Gastritis overview: Difference between revisions
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==Historical Perspective== | ==Historical Perspective== | ||
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 | 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== | ==Classification== | ||
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==Pathophysiology== | ==Pathophysiology== | ||
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 infection|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 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 infection|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.'' | ||
==Causes== | ==Causes== | ||
The most common causes of Gastritis include [[Helicobacter pylori|H. pylori]] infection, [[alcohol]] consumption, [[cigarette]] smoking, extended use of [[Non-steroidal anti-inflammatory drug|NSAIDs]] such as ([[aspirin]], [[Naproxen sodium|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|crohn's disease]], [[Constipation|constipation]], consumption of [[Poison|poisons]] and other [[caustic]] or [[corrosive]] chemical substances, [[Sarcoidosis|sarcoidosis]], [[Radiation therapy|radiation therapy]], [[Chemotherapy|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. | The most common causes of Gastritis include [[Helicobacter pylori|H. pylori]] infection, [[alcohol]] consumption, [[cigarette]] smoking, extended use of [[Non-steroidal anti-inflammatory drug|NSAIDs]] such as ([[aspirin]], [[Naproxen sodium|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|crohn's disease]], [[Constipation|constipation]], consumption of [[Poison|poisons]] and other [[caustic]] or [[corrosive]] chemical substances, [[Sarcoidosis|sarcoidosis]], [[Radiation therapy|radiation therapy]], [[Chemotherapy|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]]. | ||
==Differentiating {{PAGENAME}} from Other Diseases== | ==Differentiating {{PAGENAME}} from Other Diseases== | ||
Gastritis must be differentiated from [[peptic ulcer disease]], [[Stomach cancer|gastric cancer]], [[gastroesophageal reflux disease]] ([[Gastroesophageal reflux disease|GERD]]), [[gastroenteritis]], [[crohn's disease]], [[gastrinoma]], [[gastric adenocarcinoma]] and primary gastric lymphoma. | Gastritis must be differentiated from [[peptic ulcer disease]], [[Stomach cancer|gastric cancer]], [[gastroesophageal reflux disease]] ([[Gastroesophageal reflux disease|GERD]]), [[gastroenteritis]], [[crohn's disease]], [[gastrinoma]], [[gastric adenocarcinoma]] and primary [[gastric lymphoma]]. | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
Revision as of 13:16, 29 January 2018
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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]
Overview
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 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.
Historical Perspective
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
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).
Pathophysiology
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.
Causes
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.
Differentiating Gastritis overview from Other Diseases
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.
Epidemiology and Demographics
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.
Risk Factors
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.
Screening
There is insufficient evidence to recommend routine screening for gastritis.
Natural History, Complications, and Prognosis
Natural History
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
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
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.
Diagnosis
History and Symptoms
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.
Physical Examination
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.
Diagnostic Tests
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.
Imaging Findings
CT scan
CT scan may be helpful in the diagnosis of gastritis. Findings on CT scan suggestive of gastritis include gastric wall edema and halo sign.
X- ray
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.
Other Diagnostic Studies
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.
Treatment
Medical Therapy
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 subsalicylates, 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.
Surgery
Surgical intervention is not recommended for the management of gastritis.
Primary Prevention
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).
Secondary Prevention
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.