Gastritis

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Gastritis
Gastritis helicobacter - intermed mag.jpg
Micrograph showing gastritis. H&E stain.
Specialty Gastroenterology
Symptoms Upper abdominal pain, nausea, vomiting, bloating, loss of appetite, heartburn [1] [2]
Complications Bleeding, stomach ulcers, stomach tumors, pernicious anemia [1] [3]
DurationShort or long term [1]
Causes Helicobacter pylori , NSAIDs, alcohol, tobacco, cocaine, viruses, parasites, autoimmune [1]
Diagnostic method Endoscopy, upper gastrointestinal series, blood tests, stool tests [1]
Differential diagnosis Myocardial infarction, inflammation of the pancreas, gallbladder problems, peptic ulcer disease [2]
Treatment Antacids, H2 blockers, proton pump inhibitors, antibiotics, sucralfate, bismuth subsalicylate, [1] antiemetics
Frequency~50% of people [4]
Deaths50,000 (2015) [5]

Gastritis is the inflammation of the lining of the stomach. [1] It may occur as a short episode or may be of a long duration. [1] There may be no symptoms but, when symptoms are present, the most common is upper abdominal pain (see dyspepsia). [1] Other possible symptoms include nausea and vomiting, bloating, loss of appetite and heartburn. [1] [2] Complications may include stomach bleeding, stomach ulcers, and stomach tumors. [1] When due to autoimmune problems, low red blood cells due to not enough vitamin B12 may occur, a condition known as pernicious anemia. [3]

Contents

Common causes include infection with Helicobacter pylori and use of nonsteroidal anti-inflammatory drugs (NSAIDs). [1] When caused by H. pylori this is now termed Helicobacter pylori induced gastritis, and included as a listed disease in ICD11. [6] [7] Less common causes include alcohol, smoking, cocaine, severe illness, autoimmune problems, radiation therapy and Crohn's disease. [1] [8] Endoscopy, a type of X-ray known as an upper gastrointestinal series, blood tests, and stool tests may help with diagnosis. [1] The symptoms of gastritis may be a presentation of a myocardial infarction. [2] Other conditions with similar symptoms include inflammation of the pancreas, gallbladder problems, and peptic ulcer disease. [2]

Prevention is by avoiding things that cause the disease. [4] [ examples needed ] Treatment includes medications such as antacids, H2 blockers, or proton pump inhibitors. [1] During an acute attack drinking viscous lidocaine may help. [9] If gastritis is due to NSAIDs these may be stopped. [1] If H. pylori is present it may be treated with a combination of antibiotics such as amoxicillin and clarithromycin. [1] For those with pernicious anemia, vitamin B12 supplements are recommended either by mouth or by injection. [3] People are usually advised to avoid foods that bother them. [10]

Gastritis is believed to affect about half of people worldwide. [4] In 2013 there were approximately 90 million new cases of the condition. [11] As people get older the disease becomes more common. [4] It, along with a similar condition in the first part of the intestines known as duodenitis, resulted in 50,000 deaths in 2015. [5] H. pylori was first discovered in 1981 by Barry Marshall and Robin Warren. [12]

Signs and symptoms

A peptic ulcer may accompany gastritis. Endoscopic image. 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. [13] Pain is usually located in the upper central portion of the abdomen, [14] 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: [13]

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. [15] [1]

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). [16] Gastritis caused by H. pylori infection is termed Helicobacter pylori induced gastritis, and listed as a disease in ICD11. [6] [7] 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. [17]

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.[ citation needed ]

Diet

Evidence does not support a role for specific foods, including spicy foods and coffee, in the development of peptic ulcers. [18] People are usually advised to avoid foods that bother them. [10] 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. [19]

Pathophysiology

Acute

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. 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. [20] 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. [21] [22] [23] 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. [24] 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 stimulate hydrochloric acid secretion. High doses of alcohol do not stimulate secretion of acid. [25]

Chronic

Chronic gastritis refers to a wide range of problems of the gastric issues. [20] 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. [24] 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. [26]

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. [20]

Diagnosis

Updated Sydney System for visual classification of gastritis on histopathology. 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:

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: [28]

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 0Stage IStage IIStage II
Mild atrophy (score 1)Stage IStage IStage IIStage III
Moderate atrophy (score 2)Stage IIStage IIStage IIIStage IV
Severe atrophy (score 3)Stage IIIStage IIIStage IVStage IV

Treatment

Antacids are a common treatment for mild to medium gastritis. [29] 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. [29] [30]

Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. [31] 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. [32]

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. [33]

See also

Related Research Articles

<span class="mw-page-title-main">Peptic ulcer disease</span> Ulcer of an area of the gastrointestinal tract

Peptic ulcer disease is a break in the inner lining of the stomach, the first part of the small intestine, or sometimes the lower esophagus. An ulcer in the stomach is called a gastric ulcer, while one in the first part of the intestines is a duodenal ulcer. The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain, and upper abdominal pain that improves with eating. With a gastric ulcer, the pain may worsen with eating. The pain is often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. About a third of older people with peptic ulcers have no symptoms. Complications may include bleeding, perforation, and blockage of the stomach. Bleeding occurs in as many as 15% of cases.

Heartburn, also known as pyrosis, cardialgia or acid indigestion, is a burning sensation in the central chest or upper central abdomen. Heartburn is usually due to regurgitation of gastric acid into the esophagus. It is the major symptom of gastroesophageal reflux disease (GERD).

<i>Helicobacter pylori</i> Species of bacteria

Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, flagellated, helical bacterium. Mutants can have a rod or curved rod shape, that exhibit less virulence. Its helical body is thought to have evolved to penetrate the mucous lining of the stomach, helped by its flagella, and thereby establish infection. The bacterium was first identified as the causal agent of gastric ulcers in 1983 by the Australian doctors Barry Marshall and Robin Warren. In 2005 they were awarded the Nobel Prize in Physiology or Medicine for this discovery.

<i>Helicobacter</i> Genus of bacteria

Helicobacter is a genus of gram-negative bacteria possessing a characteristic helical shape. They were initially considered to be members of the genus Campylobacter, but in 1989, Goodwin et al. published sufficient reasons to justify the new genus name Helicobacter. The genus Helicobacter contains about 35 species.

<span class="mw-page-title-main">Barry Marshall</span> Australian physician (born 1951)

Barry James Marshall is an Australian physician, Nobel Laureate in Physiology or Medicine, Professor of Clinical Microbiology and Co-Director of the Marshall Centre at the University of Western Australia. Marshall and Robin Warren showed that the bacterium Helicobacter pylori plays a major role in causing many peptic ulcers, challenging decades of medical doctrine holding that ulcers were caused primarily by stress, spicy foods, and too much acid. This discovery has allowed for a breakthrough in understanding a causative link between Helicobacter pylori infection and stomach cancer.

Coffee ground vomitus refers to a particular appearance of vomit. Within organic heme molecules of red blood cells is the element iron, which oxidizes following exposure to gastric acid. This reaction causes the vomitus to look like ground coffee.

<span class="mw-page-title-main">Achlorhydria</span> Lack of hydrochloric acid production in the digestive organs

Achlorhydria and hypochlorhydria refer to states where the production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low, respectively. It is associated with various other medical problems.

<span class="mw-page-title-main">Gastrointestinal disease</span> Illnesses of the digestive system

Gastrointestinal diseases refer to diseases involving the gastrointestinal tract, namely the esophagus, stomach, small intestine, large intestine and rectum; and the accessory organs of digestion, the liver, gallbladder, and pancreas.

Indigestion, also known as dyspepsia or upset stomach, is a condition of impaired digestion. Symptoms may include upper abdominal fullness, heartburn, nausea, belching, or upper abdominal pain. People may also experience feeling full earlier than expected when eating. Indigestion is relatively common, affecting 20% of people at some point during their life, and is frequently caused by gastroesophageal reflux disease (GERD) or gastritis.

<span class="mw-page-title-main">Atrophic gastritis</span> Chronic inflammation and degradation of the stomach lining

Atrophic gastritis is a process of chronic inflammation of the gastric mucosa of the stomach, leading to a loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. As a result, the stomach's secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired, leading to digestive problems. The most common are pernicious anemia possibly leading to vitamin B12 deficiency; and malabsorption of iron, leading to iron deficiency anaemia. It can be caused by persistent infection with Helicobacter pylori, or can be autoimmune in origin. Those with autoimmune atrophic gastritis (Type A gastritis) are statistically more likely to develop gastric carcinoma, Hashimoto's thyroiditis, and achlorhydria.

<span class="mw-page-title-main">Ménétrier's disease</span> Premalignant stomach disorder

Ménétrier disease is a rare, acquired, premalignant disease of the stomach characterized by massive gastric folds, excessive mucus production with resultant protein loss, and little or no acid production (achlorhydria). The disorder is associated with excessive secretion of transforming growth factor alpha (TGF-α). It is named after a French physician Pierre Eugène Ménétrier, 1859–1935.

Timeline of peptic ulcer disease and <i>Helicobacter pylori</i>

This is a timeline of the events relating to the discovery that peptic ulcer disease and some cancers are caused by H. pylori. In 2005, Barry Marshall and Robin Warren were awarded the Nobel Prize in Physiology or Medicine for their discovery that peptic ulcer disease (PUD) was primarily caused by Helicobacter pylori, a bacterium with affinity for acidic environments, such as the stomach. As a result, PUD that is associated with H. pylori is currently treated with antibiotics used to eradicate the infection. For decades prior to their discovery, it was widely believed that PUD was caused by excess acid in the stomach. During this time, acid control was the primary method of treatment for PUD, to only partial success. Among other effects, it is now known that acid suppression alters the stomach milieu to make it less amenable to H. pylori infection.

<span class="mw-page-title-main">Duodenitis</span> Medical condition

Duodenitis is inflammation of the duodenum. It may persist acutely or chronically.

A stress ulcer is a single or multiple mucosal defect usually caused by physiological stress which can become complicated by upper gastrointestinal bleeding. These ulcers can be caused by shock, sepsis, trauma or other conditions and are found in patients with chronic illnesses. These ulcers are a significant issue in patients in critical and intensive care.

<span class="mw-page-title-main">Stomach disease</span> Medical condition

Stomach diseases include gastritis, gastroparesis, Crohn's disease and various cancers.

<span class="mw-page-title-main">Troxipide</span> Chemical compound

Troxipide is a drug used in the treatment of gastroesophageal reflux disease. Troxipide is a systemic non-antisecretory gastric cytoprotective agent with anti-ulcer, anti-inflammatory and mucus secreting properties irrespective of pH of stomach or duodenum. Troxipide is currently marketed in Japan (Aplace), China (Shuqi), South Korea (Defensa), and India (Troxip). It is used for the management of gastric ulcers, and amelioration of gastric mucosal lesions in acute gastritis and acute exacerbation of chronic gastritis.

<span class="mw-page-title-main">Gastric folds</span> Coiled sections of tissue that exist in the mucosal and submucosal layers of the stomach

The gastric folds are coiled sections of tissue that exist in the mucosal and submucosal layers of the stomach. They provide elasticity by allowing the stomach to expand when a bolus enters it. These folds stretch outward through the action of mechanoreceptors, which respond to the increase in pressure. This allows the stomach to expand, therefore increasing the volume of the stomach without increasing pressure. They also provide the stomach with an increased surface area for nutrient absorption during digestion. Gastric folds may be seen during esophagogastroduodenoscopy or in radiological studies.

Helicobacter felis is a bacterial species in the Helicobacteraceae family, Campylobacterales order, Helicobacter genus. This bacterium is Gram-negative, microaerophilic, urease-positive, and spiral-shaped. Its type strain is CS1T. It can be pathogenic.

<span class="mw-page-title-main">Acid peptic diseases</span> Overview of the acid peptic diseases of the stomach and gastrointestinal tract

Acid peptic diseases, such as peptic ulcers, Zollinger-Ellison syndrome, and gastroesophageal reflux disease, are caused by distinct but overlapping pathogenic mechanisms involving acid effects on mucosal defense. Acid reflux damages the esophageal mucosa and may also cause laryngeal tissue injury, leading to the development of pulmonary symptoms.

Helicobacter heilmannii sensu lato refers to a group of bacterial species within the Helicobacter genus. The Helicobacter genus consists of at least 40 species of spiral-shaped flagellated, Gram-negative bacteria of which the by far most prominent and well-known species is Helicobacter pylori. H. pylori is associated with the development of gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and various subtypes of extranodal marginal zone lymphomas, e.g. those of the stomach, small intestines, large intestines, and rectum. H. pylori has also been associated with the development of bile duct cancer and has been associated with a wide range of other diseases although its role in the development of many of these other diseases requires further study.

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