Gastritis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Gastritis is inflammation of the gastric mucosa. In the Greek gastro- means the stomach and -itis means inflammation. Depending on the cause, it may persist acutely or chronically and may coincide with more serious conditions such as atrophy of the stomach. In 1728, a German physician named Georg Ernst Stahl first used the term “gastritis” to describe inflammation of the inner lining of the stomach. In 1982, Robin Warren and Barry Marshall discovered Helicobacter pylori which further led to the identification and classification of different gastritides. In 2005, gastritis staging using the OLGA (Operative Link on Gastritis Assessment) staging system for reporting gastric histology was introduced. Gastritis, depending on the causes may be classified into acute gastritis, chronic gastritis, atrophic gastritis, and H.pylori associated gastritis. In the majority of patients presenting with acute gastritis, the initial acute phase is subclinical and is of short duration (about 7 to 10 days). Acute gastritis also referred to as reactive gastritis occurs as a result of the trigger by factors such as NSAIDs, stress, bile reflux, radiation, alcohol abuse, cocaine addiction and ischemic damage. In chronic gastritis, the H. pylori infection persists leading to accumulation of large number chronic inflammatory cells leading to active chronic gastritis. Gastritis must be differentiated from peptic ulcer disease, gastric cancer, gastroesophageal reflux disease (GERD), gastroenteritis, crohn’s disease, gastrinoma, gastric adenocarcinoma and primary gastric lymphoma. In acute gastritis, the prevalence of eosinophilic gastritis is approximately 6.3 per 100,000 individuals worldwide. The incidence of new cases of H.pylori infection each year ranges from 3,000 to 10,000 per 100,000 individuals in developing countries. It has been observed that with advancing age, the incidence of H.pylori infection is increased. Common risk factors in the development of Gastritis include alcohol, NSAIDs, cocaine, autoimmune gastritis, crohn’s disease, HIV/AIDS and bacterial infections such as Helicobacter pylori. Less common risk factors in the development of Gastritis include, food poisoning (bacterial gastroenteritis), autoimmune gastritis predisposing to vitamin B-12 deficiency and other autoimmune disorders such as Hashimoto’s disease and type 1 diabetes, stress as a result of major surgery or trauma or other illness, traumatic injury, burns or severe infections, bile reflux, low fiber diet, processed food as the primary source, pernicious anemia and viral and parasitic infections. There is insufficient evidence to recommend routine screening for gastritis. The increased risk of developing duodenal and peptic ulcers have been observed in individuals with persistent gastritis. Biopsies and routine evaluations may help predict the progression of gastritis to the conditions such as the peptic ulcer disease. Complications of gastritis may include, peptic ulcers, gastrointestinal perforation, gastrointestinal bleeding, gastric polyp, anemia due to erosive gastritis, vitamin B12 deficiency, pernicious anemia, gastric outlet obstruction. Prognosis for gastritis is majorly dependent upon the type of gastritis and etiological factors. In chronic gastritis associated with Helicobacter pylori infection, the prognosis is good. The triple therapy regimen may not be as effective when compared to quadruple bismuth-based regimen has proven to be very effective comparatively. If left untreated, Helicobacter pylori infection associated chronic gastritis, may progress to develop peptic ulcer disease, adenocarcinoma and MALT lymphoma.

In 1728, a German physician named Georg Ernst Stahl first used the term “gastritis” to describe inflammation of the inner lining of the stomach. In 1982, Robin Warren and Barry Marshall discovered Helicobacter pylori which further led to the identification and classification of different gastritides. in 1990, A New Classification of Gastritis called the Sydney System was presented to the World Congress of Gastroenterology in Sydney and was later published as six papers in the Journal of gastroenterology and hepatology. In 1994, at the international workshop on the histopathology of gastritis held at Houston, The updated Sydney System for the classification and grading of gastritis was introduced. In 2005, gastritis staging using the OLGA (Operative Link on Gastritis Assessment) staging system for reporting gastric histology was introduced.

Classification and grading of Gastritis based on the Updated Sydney System emphasizes the importance of combining topographical, morphological, and etiological information into a schema that would help to generate reproducible and clinically useful diagnoses. In clinical practice, Gastritis staging is done using the OLGA (Operative Link on Gastritis Assessment) staging system for reporting gastric histology. Gastritis staging integrates the atrophy score (obtained by biopsy) and the atrophy topography (achieved through directed biopsy mapping).

Gastritis depending on the causes may be classified into acute gastritis, chronic gastritis, atrophic gastritis, and H.pylori associated gastritis. In acute gastritis, the majority of patients, the initial acute phase of gastritis is subclinical and is of short duration (about 7 to 10 days). Acute gastritis also referred to as reactive gastritis occurs as a result of the trigger by factors such as NSAIDs, stress, bile reflux, radiation, alcohol abuse, cocaine addiction and ischemic damage. In chronic gastritis, the H. pylori infection persists leading to accumulation of large number chronic inflammatory cells leading to active chronic gastritis.

The most common causes of Gastritis include H. pylori infection, alcohol consumption, cigarette smoking, extended use of NSAIDs such as (aspirin, naproxen, ibuprofen), stress, autoimmune gastritis and excessive consumption of coffee and acidic beverages. Less common causes of Gastritis include cocaine addiction, bile reflux, crohn’s disease, constipation, consumption of poisons and other caustic or corrosive chemical substances, sarcoidosis, radiation therapy, chemotherapy drugs, iron and potassium supplements, stress as a result of major surgery or trauma or other illness, infections can be caused by viruses such as HSV, cytomegalovirus CMV (mostly seen in immunocompromised individuals), parasitic infections and fungal infections.

Gastritis must be differentiated from peptic ulcer disease, gastric cancer, gastroesophageal reflux disease (GERD), gastroenteritis, crohn’s disease, gastrinoma, gastric adenocarcinoma and primary gastric lymphoma.

In acute gastritis, the prevalence of eosinophilic gastritis is approximately 6.3 per 100,000 individuals worldwide. The incidence of new cases of H.pylori infection each year ranges from 3,000 to 10,000 per 100,000 individuals in developing countries. It has been observed that the incidence of H.pylori infection increases with advancing age. In united states, 20% of adolescents are infected with H. pylori when compared to 90% in developing countries by the age of 5. In United States, H. pylori infection associated gastritis is more common in African Americans (54%), Hispanics (52%), and the elderly compared to Whites(21%). In acute gastritis, females are usually more affected than men. In H. pylori infection associated gastritis, males are more commonly affected than females. The incidence rates of H.pylori infection are high in Japan, Columbia, Costa Rica and China, and comparatively low in the United States. H.pylori infection is common in southern and eastern Europe, Mexico, South America, Africa, most Asian countries, and aboriginal people in North America.

Common risk factors in the development of gastritis include alcohol, NSAIDs, cocaine, autoimmune gastritis, crohn’s disease, HIV/AIDS and bacterial infections such as Helicobacter pylori. Less common risk factors in the development of gastritis include, food poisoning (bacterial gastroenteritis), autoimmune gastritis predisposing to vitamin B-12 deficiency and other autoimmune disorders such as Hashimoto’s disease and type 1 diabetes, stress as a result of major surgery or trauma or other illness, traumatic injury, burns or severe infections, bile reflux, low fiber diet, processed food as the primary source of diet, pernicious anemia and viral and parasitic infections.

There is insufficient evidence to recommend routine screening for gastritis.

Gastritis is a common inflammatory disease. Gastritis usually persists throughout life and the chance of spontaneous remission is rare. Gastritis is most commonly associated with Helicobacter pylori infection. The gastric mucosa undergoes inflammatory changes which may finally lead to atrophic gastritis. Chronic gastritis is commonly observed as a manifestation of progression of many gastric conditions. Gastric secretory functions are usually impaired due to inflammation and atrophy of the gastric mucosa. Increase in the prevalence of gastritis is attributed to the increasing age and the onset varies among different ethnicities. The increased risk of developing duodenal and peptic ulcers have been observed in individuals with persistent gastritis. Biopsies and routine evaluations may help predict the progression of gastritis to the conditions such as the peptic ulcer disease.

Complications of gastritis may include, peptic ulcers, gastrointestinal perforation, gastrointestinal bleeding, gastric polyp, anemia due to erosive gastritis, vitamin B12 deficiency, pernicious anemia, gastric outlet obstruction, increased risk of developing benign or malignant growths in the lining of the stomach which may lead to stomach cancer.

Prognosis for gastritis is majorly dependent upon the type of gastritis and etiological factors. In acute gastritis, the condition improves upon refraining from risk factors such as NSAIDs, alcohol, cigarette smoking, acidic food, and beverages. In autoimmune gastritis, prognosis for vitamin B12 deficiency when treated with cyanocobalamin therapy is good. Although in autoimmune gastritis, there is an increased risk for carcinoid tumors and gastric adenocarcinoma. In chronic gastritis associated with Helicobacter pylori infection, the prognosis is good. The triple therapy regimen may not be as effective when compared to quadruple bismuth-based regimen which has proven to be very effective comparatively. Helicobacter pylori infection associated chronic gastritis, if left untreated may progress to develop peptic ulcer disease, adenocarcinoma and MALT lymphoma.

It is important to reviews a patient’s history regarding medications, alcohol intake, smoking, and other risk factors that may be associated with gastritis.. Symptoms of gastritis may be silent or manifest as abdominal discomfort, nausea, vomiting, and/or gastrointestinal bleeding. Individuals with gastritis experience abdominal pain and gastric disturbances. Symptoms as a result of gastritis are upper abdominal pain or discomfort, dyspepsia (indigestion), nausea, vomiting of blood or dark brown/coffee-ground like vomitus, bloating sensation in the upper abdomen, belching, heartburn, loss of appetite, malena (dark stools), gastric hemorrhage, fever, lethargy, halitosis, epigastric pain or abdominal pain, early satiety, fatigue and diarrhea.

Patients with gastritis may appear pale. Some patients may appear fatigued and in distress if associated with abdominal pain. Vital signs generally appear to be normal. If associated with gastrointestinal bleed, vital signs include tachycardia. Pallor may observed in patients presenting with melena and hematemesis. On examination of the eyes, conjunctival pallor may be observed. Halitosis may be observed in case of chronic gastritis. Chest tenderness may be present on palpation in case of Helicobacter pylori infection associated gastritis. Abdominal pain or discomfort may be observed. Epigastric tenderness may be present. Gastritis associated with gastric ulcers may result in blood loss and the stool test may be guaiac-positive.

Endoscopic diagnostic tests are biopsy-based diagnostic methods for gastritis associated with H. pylori infection. These include histology, rapid urease testing, culture and polymerase chain reaction (PCR).

The nonendoscopic diagnostic testing methods for gastritis associated with H. pylori include antibody tests, urea breath test, and fecal antigen test.

CT scan may be helpful in the diagnosis of gastritis. Findings on CT scan suggestive of gastritis include gastric wall edema and halo sign.

An x-ray may be helpful in the diagnosis of gastritis. Series of x-rays of the esophagus, stomach and duodenum known as the upper gastrointestinal series or barium swallow aid in determining the condition. In barium swallow procedure, the patient is made to ingest a white liquid which contains barium. The ingested barium liquid lines the gastrointestinal tract and helps in visualizing the ulcers better when the x-ray is taken.

In Helicobacter pylori infection which is the most common cause of gastritis, a non-invasive test such as the urea breath test is used to determine the presence of H. pylori in the stomach.

Medical therapy for gastritis depends on its specific cause. Medications known to cause gastritis such as NSAIDs (aspirin, naproxen, ibuprofen) should be discontinued. Smoking cessation and abstenance from alcohol consumption is recommended. Medications to decrease gastric acid production such as proton pump inhibitors (PPI) are recommended. In cases of Helicobacter pylori infection, antimicrobial drugs are recommended. Helicobacter infection typically responds well to the triple therapy protocol (consisting of two antibiotics, and a proton pump inhibitor). Regimens that work well include PCA or PCM triple therapy (PPI, clarithromycin, amoxicillin) or (PPI, clarithromycin, metronidazole). Quadruple therapy has a >90% success rate and includes PPIs, bismuth subsalicylate, metronidazole, and tetracycline. Indications for treatment of H. pylori infection include past or present duodenal and/or gastric ulcer, with or without complications, following resection of gastric cancer, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, atrophic gastritis, dyspepsia, and patients with first-degree relatives with gastric cancer. Factors involved in choosing treatment regimens include prevalence of H. pylori infection, prevalence of gastric cancer, resistance to antibiotics, availability of bismuth, availability of endoscopy and H. pylori tests, ethnicity, drug allergies and tolerance, previous treatments and outcome, adverse effects, effectiveness of local treatment and recommended dosages and treatment duration.

Surgical intervention is not recommended for the management of gastritis.

Effective measures for the primary prevention of gastritis include avoiding long term or extended use of medications such as NSAIDs, abstenance from alcohol, cessation of cigarette smoking, coffee or acidic beverages, spicy foods and avoiding stress. Inculcating healthy eating habits, exercising regularly and maintaining healthy body weight may help in avoiding gastritis. Effective measures for primary prevention of the H. pylori infection include hand washing (antibacterial soaps), avoid contaminated food and water, maintain proper hygiene (hand sanitizers, antiseptic washes) and avoid close contact with infected family members ( e.g., kissing, by sharing eating utensils and drinking glasses).

The secondary prevention strategies for gastritis following H. pylori infection to prevent recurrence of peptic ulcer disease and gastric cancer include the use of antibiotics to prevent recurrence of infection and the post treatment confirmation of H. pylori eradication after treatment using diagnostic tests.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

In 1728, Georg Ernst Stahl, a German physician first used the term “gastritis” to describe inflammation of the inner lining of the stomach. In 1982, Robin Warren and Barry Marshall discovered Helicobacter pylori which further led to the identification and classification of different gastritides. In 1990, a new classification of gastritis called the Sydney system was presented to the World Congress of gastroenterology in Sydney and was later published as six papers in the Journal of gastroenterology and hepatology. In 1994, the updated Sydney System for the classification and grading of gastritis was introduced at the International Workshop on the histopathology of gastritis held at Houston. In 2005, gastritis staging using the OLGA (Operative Link on Gastritis Assessment) staging system for reporting gastric histology was introduced.

• In 1728, George Stahl first noted inflammation of the inner lining of the stomach as “gastritis”.
• In 1771, Giovanni Morgagni described “erosive” and “ulcerating gastritis”.
• In 1855, Baron Carl von Rokitansky described “hypertrophic gastritis”.
• In 1870, Samuel Fenwick described gastric atrophy.
• In 1944, Warren & Meissner described intestinal metaplasia as feature of chronic gastritis.
• In 1947, Sir Ian Jeffreys Wood, performed first gastric biopsy with semi-flexible biopsy tube and defined “gastritis” by histopathology.
• In 1956, Louis Streifeneder and Eddy Palmer introduced flexible fiber optic endoscope.
• In 1982, Robin Warren and Barry Marshall discovered Helicobacter pylori which further led to the identification and classification of different gastritides.^[1]
• In 1990, a new classification of gastritis called the Sydney system was presented to the World Congress of gastroenterology in Sydney and was later published as six papers in the Journal of gastroenterology and hepatology.^[2][3]
• In 1994, the updated Sydney system for the classification and grading of gastritis was introduced at the international workshop on the histopathology of gastritis held at Houston.^[3]
• In 2005, gastritis staging using the OLGA (Operative Link on Gastritis Assessment) staging system for reporting gastric histology was introduced. Gastritis staging combines the atrophy score which is determined by biopsy and the atrophy topography which is determined by directed biopsy mapping.^[4][5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]}}

The Updated Sydney System establishes the classification and grading of gastritis which underlines the significance of combining topographical, morphological, and etiological information to help arrive at clinical diagnosis. In clinical practice, gastritis staging is done using the OLGA (Operative Link on Gastritis Assessment) staging system for reporting gastric histology. Gastritis staging combines the atrophy score which is determined by biopsy and the atrophy topography which is determined by directed biopsy mapping.

• The Updated Sydney System establishes the classification and grading of gastritis which underlines the significance of combining topographical, morphological, and etiological information to help arrive at clinical diagnosis. ^[1]
  

• In clinical practice, gastritis staging is done using the OLGA (Operative Link on Gastritis Assessment) staging system for reporting gastric histology. Gastritis staging combines the atrophy score which is determined by biopsy and the atrophy topography which is determined by directed biopsy mapping. ^{[2] [3]}

Sydney system for grading of chronic gastritis^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Gastritis depending on the causes may be classified into acute gastritis, chronic gastritis, atrophic gastritis, and H. pylori associated gastritis. In the majority of patients with acute gastritis, the initial acute phase of gastritis is subclinical and is of short duration (about 7 to 10 days). Acute gastritis also referred to as reactive gastritis occurs as a result of the trigger by factors such as NSAIDs, stress, bile reflux, radiation, alcohol abuse, cocaine addiction, and ischemic damage. In chronic gastritis, the H. pylori infection persists leading to accumulation of large number chronic inflammatory cells leading to active chronic gastritis.

• Acute gastritis also referred to as reactive gastritis occurs as a result of the trigger by factors such as NSAIDs, stress, bile reflux, radiation, alcohol abuse, cocaine addiction, and ischemic damage. The outcome of these triggers may result in ulcers, hemorrhage and erosion of the gastric mucosa.

• The decrease in the prostaglandin synthesis is thought to be the reason for the injury to the gastric mucosa. The gastric mucosa is safeguarded from the deleterious effects of the gastric acid by mechanisms promoted by the prostaglandins.
• In the majority of patients, the initial acute phase of gastritis is subclinical and is of short duration (about 7 to 10 days).
• In the majority of cases of H. pylori infection, the infection is not eliminated and there will be gradual accumulation of chronic inflammatory cells over the next 3 or 4 weeks.^[1] In H. pylori infection, the organisms are spontaneously cleared in a small minority of people, especially in childhood.
• Following transmission, H. pylori penetrates the gastric mucosa and multiplies close to the surface epithelial cells.
• Following adhesion to epithelial cells, the bacteria releases lipopolysaccharides (endotoxin) and chemotactic mediators which penetrate the surface epithelial cells.^[2][3]

Histological features observed includes:

• Hyperemia
• Acute inflammation
• Increased polymorphonuclear neutrophil in the superficial lamina propria
• Erosion of the surface epithelium
• Sloughing
• Mucosal necrosis to a greater extent
• Scarring (later sequelae)

In the majority of cases, the H. pylori infection persists leading to accumulation of large number of chronic inflammatory cells leading to active chronic gastritis.

• The major diagnostic feature of chronic gastritis is an influx of lymphocytes and plasma cells (normally the antral mucosa is devoid of plasma cells and lymphocytes). Hence the presence of these cells is indicative of gastritis.^[4]
• H. pylori colonizes more in the antrum than the corpus. Hence there is increased inflammatory cell infiltration in the antrum.
• The direct acting antigens of H. pylori like lipopolysaccharides and urease along with interleukins 1 and 6, activate T-helper cells which produce the variety of cytokines including IL-4, IL-5, and IL-6.
• These interleukins differentiate into plasma cells releasing cytokines and anti-H.pylori infection like IgM-opsonizing and complement-fixing antibodies.
• The main role of the mucosa in the immune response is that the IgA prevents bacterial adhesion and IgG causes opsonization and complement activation.
• Due to the acidic environment, the antibodies produced quickly lose their adhesive properties and catalase produced by H. pylori protects against polymorphs.
• However, this immune response is insufficient to eradicate the organism leading to the development of immune response directed towards preventing the damaging effects of the H. pylori.
• Hence the persistent antigenic stimulation leads to the formation of lymphoid follicles, which is the consistent feature of chronic H. pylori infection.
• These lymphoid follicles in the gastric mucosa constitutes mucosa-associated lymphoid tissue (MALT) from which gastric marginal zone B-cell lymphoma (MALToma) arises.

Also, these polymorphs accumulate around the pit isthmus, which is a proliferative compartment, causing lethal damage to stem cells resulting in glandular atrophy.

• Variable epithelial degeneration
• Neutrophil infiltration in the epithelium and the lamina propria
• Variable H. pylori colonization
• Lymphocytes and plasma cell infiltration
• Lymphoid follicles (typical feature of chronic gastritis)
• Around one-fifth of cases with an inflamed cardia may undergo intestinal metaplasia. ^[5]

• 
  Chronic gastritis – Intermedicate Magnification, By Nephron (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons ^[6]
• 
  Chronic gastritis – Very-High Magnification, By Nephron (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons ^[7]

Sydney system for grading of chronic gastritis^[8]

Atrophy of stomach is defined as loss of glandular tissue due to continuous mucosal injury. This leads to thinning of gastric mucosa.

• The prevalence and severity of atrophy of stomach increases with age among the patient’s chronic gastritis due to longer duration of H. pylori infection.
• Due to glandular atrophy, the prevalence of H. pylori positivity decreases. The main reasons are as follows:

• Due to intestinal metaplasia that is usually present in atrophic stomach, the organisms are absent as they usually colonize only gastric epithelium.
• As H. pylori requires partially acidic environment to thrive, hypochlorhydria creates hostile environment to H. pylori to survive.^[9]
• The metaplastic epithelium secretes acidic glycoproteins which create the most hostile environment for H. pylori.

• Hence, based on above reasons, failure to demonstrate H. pylori does not deny the role of the organism in atrophic gastritis.

• The continuous mucosal injury due to long-standing H. pylori infection, leads to atrophy of stomach.
• This continuous pathological process results in erosion or ulceration of the mucosa leading to the destruction of the glandular layer and followed by fibrous replacement.
• The destruction of the glandular basement membrane and the sheath of supporting cells prevents orderly regeneration. This uneven regeneration follows a divergent differentiation pathway producing metaplastic glands (pseudo-pyloric appearance) which are composed of cells of the ‘ulcer-associated cell lineage’ (UACL).^[10]

• Reduced number of oxyntic cells. No intestinal metaplasia
• The mucosa is infiltrated with neutrophils
• H. pylori is not seen on H&E stain.
• Immunohistochemical stain of H. pylori detects the organisms.

• Erosive Gastritis:
  • Erosive gastritis results due to the loss of superficial epithelium, it usually does not extend beyond the muscularis mucosa.
  • The crypts may present as dilatations and contain acute inflammatory cells.

Chronic gastritis {{#ev:youtube|Wvn5TiiIB4Q}}

Atrophic gastritis {{#ev:youtube|760GB43AZqE}}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

The most common causes of gastritis include H. pylori infection, alcohol consumption, cigarette smoking, extended use of NSAIDs such as (aspirin, naproxen, ibuprofen), stress, autoimmune gastritis, and excessive consumption of coffee and acidic beverages. Less common causes of gastritis include cocaine addiction, bile reflux, crohn’s disease, constipation, consumption of poisons and other caustic or corrosive chemical substances, sarcoidosis, radiation therapy, chemotherapy drugs, iron and potassium supplements; stress as a result of major surgery, trauma, or other illness; infections caused by viruses such as HSV, cytomegalovirus (mostly seen in immunocompromised individuals), parasitic infections, and fungal infections.

The causes may be divided into common and less common causes: ^{[1][2][3][4][5][6][7][8][9][10]}

• Helicobacter pylori (H. pylori) infection
• Excessive alcohol consumption (usually results in acute gastritis)
• Smoking cigarettes
• Long term or extended use of NSAIDs (aspirin, naproxen, ibuprofen) leads to the damage of stomach lining
• Autoimmune response
• Stress resulting in excessive gastric acid secretion
• Excessive consumption of coffee and acidic beverages

• Cocaine addiction
• Bile reflux
• Constipation (Constant straining and dryness of the colon leads to infection and inflammation)
• Crohn’s disease
• Consumption of poisons and other caustic or corrosive chemical substances
• Sarcoidosis
• Radiation therapy
• Chemotherapy drugs
• Iron and potassium supplements
• Stress as a result of major surgery or trauma or other illness
• Infections caused by:
  • Viruses such as HSV, cytomegalovirus (mostly seen in immunocompromised individuals)
  • Parasites
  • Fungi

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Gastritis must be differentiated from peptic ulcer disease, gastric cancer, gastroesophageal reflux disease (GERD), gastroenteritis, crohn’s disease, gastrinoma, gastric adenocarcinoma and primary gastric lymphoma.

Differentiating gastritis from other Diseases:

• Acute Gastritis
  • Crohn’s Disease
  • Gallstones (Cholelithiasis)
  • Cholecystitis
  • Gastric cancer
  • Peptic Ulcer Disease
  • Viral Gastroenteritis
  • Acute Complications of Sarcoidosis
  • B-Cell Lymphoma
• Chronic Gastritis
  • Atrophic Gastritis
  • Gastroesophageal Reflux Disease (GERD)
  • Crohn’s Disease
• Atrophic Gastritis
  • Chronic Gastritis
  • Functional (Nonulcer) Dyspepsia
  • Gastroesophageal Reflux Disease (GERD)
  • Pernicious Anemia
• Stress related/induced Gastritis
  • Alcoholic gastropathy
  • Nonsteroidal anti-inflammatory drug, (NSAID) induced gastritis
  • Peptic Ulcer Disease
  • Uremic gastropathy
• Helicobacter Pylori-associated Gastritis
  • Autoimmune gastritis
  • Nonspecific chronic inactive gastritis
  • Gastritis in patients with Crohn’s disease involving the stomach
  • Gastropathy in the setting of chronic conditions (eg, portal hypertensive gastropathy)
  • Lymphocytic gastritis
• Other differentials
  • Ménétrier disease (Rare disorder)
  • Aortic aneurysm (ruptured)
  • Candida
  • Crohn’s Disease
  • Cytomegalovirus (CMV) in HIV
  • Diseases of the biliary system
  • Drugs
  • Esophageal varices
  • Functional dyspepsia
  • Gastric carcinoma
  • Gastroduodenal ulcer
  • Intoxication
  • Liver failure
  • Lymphocytic gastritis
  • Mallory-Weiss Tear
  • Menetrier’s Disease
  • Pancreas carcinoma
  • Pancreatitis
  • Peptic ulcer
  • Perforated ulcer
  • Radiation
  • Reflux esophagitis
  • Renal Failure
  • Respiratory failure
  • Sarcoidosis
  • Sepsis
  • Shock
  • Surgery
  • Syphilis
  • Trauma
  • Tuberculosis
  • Volvulus
  • Zollinger-Ellison Syndrome

• The table below differentiates gastritis from other conditions:^{[1][2][3][4][5][6][7][8][9]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

In acute gastritis, the prevalence of eosinophilic gastritis is approximately 6.3 per 100,000 individuals worldwide. The incidence of new cases of H. pylori infection each year ranges from 3,000 to 10,000 per 100,000 individuals in developing countries. It has been observed that with advancing age, the incidence of H. pylori infection increases. In united states, 20% of adolescents are infected with H. pylori when compared to 90% by 5 years of age in developing countries. In United States, H. pylori infection associated gastritis is more common in African Americans (54%), Hispanics (52%), and the elderly compared to Whites (21%). In acute gastritis, females are usually more affected than men. In H. pylori infection associated gastritis, males are more commonly affected than females. The incidence rates of H. pylori infection are high in Japan, Columbia, Costa Rica and China, and comparatively low in the United States. H. pylori infection is common in Southern and Eastern Europe, Mexico, South America, Africa, most Asian countries, and aboriginal people in North America.

• Chronic Gastritis:
  • The incidence of new cases of H. pylori infection each year ranges from 3,000 to 10,000 per 100,000 individuals in developing countries. ^[1]
  • The incidence of new cases of H. pylori infection each year is around 500 per 100,000 individuals in developed countries.^[1]
• It has been observed that with advancing age, the incidence of H. pylori infection increases. ^[2]

• Acute Gastritis:
  • The prevalence of eosinophilic gastritis is approximately 6.3 per 100,000 individuals worldwide. ^[3]

• H. pylori infection associated gastritis:
  • All age groups may develop H. pylori infection.
  • The prevalence of infection increases with age.^[4]
  • About 30%-50% of H. pylori infections are acquired during childhood which increases to 90% during adulthood in developing countries.^[5]
  • H. pylori infection in developed countries is less common in children and reaches up to 60% with increasing age.^[6]
  • In United States, 20% of adolescents are infected with H. pylori when compared to 90% by 5 years of age in developing countries.^[7]
  • Children differ from adults with respect to H. pylori infection in terms of:^[8][9]
    • Prevalence of infection
    • High rate of antibiotic resistance
    • The near-absence of gastric malignancies
    • Age specific problems with diagnostic tests and medications

• In United States, H. pylori infection associated gastritis is more common in African Americans (54%), Hispanics (52%), and the elderly compared to Whites (21%).^[10][11]

• In acute gastritis, females are usually more affected than men.
• In H. pylori infection associated gastritis, males are more commonly affected than females.^[12]

• H. pylori infection associated gastritis is common in Southern and Eastern Europe, Mexico, South America, Africa, most Asian countries, and aboriginal people in North America.^[13][14]

• The incidence of new cases of H. pylori infection each year is 0.5 percent in developed countries.^[1]
• The prevalence of H. pylori is declining in the United States.
• In developed countries such as the United States, children acquire the H. pylori infection at a rate of about less than 1% per year.
• It is estimated that 30%-40% of the US population is infected with H. pylori.^[15][16]
• In United States, approximately 25% of children between 6-19 years old are infected.^[17]
• The incidence rates of H. pylori infection are high in Japan, Columbia, Costa Rica and China, and comparatively low in the United States.

• The prevalence of H. pylori is higher in developing countries than that in developed countries.^[18]
• The incidence of new cases of H.pylori infection each year ranges from 3,000 to 10,000 per 100,000 individuals in developing countries.^[1]
• In the developing countries, children in the age group of 2 to 8 years acquire the H.pylori infection at a rate of about 10% per year.
• H. pylori infection is common in Southern and Eastern Europe, Mexico, South America, Africa, most Asian countries, and aboriginal people in North America.^[13][14]

Prevalence of H. pylori infection globally^[19]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Common risk factors in the development of gastritis include alcohol, NSAIDs, cocaine, crohn’s disease, HIV/AIDS, and bacterial infections such as Helicobacter pylori. Less common risk factors in the development of gastritis include food poisoning (bacterial gastroenteritis), autoimmune disorders such as pernicious anemia , Hashimoto’s disease and type 1 diabetes; stress as a result of major surgery, trauma or other illness; traumatic injury, burns, severe infections, bile reflux, low fiber diet, processed food as the primary diet, and viral and parasitic infections.

• Common risk factors in the development of gastritis include alcohol, NSAIDs, cocaine, crohn’s disease, HIV/AIDS and bacterial infections such as Helicobacter pylori.^{[1][2][3][4][5][6][7][8][9][10]}

• Common risk factors in the development of gastritis include:
  • Excessive amounts of alcohol (acute gastritis)
  • Cigarette smoking
  • Excessive amounts of caffeine or acidic beverages
  • Medications such as aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Cocaine addiction
  • Stress resulting in excessive gastric acid secretion
  • Bacterial infection such as Helicobacter pylori (H. pylori)
  • Increasing age
  • HIV/AIDS

• Less common risk factors in the development of gastritis include:
  • Food poisoning (bacterial gastroenteritis)
  • Autoimmune disorders such as pernicious anemia , Hashimoto’s disease and type 1 diabetes
  • Stress as a result of major surgery, trauma, or other illness
  • Traumatic injury, burns, or severe infections
  • Bile reflux
  • Low fiber diet
  • Processed food as the primary diet
  • Viral and parasitic infections

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

There is insufficient evidence to recommend routine screening for gastritis

There is insufficient evidence to recommend routine screening for gastritis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Gastritis may be seen as a commonly occurring inflammatory disease in many individuals. Gastritis usually persists throughout life and the chance of spontaneous healing is rare. Gastritis is mostl associated with the presence of Helicobacter pylori infection. The gastric mucosa undergoes inflammation and may lead to atrophic gastritis. Chronic gastritis is a condition which is commonly observed as a manifestation of pathogenesis of many gastric disease conditions. Gastric secretory functions are usually impaired due to the gastric mucosa undergoing inflammation and atrophy. Increase in the prevalence of gastritis is attributed to the increasing age and the onset varies among different ethnicities. The increased risk of developing duodenal and peptic ulcers have been observed in individuals with persistent gastritis. Biopsies and routine evaluations may help predict the progression of gastritis to further conditions such as the peptic ulcer disease. Complications of Gastritis may include, peptic ulcers, gastrointestinal perforation, gastrointestinal bleeding, gastric polyp, anemia due to erosive gastritis, vitamin B12 deficiency, pernicious anemia, gastric outlet obstruction, increased risk of developing benign or malignant growths in the lining of the stomach which may lead to stomach cancer. Prognosis for gastritis is majorly dependent upon the type of gastritis and etiological factors. In Acute gastirtis, the condition improves upon refraining from risk factors such as NSAIDs, alcohol, cigarette smoking, acidic food, and beverages. In Autoimmune gastirtis, prognosis is usually good for vitamin B12 deficiency when treated with cyanocobalamin therapy. Although in Autoimmune gastritis, there is an increased risk for carcinoid tumors and gastric adenocarcinoma. In Chronic gastirtis associated with Helicobacter pylori infection, the prognosis is good. The triple therapy regimen may not be effective when compared to quadruple bismuth-based regimen is has proven to be very effective comparatively. In individuals with Helicobacter pylori infection associated chronic gastritis, if left untreated may progress to develop peptic ulcer disease, adenocarcinoma and MALT lymphoma.

Gastritis is a common inflammatory disease. Gastritis usually persists throughout life and the chance of spontaneous healing is rare. Gastritis is most commonly associated with Helicobacter pylori infection. The gastric mucosa undergoes inflammatory changes which may finally lead to atrophic gastritis. Chronic gastritis is commonly observed as a manifestation of progression of many gastric conditions. Gastric secretory functions are usually impaired due to inflammation and atrophy of the gastric mucosa. Increase in the prevalence of gastritis is attributed to the increasing age and the onset varies among different ethnicities. The increased risk of developing duodenal and peptic ulcers have been observed in individuals with persistent gastritis. Biopsies and routine evaluations may help predict the progression of gastritis to the conditions such as the peptic ulcer disease. ^[1][2][3]

• Acute gastritis Complications:
  • Ulcer bleed
  • Bleeding as a result of gastric erosion
  • Anemia as a result of the bleeding from the ulcer or due to the gastric erosion
  • Gastric outlet obstruction

• Chronic gastritis Complications:
  • Atrophic gastritis
  • Peptic ulcers
  • Gastrointestinal Perforation
  • Gastrointestinal Bleeding
  • Anemia due to erosive gastritis
  • Stomach cancer
  • Vitamin B12 deficiency
  • Pernicious anemia
  • Increased risk of developing benign or malignant growths in the lining of the stomach.

• Atrophic gastritis Complications:
  • Atrophic gastirtis as a result of Helicobacter pylori infection:
    • Gastric ulceration
    • Gastric cancer (adenocarcinoma)
  • Atrophic gastritis as a result of atrophic gastritis due to Autoimmune gastritis:
    • Gastric polyp
    • Gastric cancer (adenocarcinoma)
    • Pernicious anemia

• Stress Induced gastritis Complications:
  • Rarely, stress-induced gastritis may lead to severe bleeding that can prove fatal and leads to a life-threatening situation.

• Helicobacter pylori-associated gastirtis Complications:
  • Chronic Helicobacter pylori-associated gastritis increases the risk for mucosa-associated lymphoid tissue (MALT) lymphoma.
  • Gastric and duodenal ulcers
  • Gastric adenocarcinoma
  • Pseudomembranous colitis following H. pylori treatment
  • B12 and iron deficiency anemia
  • Post Treatment complication of of Helicobacter pylori infection is Clostridium difficile infection

• Prognosis for gastritis is majorly dependent upon the type of gastritis and etiological factors:
  • In Acute gastritis, the condition improves upon refraining from risk factors such as NSAIDs, alcohol, cigarette smoking, acidic food, and beverages. ^[4]
  • In Autoimmune gastritis, prognosis is usually good for vitamin B12 deficiency when treated with cyanocobalamin therapy. Although in autoimmune gastritis, there is an increased risk for carcinoid tumors and gastric adenocarcinoma. ^{[5] [6]}
  • In Chronic gastirtis associated with Helicobacter pylori infection, the prognosis is good.
    • The triple therapy regimen may not be effective when compared to quadruple bismuth-based regimen is has proven to be very effective comparatively. ^[7]
    • In individuals with Helicobacter pylori infection associated chronic gastritis, if left untreated may progress to develop peptic ulcer disease, adenocarcinoma and MALT lymphoma.

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