gastritis, for which the most common cause is a Helicobacter pylori infection. <ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name="NID2013" />

Helicobacter pylori

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.g., ulcer disease, stomach cancers, and some distinct extragastric disorders).<ref>Template:Cite journal</ref> Gastritis caused by H. pylori infection is termed Helicobacter pylori induced gastritis, and listed as a disease in ICD11.<ref name="Maastricht 2022">Template:Cite journal</ref><ref name="ICD11">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> More than 80% 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.<ref>Template:Cite journal</ref>

Critical illness

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.Template:Cn

Diet

Evidence does not support a role for specific foods, including spicy foods and coffee, in the development of peptic ulcers.<ref>Template:Cite book</ref> People are usually advised to avoid foods that bother them.<ref name=Hold2012/> There is little specific advice on diet published by authoritative sources. The National Health Service of the United Kingdom advises avoiding spicy, acidic or fried foods which may irritate the stomach.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Pathophysiology

Acute

File:Histopathology of early acute superficial gastritis.png

Early acute superficial gastritis: Marked neutrophilic infiltrates appear in the mucous neck region and lamina with a pit microabscess. This case was caused by Helicobacter pylori.

Acute erosive gastritis typically involves discrete foci of surface necrosis due to damage to mucosal defenses.<ref name=merckgastritis>Template:Cite news</ref> 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.<ref>Template:Cite journalTemplate:Dead link</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> 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.<ref name=Siegelbaum>Template:Cite news</ref> 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.Template:Cn

Also, 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.<ref>Template:Cite journal</ref>

Chronic

Chronic gastritis refers to a wide range of problems of the gastric issues.<ref name=merckgastritis/> 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.<ref name=Siegelbaum/> 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.<ref name='DS00488'>Template:Cite news</ref>

Metaplasia

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.<ref name=merckgastritis/>

Diagnosis

File:Updated Sydney System for visual classification of gastritis.png

Updated Sydney System for visual classification of gastritis on histopathology.

Often, a diagnosis can be made based on patients' description of their symptoms. 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
• Urinalysis
• Stool sample, to look for blood in the stool
• X-rays
• Endoscopy, to check for stomach lining inflammation and mucous erosion
• Stomach biopsy, to test for gastritis and other conditions<ref>Template:Cite news</ref>

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:<ref name=Carrasco>Template:Cite journal Template:CC-notice</ref>

		Corpus
		No atrophy (score 0)	Mild atrophy (score 1)	Moderate atrophy (score 2)	Severe atrophy (score 3)
Antrum (including incisura angularis)
	No atrophy (score 0)	Stage 0	Stage I	Stage II	Stage II
	Mild atrophy (score 1)	Stage I	Stage I	Stage II	Stage III
	Moderate atrophy (score 2)	Stage II	Stage II	Stage III	Stage IV
	Severe atrophy (score 3)	Stage III	Stage III	Stage IV	Stage IV

Treatment

Antacids are a common treatment for mild to medium gastritis.<ref name="Overview">Template:Cite journal</ref> When antacids do not provide enough relief, medications such as H₂ blockers and proton-pump inhibitors that help reduce the amount of acid are often prescribed.<ref name="Overview"/><ref name="pmid18457460">Template:Cite journal</ref>

Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine.<ref>Template:Cite journal</ref> 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.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Several regimens are used to treat H. pylori infection. Most use a combination of two antibiotics and a proton pump inhibitor. Sometimes bismuth is added to the regimen.

History

In 1,000 A.D, Avicenna first gave the description of stomach cancer. In 1728, 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 1808 and 1831, French physician François-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 of ascites, typhoid fever, and meningitis. In 1854, Charles Handfield Jones and Wilson 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 described hypertrophic gastritis. In 1859, British physician, William Brinton first described about acute, subacute, and chronic gastritis. In 1870, Samuel Fenwick noted that pernicious anemia causes glandular atrophy 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 the intestinal metaplasia of the stomach as a feature of chronic gastritis.<ref name="Guyula 2013">Template:Cite book</ref>

See also

• Gastroenteritis
• Esophagitis

Further reading

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