Gastritis

Gastritis is inflammation of the lining of the stomach.[1] It may occur as a short episode or it may have a long duration.[1] There may be no symptoms but, when symptoms are present, the most common is upper abdominal pain.[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]

Gastritis
Micrograph showing gastritis. H&E stain.
SpecialtyGastroenterology
SymptomsUpper abdominal pain, nausea, vomiting, bloating, loss of appetite, heartburn[1][2]
ComplicationsBleeding, stomach ulcers, stomach tumors, pernicious anemia[1][3]
DurationShort or long term[1]
CausesHelicobacter pylori, NSAIDs, alcohol, smoking, cocaine, severe illness, autoimmune problems[1]
Diagnostic methodEndoscopy, upper gastrointestinal series, blood tests, stool tests[1]
Differential diagnosisMyocardial infarction, inflammation of the pancreas, gallbladder problems, peptic ulcer disease, gastric cancer, Ménétrier's disease, cholecystitis, Zollinger-Ellison syndrome, dyspepsia, celiac disease[4][2]
TreatmentAntacids, H2 blockers, proton pump inhibitors, antibiotics[1]
Frequency~50% of people[5]
Deaths50,000 (2015)[6]

Common causes include infection with Helicobacter pylori and use of nonsteroidal anti-inflammatory drugs (NSAIDs).[1] Less common causes include alcohol, smoking, cocaine, severe illness, autoimmune problems, radiation therapy and Crohn's disease.[1][7] 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.[5] Treatment includes medications such as antacids, H2 blockers, or proton pump inhibitors.[1] During an acute attack drinking viscous lidocaine may help.[8] 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.[9]

Gastritis is believed to affect about half of people worldwide.[5] In 2013 there were approximately 90 million new cases of the condition.[10] As people get older the disease becomes more common.[5] It, along with a similar condition in the first part of the intestines known as duodenitis, resulted in 50,000 deaths in 2015.[6]

Signs and symptoms
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.[1] Pain is usually located in the upper central portion of the abdomen,[11] 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:

Cause

Common causes include Helicobacter pylori and NSAIDs.[1] Less common causes include alcohol, cocaine, severe illness, radiation exposure, and Crohn disease, among others.[1] Cases of exercise induced bleeding as a result of gastritis have also been reported.[13]

Infections

Helicobacter

Helicobacter species such as H. suis (most often), H. felis, H. bizzozeronii, and H. salomonis have been associated with chronic gastritis and peptic ulcers in humans and, importantly, with higher risk for MALT lymphoma compared to H. pylori.[14] Other causes may include Helicobacter heilmannii sensu lato.[15]

Helicobacter pylori(HP) 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, some distinct extragastric disorders).[16] However, over 80 percent 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] HP infection is specific to a certain type of gastritis called follicular gastritis, it is also present in 50% of Russell body gastritis, in which the lamina propria contains plasma cells with prominent intracytoplasmic inclusions of immunoglobulins.[18]

Viral

Gastritis can be induced by viral infections such as cytomegalovirus, herpes simplex virus (rare and restricted to immunosuppressed patients), varicella zoster virus only diagnosed by PCR, intranuclear viral inclusions are eosinophilic and have ground-glass appearance in epithelial cells (antiviral treatment is effective and most cases resolve within 2 weeks), Epstein-Barr virus (Although EBV may not cause a primary gastritis, EBV infection is associated with gastric pathology) or adenovirus.[19][18]

Fungi

Infections with fungi like Zygomycota, Histoplasma capsulatum, Aspergillus (rare) or Candida can cause gastritis.[18]

Parasites

Gastric giardiasis only occurs in those with intestinal giardiasis, with 11% of people with intestinal giardiasis have concurrent gastric giardiasis. Symptoms include dyspepsia, epigastric pain, and abdominal distension. Chronic atrophic gastritis is common, but whether this can be entirely attributed to giardiasis is uncertain.[18]

Anisakiasis[18]

Cryptosporidiosis[18]

Leishmaniasis[18]

Strongyloidiasis[18]

Toxoplasmosis[18]

Critical illness

Gastritis may also develop after major surgery or traumatic injury ("Cushing ulcer"), burns ("Curling ulcer"), or severe infections.[1]

Diet

Evidence does not support a role for specific foods including spicy foods and coffee in the development of peptic ulcers.[20] People are usually advised to avoid foods that bother them.[9] Eating spicy foods can cause gastritis by irritating the stomach lining.[21]

Other

Pathophysiology

Active gastritis is characterized by granulocyte and agranulocyte infiltration of the mucosa of the antrum and body.[23][24] The term pangastritis refers to an inflammation in the stomach as a whole.

Acute

Acute gastritis refers to how fast the symptoms have come on.[25] 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.[26] 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.[27] Additionally, severe physiologic stress ("stress ulcers") from sepsis, hypoxia, trauma, or surgery, is also a common etiology for acute erosive gastritis. This form of gastritis can occur in more than 5% of hospitalized patients.

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.[28] It differs from active gastritis which is when neutrophils are present.[25]

Acute erosive gastropathy

Acute erosive gastropathy or stress gastritis is a type of acute gastritis caused by various health problems (injuries, burns, or sepsis) that reduce the blood flow to the stomach lining.[1]

Chronic

Chronic gastritis refers to a wide range of problems of the gastric tissues.[24]

Gastric syphilis

A previous history with the syphilis disease has not been encountered in about 13% of patients who experience epigastric pain/fullness, tenderness, and upper gastrointestinal bleeding as symptoms. Gastric syphilis should be considered especially in patients who are at risk for sexually transmitted diseases, have unusual endoscopic findings, or do not respond to standard therapy for presumed peptic ulcer disease.[18]

Complications

Complications include hemorrhage, gastric outlet obstruction, and perforation, with up to 17% of patients receiving surgical treatment due to these complications.[18]

Hyperplastic gastropathy

Hyperplastic gastropathy is characterised with enlarged gastric folds, inflammation and clinical manifestations similar to Ménétrier disease. It has also been described as being associated with H. pylori infection.[18]

Atrophic gastritis

Bile reflux gastritis

Bile reflux gastritis can result from excess bile in the duodenum, lack of a pylorus as a barrier to retrograde flow, and/or decreased anterograde peristalsis of the stomach and duodenum. This can occur following gastric or biliary surgery or as primary biliary reflux. The most common predisposing surgeries are those that either remove, disrupt or bypass the pylorus, resulting in unopposed reflux of duodenal contents. Primary biliary reflux occurs in the absence of gastric surgery. Risk factors include gallbladder dysfunction and gastric or duodenal dysmotility. Individuals with bile reflux gastritis have been shown to have a decreased frequency of migratory motor complexes, suggesting that the gastritis might be related to a prolonged mucosal exposure to bile. Diagnosis is done with checking for biliary reflux and histologic changes of gastritis.[29]

Idiopathic chronic gastritis

Idiopathic chronic gastritis occur in about 15 to 25% of cases.[19]

Chronic erosive gastropathy

Chronic erosive gastropathy or hemorrhagic gastropathy is a type of chronic gastritis caused by the disregulation of 3 substances located in the stomach, acetylcholine, gastrin and histamine. It is also called stress gastritis because physiologic stress cause elevated ACH and histamine in the stomach resulting in increased acid production.[22]

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.[24]

Collagenous gastritis

Collagenous gastritis (CG) is a rare form of chronic gastritis characterised by the deposition of subepithelial collagen band thicker than 10 μm and a chronic inflammation of the lamina propria. The clinical features for the children and adults are generally not the same. Children often present symtpoms of iron anemia and the adults with gastrointestinal tract involvement, being associated with collagenous colitis or collagenous sprue, and chronic watery diarrhea. There is no established treatment for CG.[30]

Lymphocytic gastritis

Lymphocytic gastritis (LG) is a special case of chronic gastritis characterized by a high number of lymphocytes in the epithelium, the foveolar epithelium and the lamina propria. (typically between 40 and 60 per 100 epithelial cells). It is strongly associated with varioliform gastritis with up to 82% of cases.[31] This type of gastritis is also associated with HP infection.[18]

Varioliform gastritis

Varioliform gastritis (VG) is a special case of chronic gastritis characterised by nodules, gastric folds thickening and erosions. The frequency of varioliform gastritis is estimated to be found in 0.3 to 2.8% of upper gastrointestinal endoscopies. The diagnosis can be made by endoscopic examination.[32]

Eosinophilic gastroenteritis

Another type of chronic gastritis is eosinophilic gastroenteritis.

Diagnosis

Treatment with proton-pump inhibitors leads to false-negative results in both invasive and non-invasive diagnostic tests.[4] Often, a diagnosis can be made based on the person's description of their symptoms, but other methods which may be used to verify gastritis include:

  • Blood tests:
    • Liver, kidney, gallbladder, or pancreas functions
    • Biomarkers count such as pepsinogen 3, group I (pepsinogen A) (PGI), progastricsin (PGII) and little gastrin I (G-17). PGII alone is considered as a reliable biomarker of gastric inflammation[33]
  • Stool sample, to look for blood or signs of H. pylori infection in the stool[1]
  • Various tests to look for HP infection[18]
  • Upper GI series to check for signs of gastritis or gastropathy[1]
  • Endoscopy, to check for stomach lining inflammation and mucous erosion. Magnifying endoscopy combined with staining can facilitate the pathologic classification of chronic gastritis.[12][4]
  • Stomach biopsy (2 to 3 pieces of tissues each at the antrum, gastric angle and gastric body should be obtained, and additional biopsies can be obtained from areas with suspected lesions), to test for gastritis, (specially biopsies of antral and oxyntic mucosa for HP and H. heilmannii detection as HP and H. heilmannii are antrum-dominant infections[18]) and other conditions (gold standard)[12][4][1] [19]
  • Electronic magnifying chromoendoscopy and confocal laser microendoscopy have certain value in the diagnosis and differential diagnosis of chronic gastritis.[12]
  • Nasogastric test for testing for stress induced gastritis.[22]
  • The range of intestinal metaplasia and its subtypes have certain values that predict the risk of gastric cancer. AB-PAS and HID-AB mucous staining can differentiate the intestinal metaplasia subtypes.[12]

Chronic gastritis

Endoscopy combined with histopathologic examination can diagnose the two basic types of chronic gastritis, chronic non-atrophic gastritis and chronic atrophic gastritis.[12]

Grading system

Since 1992, chronic gastritis lesions are classified according to the Sydney system, a system in which the primary goal is to provide guidelines related to the aspect of biopsies and how to write a report. Chronic gastritis has five histologic changes: H. pylori, activity, inflammatory reaction, atrophy and intestinal metaplasia, which can be further divided into 4 grades: none, mild, moderate and severe (0, +, ++, +++). These grading standards are based on the pathologic diagnostic criteria for chronic gastritis in China, and the Sydney system.[12] The OLGA and OLGIM staging systems (proposed by the International Atrophy Study Group) can reflect the severity and extent of gastric mucosal atrophy in patients with chronic gastritis. Studies have shown that these staging systems can also predict accurately the risk of gastric cancer. The OLGA staging system is based on the Sydney system.[12]

Gastric syphilis

Radiologic studies often show fibrotic narrowing and rigidity of the gastric wall; other findings include mucosal nodules and hypertrophic, irregular folds. Endoscopically, mucosal nodularity, erosions, or ulcers with heaped up edges are common. The antrum seems to be preferentially involved. On biopsy, the main finding is gastric mucosa that shows marked expansion of the lamina propria by a dense infiltrate of plasma cells that sometimes displays perivascular cuffing. Occasional intraepithelial neutrophils, glandular injury, granulomas, and a secondary vasculitis have also been described. At times, the lymphocytic inflammation can be so intense with lymphoepithelial lesions and atypical cytologic features that it can raise concern for malignant lymphoma. In these cases, lymphocyte clonality studies may be necessary to exclude malignancy. The diagnosis rests upon demonstration of spirochetes by silver histochemical stains or anti-Treponema immunohistochemistry; the latter is preferable due to the ease of interpretation and improved sensitivity. Ancillary tests include serologic studies and molecular methods. The Venereal Disease Research Laboratory (VDRL), rapid plasma reagin (RPR), unheated serum reagin (USR), and toluidine red unheated serum (TRUST) tests offer the advantages of being quick and inexpensive, but come with the drawbacks of being insensitive in early and late disease as well as false-negatives and false-positives. Polymerase chain reaction (PCR), albeit more expensive, is both sensitive and specific, and can be particularly helpful in detecting early infection.[18]

CMV

The CMV-infected stomach can show mucosal edema, erythema, congestion, erosions, or ulcers. CMV gastritis can also present with hypertrophic gastric folds, also known as hypertrophic gastropathy, and can resemble Ménétrier disease both endoscopically and microscopically. Infected patients can also present with protein-losing enteropathy; in fact, some authors have speculated that CMV may be a cause of Ménétrier disease. Microscopically, gastric mucosa involved by CMV tends be ulcerated, with the lamina propria expanded by a mixed or plasma cell rich inflammatory infiltrate. Epithelial apoptosis in the mid-zone of the mucosa may be a subtle finding that should prompt a search for viral inclusions. In contrast to other segments of the tubular GI tract such as the colon, most cases of CMV gastritis do not show aggregates of macrophages surrounding viral inclusions or a perivascular distribution. In cases with hypertrophic gastropathy, additional findings include marked foveolar hyperplasia, intramucosal cyst formation, atrophic appearing oxyntic glands, and increased intra-epithelial T lymphocytes.[18]

Treatment

Treatment may include medications such as antacids, H2 blockers, or proton pump inhibitors.[1] For stress induced gastritis, the mainstay of treatment is PPI administration, and the second line is the use of histamine blockers.[22] Ursodeoxycholic acid is an adequate treatment of bile reflux gastritis.[29]

Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine.[34] They include the medications sucralfate, rebamipide,[35] and misoprostol. If NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken.[36]

Treatment in gastritis include cessation of alcohol, smoking, anti-inflammatory drugs, spicy food, as well as managing stress.[4]

Surgery

Bile reflux gastritis

Surgical management of bile reflux aims to divert bile away from the stomach. The most commonly utilized procedures include interposed isoperistaltic jejunal (Henley) loop, Braun enteroenterostomy and a roux-en-Y procedure. A roux-en-y choledochojejunostomy can be used to divert bile directly from the biliary tree after cholecystectomy. These procedures are effective in relieving symptoms but can be complicated by stomal ulcerations, roux stasis syndrome, and bezoar formation. [29]

Epidemiology

Gastritis is believed to affect about half of people worldwide.[5] In 2013 there were approximately 90 million new cases of the condition.[37] As people get older the disease becomes more common.[5] It, along with a similar condition in the first part of the intestines known as duodenitis, resulted in 50,000 deaths in 2015.[6]

Prognosis

There is an increased risk of gastric cancer in patients with intraepithelial neoplasia. Studies found that methylation of the AMPH, PCDH10, RSPO2, SORCS3 and ZNF610 genes could predict the progress of gastric mucosal lesions. Age is related to histological atrophy and even the appearance of intestinal metaplasia, in addition to genetic factors, H. pylori infection, dietary conditions, and lifestyle. After integrating a variety of factors, the "stomach age" can reflect the aging of gastric mucosal cells. The concept of stomach age is based on the telomeres length of mucosal cells. And the fact that the stomach lining tends to thin with age.[38][12]

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 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 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 hypetrophic 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 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.

See also

References
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Classification
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