Acute gastritis is a term covering a broad spectrum of entities that induce inflammatory changes in the gastric mucosa. Several different etiologies share the same general clinical presentation. However, they differ in their unique histologic characteristics. The inflammation may involve the entire stomach (eg, pangastritis) or a region of the stomach (eg, antral gastritis). Acute gastritis can be broken down into two categories: erosive (eg, superficial erosions, deep erosions, hemorrhagic erosions) and nonerosive (generally caused by Helicobacter pylori). See the images below.
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Acute gastritis with superficial erosions.
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Mucosal erythema and edema consistent with acute gastritis.
No correlation exists between microscopic inflammation (histologic gastritis) and the presence of gastric symptoms (eg, abdominal pain, nausea, vomiting). In fact, most patients with histologic evidence of acute gastritis (inflammation) are asymptomatic. The diagnosis is usually obtained during endoscopy performed for other reasons. Acute gastritis may present with an array of symptoms, the most common being nondescript epigastric discomfort.
Other symptoms include nausea, vomiting, loss of appetite, belching, and bloating. Occasionally, acute abdominal pain can be a presenting symptom. This is the case in phlegmonous gastritis (gangrene of the stomach) where severe abdominal pain accompanied by nausea and vomiting of potentially purulent gastric contents can be the presenting symptoms. Fever, chills, and hiccups also may be present.
The diagnosis of acute gastritis may be suspected from the patient's history and can be confirmed histologically by biopsy specimens taken at endoscopy.
Epidemiologic studies reflect the widespread incidence of gastritis. In the United States, it accounts for approximately 1.8-2.1 million visits to doctors' offices each year. It is especially common in people older than 60 years.
See related CME at Evaluation of Acute Abdominal Pain Reviewed.
Acute gastritis has a number of causes, including certain drugs; alcohol; bile; ischemia; bacterial, viral, and fungal infections; acute stress (shock); radiation; allergy and food poisoning; and direct trauma. The common mechanism of injury is an imbalance between the aggressive and the defensive factors that maintain the integrity of the gastric lining (mucosa).
Acute erosive gastritis can result from an exposure to a variety of agents or factors. This is referred to as reactive gastritis. These agents/factors include nonsteroidal anti-inflammatory drugs (NSAIDs), alcohol, cocaine, stress, radiation, bile reflux, and ischemia. The gastric mucosa exhibits hemorrhages, erosions, and ulcers. NSAIDs, such as aspirin, ibuprofen, and naproxen, are the most common agents associated with acute erosive gastritis. This results from both oral and systemic administration of these agents, either in therapeutic doses or in supratherapeutic doses.
Because of gravity, the inciting agents lie on the greater curvature of the stomach. This partly explains the development of acute gastritis distally over or near the greater curvature of the stomach in the case of orally administered NSAIDs. However, the major mechanism of injury is the reduction in prostaglandin synthesis. Prostaglandins are chemicals responsible for maintaining the mechanisms that result in the protection of the mucosa from the injurious effects of the gastric acid. Long-term effects of such ingestions can include fibrosis and stricture formation.
Bacterial infection is another cause of acute gastritis. The corkscrew-shaped bacterium called H pylori is the most common cause of gastritis. Complications result from a chronic infection rather than from an acute infection. The prevalence of H pylori in otherwise healthy individuals varies depending on age, socioeconomic class, and country of origin. The infection is usually acquired in childhood. In the Western world, the number of people infected with H pylori increases with age.
Evidence of H pylori infection can be found in 20% of individuals younger than 40 years and in 50% of individuals older than 60 years. How the bacterium is transmitted is not entirely clear. Transmission is likely from person to person through the oral-fecal route or through the ingestion of contaminated water or food. This is why the prevalence is higher in lower socioeconomic classes and in developing countries. H pylori is associated with 60% of gastric ulcers and 80% of duodenal ulcers.
H pylori gastritis typically starts as an acute gastritis in the antrum, causing intense inflammation, and over time, it may extend to involve the entire gastric mucosa resulting in chronic gastritis.
The acute gastritis encountered with H pylori is usually asymptomatic. The bacterium imbeds itself in the mucous layer, a protective layer that coats the gastric mucosa. It protects itself from the acidity of the stomach through the production of large amounts of urease, an enzyme that catalyzes the breakdown of urea to the alkaline ammonia and carbon dioxide. The alkaline ammonia neutralizes the gastric acid in the immediate vicinity of the bacterium conferring protection.
H pylori also has flagella that enable it to move and help it to penetrate the mucous layer so that it comes into contact with the gastric epithelial cells. It also has several adhesion molecules that help it to adhere to these cells. It produces inflammation by activating a number of toxins and enzymes that activate IL-8, which eventually attracts polymorphs and monocytes that cause acute gastritis.
Antigen-presenting cells activate lymphocytes and other mononuclear cells that lead to chronic superficial gastritis. The infection is established within a few weeks after the primary exposure to H pylori. It produces inflammation via the production of a number of toxins and enzymes. The intense inflammation can result in the loss of gastric glands responsible for the production of acid. This is referred to as atrophic gastritis. Consequently, gastric acid production drops. The virulence genotype of the microbe is an important determinant for the severity of the gastritis and the formation of intestinal metaplasia, the transformation of gastric epithelium. This transformation can lead to gastric cancer.
Reactive gastropathy is the second most common diagnosis made on gastric biopsy specimens after H pylori gastritis. This entity is believed to be secondary to bile reflux and was originally reported after partial gastrectomy (Billroth I or II). It is now considered to represent a nonspecific response to a variety of other gastric irritants.
Helicobacter heilmanii is a gram-negative, tightly spiraled, helical-shaped organism with 5-7 turns. The prevalence of H heilmanii is extremely low (0.25-1.5%). The source of H heilmanii infection is unclear, but animal contact is thought to be the means of transmission.
Tuberculosis is a rare cause of gastritis, but an increasing number of cases have developed in patients who are immunocompromised. Gastritis caused by tuberculosis is generally associated with pulmonary or disseminated disease.
Secondary syphilis of the stomach is a rare cause of gastritis.
Phlegmonous gastritis is an uncommon form of gastritis caused by numerous bacterial agents, including streptococci, staphylococci, Proteus species, Clostridium species, and Escherichia coli. Phlegmonous gastritis usually occurs in individuals who are debilitated. It is associated with a recent large intake of alcohol, a concomitant upper respiratory tract infection, and AIDS. Phlegmonous means a diffuse spreading inflammation of or within the connective tissue. In the stomach, it implies infection of the deeper layers of the stomach (submucosa and muscularis). As a result, purulent bacterial infection may lead to gangrene.
Phlegmonous gastritis is rare. The clinical diagnosis is usually established in the operating room, as these patients present with an acute abdominal emergency requiring immediate surgical exploration. Without appropriate therapy, it can progress to peritonitis and death.
Viral infections can cause gastritis. Cytomegalovirus (CMV) is a common viral cause of gastritis. It is usually, but not always, encountered in individuals who are immunocompromised, including those with cancer, on immunosuppression medications, after transplants, and AIDS. Yamamoto et al described a case of gastritis due to concurrent infection with Epstein-Barr virus (EBV) and CMV in an immunocompetent adult.[1] Gastric involvement can be localized or diffuse.
Fungal infections that cause gastritis include Candida albicans and histoplasmosis. Gastric phycomycosis is another rare lethal fungal infection. The common predisposing factor is immunosuppression. C albicans rarely involves the gastric mucosa. When isolated in the stomach, the most common locations tend to be within a gastric ulcer or an erosion bed. It is generally of little consequence. Disseminated histoplasmosis can involve the stomach. The usual presenting clinical feature is bleeding from gastric ulcers or erosions on giant gastric folds.
Parasitic infections are rare causes of gastritis. Anisakidosis is caused by a nematode that embeds itself in the gastric mucosa along the greater curvature. Anisakidosis is acquired by eating contaminated sushi and other types of contaminated raw fish. It often causes severe abdominal pain that subsides within a few days. This nematode infection is associated with gastric fold swelling, erosions, and ulcers.
Ulcero-hemorrhagic gastritis is most commonly seen in patients who are critically ill. Ulcero-hemorrhagic gastritis is believed to be secondary to ischemia related to hypotension and shock or to the release of vasoconstrictive substances, but the etiology is often unknown. The gastric mucosa reveals multiple petechiae, mostly in the fundus and body, or exhibits a diffusely hemorrhagic pattern. The gross pathology may resemble that of NSAID- or other ingestion-induced gastritis, except that the location of injury is different. This form of gastritis can be life-threatening if the patient experiences hemorrhaging and may even require emergency gastrectomy.
Inflammatory bowel disease and microscopic colitis appear to be inversely associated with H pylori infection.[2] Microscopic evidence of acute gastritis can be seen in patients with Crohn disease, though clinical manifestations are rare (occurring in only about 2-7% of patients with Crohn disease). Focally enhancing gastritis is now recognized as a condition seen in both Crohn disease and ulcerative colitis.
Eosinophilic gastritis is often seen in conjunction with eosinophilic gastroenteritis but can be associated with various disorders, including food allergies (eg, cow milk, soy protein), collagen vascular diseases, parasitic infections, gastric cancer, lymphoma, Crohn disease, vasculitis, drug allergies, and H pylori infections. An eosinophilic infiltrate is seen involving the gastric wall or epithelium.
Acute gastritis has a number of causes, including certain drugs; alcohol; bacterial, viral, and fungal infections; acute stress (shock); radiation; allergy and food poisoning; bile; ischemia; and direct trauma.
Causes of acute gastritis include the following:
Drugs - NSAIDs, such as aspirin, ibuprofen, and naproxen; cocaine; iron; colchicine, when at toxic levels, as in patients with failing renal or hepatic function; kayexalate; chemotherapeutic agents, such as mitomycin C, 5-fluoro-2-deoxyuridine, and floxuridine
Potent alcoholic beverages, such as whisky, vodka, and gin
Bacterial infections -H pylori (most frequent), H heilmanii (rare), streptococci (rare), staphylococci (rare), Proteus species (rare), Clostridium species (rare), E coli (rare), tuberculosis (rare), secondary syphilis (rare)
Bile: The reflux of bile (an alkaline medium is important for the activation of digestive enzymes in the small intestine) from the small intestine to the stomach can induce gastritis.
Ischemia: This term is used to refer to damage induced by decreased blood supply to the stomach. This rare etiology is due to the rich blood supply to the stomach.
Data from a national administrative database (2009-2011) revealed standardized estimated prevalence rates of 6.3 per 100,000 population for eosinophilic gastritis and 3.3 per 100,000 population for eosinophilic colitis; women were affected more often.[3]
Gastritis affects all age groups. The incidence of H pylori infection increases with age.
Gastritis generally clears spontaneously. With treatment, the mortality rate of phlegmonous gastritis is 65%.
Mortality/morbidity
The mortality/morbidity is dependent on the etiology of the gastritis. Generally, most cases of gastritis are treatable once the etiology is determined. The exception to this is phlegmonous gastritis, which has a mortality rate of 65%, even with treatment.
Complications
Complications of acute gastritis include the following:
Bleeding from an erosion or ulcer
Gastric outlet obstruction due to edema limiting an adequate transfer of food from the stomach to the small intestine
Patients may experience gnawing or burning epigastric distress, occasionally accompanied by nausea and/or vomiting. The pain may improve or worsen with eating.
Obtain the following information, if available:
Presence of a previous mucosal injury (eg, gastritis, peptic ulcer disease, endoscopic injury caused by polypectomy, injury caused by any surgery)
History of eating raw fish
Exposure to potentially noxious drugs or chemical agents. This includes corticosteroids or other prescription medications that can cause gastritis.
Routine use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs), especially at high doses
The physical examination findings are often normal with occasional mild epigastric tenderness. The examination tends to exhibit more abnormalities as the patient develops complications in relation to gastritis.
Four radiologic signs of acute gastritis are fairly consistent regardless of the etiology. These signs include thick folds, inflammatory nodules, coarse area gastrica, and erosions.
Thick folds are defined by a size greater than 5 mm in caliber. These folds are measured on radiographs with the stomach moderately distended. If thick folds are found in a patient who is symptomatic, H pylori is generally involved.
Nodularity of the gastric mucosa (bumpy appearance) is a second sign of acute or subacute gastritis. Its origin is uncertain. Nodules may represent erosions that have epithelialized (healed) but still have the associated edema. Compared with benign neoplastic polyps, gastritis-related nodules are smaller, and their edges are less well defined. They taper onto the adjacent mucosa, and they are seen most often in the distal stomach. Nodules due to gastritis are referred to as inflammatory. They generally line up on the folds of the gastric antrum and are a characteristic appearance of gastritis.
Enlarged area gastrica are a sign of gastritis that is not strongly associated with a specific cause. Area gastrica are small polygonal areas, 1-3 mm in diameter, separated by linear depressions on the surface of the mucous membrane of the stomach; they contain the gastric pits. Enlargement of these areas may reflect inflammatory swelling and is often associated with gastritis. Because of the loss of the mucosal layer, the barium suspension can more completely fill the intervening grooves.
Gastric erosions are noted to be one of the most specific signs of gastritis. Erosions may be linear or serpiginous. They may be accompanied by edema and may be seen on or near the greater curvature of the stomach. A double-contrast examination usually is required to best reveal gastric erosions.
Tomography scan and plain films of the abdomen can demonstrate thickening of the gastric wall in the case of phlegmonous gastritis.
Double-contrast barium radiography can demonstrate the nematodes that cause anisakidosis.
A number of H pylori tests are available. They are classified as either nonendoscopy based or endoscopy based.
Three nonendoscopy-based H pylori tests are available, as follows:
The first test is the H pylori stool antigen test (HpSA). This test is based on the detection of the H pylori antigen in the stool. It has sensitivity and specificity of greater than 90%. It can be used for both the diagnosis of H pylori and the confirmation of eradication after therapy.
The second test is the urea breath test. It uses 13C- or 14C-labeled urea taken orally. H pylori metabolizes the urea and liberates labeled carbon dioxide that is exhaled. This, in turn, can be quantified in breath samples. The sensitivity and specificity of the urea breath test is greater than 90%. This is considered the noninvasive diagnostic method of choice in situations where endoscopy is not indicated. It can also be used to confirm eradication after therapy
The third test depends on the presence of antibodies to H pylori in the serum. The major drawback to this test is that serologic assays may remain positive for as long as 3 years after eradication of the bacteria. Therefore, serologic assays are often unreliable to document eradication of H pylori. This test can be used for the diagnosis of H pylori, provided that the patient has not received any prior therapy for it.
Three endoscopy-based H pylori tests are available, as follows:
The first test is the rapid urease test (RUT). It is performed by placing a gastric biopsy specimen, obtained at endoscopy, onto a gel- or membrane-containing urea and a pH-sensitive indicator. If H pylori is present, the bacterial urease hydrolyzes urea and changes the color of the media. The sensitivity and specificity of this test is greater than 90%.
Another test is bacterial culture of H pylori. It is highly specific but is not widely used because of the degree of expertise required. It is used when antibiotic susceptibilities are necessary.
Histologic detection of H pylori in the biopsy specimen is another endoscopy-based test. Appropriate staining is achieved using such stains as hematoxylin and eosin, Warthin-Starry, Giemsa, or Genta.
American Society for Gastrointestinal Endoscopy guidelines suggest endoscopic evaluation for patients older than 50 years who have alarm features such as weight loss and anemia. For patients younger than 50 years with no alarm features who are H pylori negative, endoscopic evaluation may be considered.[5]
Mycobacterium tuberculosis may be diagnosed when acid-fast stain detects the bacilli in a biopsy specimen.
Syphilis may be diagnosed when the organism is found in the gastric mucosa. Endoscopic biopsy, silver impregnation, and fluorescent antibody techniques also can be used.
Endoscopy may reveal a thickened, edematous, nonpliable wall with erosions and reddened gastric folds. The edema can be severe resulting in gastric outlet obstruction. Ulcers and frank bleeding might be present.
The nematodes that cause anisakidosis can be seen on endoscopy.
Endoscopy can be used to help diagnose gastric syphilis and tuberculosis.
A meta-analysis has shown that for individuals who undergo endoscopy for dyspepsia, the most common finding is erosive esophagitis (though prevalence was lower when the Rome criteria were used to define dyspepsia) followed by peptic ulcers.[6]
Histologic examination of a biopsy specimen can help in establishing the etiologic agent of gastritis.
H heilmanii is better diagnosed on smears using Giemsa or Warthin-Starry silver stains than by gastric biopsy specimens via observation of a distinct morphology. A culture of H heilmanii has not been established yet, and the diagnosis of this bacterial infection is based on morphological identification by histologic examination and tissue smear cytology.
As mentioned earlier, H pylori can be found by histologic staining of a gastric mucosal biopsy specimen. It has a sensitivity and specificity of greater than 90%.
The main histologic feature of CMV infection is cytomegalic cells with intranuclear inclusions. Viral cultures, immunocytochemistry, and in situ hybridization can further aid in establishing the diagnosis.
The main histologic feature of C albicans infection is yeast forms in a biopsy specimen.
The main histologic feature of tuberculosis is necrotizing granulomas.
The main histologic feature of histoplasmosis is the presence of nonnecrotizing granulomas containing the organisms. The diagnosis of histoplasmosis requires a positive culture result from the gastric mucosal biopsy specimen.
In ulcero-hemorrhagic gastritis, the epithelium appears eroded with edema and hemorrhage with typically little inflammation. In severe cases, the lumen of the stomach may be coated with fibropurulent exudates and the lamina propria may be replaced by eosinophilic hyaline material.
In iron-induced gastritis, erosions, foveolar hyperplasia, or even hyperplastic-type polyps can be detected. Iron has been associated with infarctlike necrosis given its corrosive properties. Iron stains can highlight the golden brown pigment in tissue samples, but these are often easily visible. Of note, such findings should be differentiated from glandular siderosis seen in systemic iron overload or hemochromatosis.
Histologic features of chemotherapy-induced gastritis may include atypical epithelial cells with bizarre features at the base of the glands, limited mitoses, and pleomorphic nuclei. These characteristics may make it difficult to differentiate from an adenocarcinoma.
The findings at histology of radiation-induced gastritis include nuclear karyorrhexis (destructive fragmentation of the nucleus of a dying cell) and cytoplasmic eosinophilia of the gastric pit epithelium during the first 10 days following treatment, followed by mucosal edema, congestion, submucosal collagen bundle swelling, fibrin deposition, and telangiectasia. If extensive, hemorrhage and ulceration may be evident.
In eosinophilic gastritis, a prominent eosinophilic infiltrate is present in the gastric wall or epithelium. Distribution can be patchy, so multiple biopsy specimens should be obtained during endoscopy.
Surgical intervention is not necessary, except in the case of phlegmonous gastritis. With this entity, surgical intervention with resection of the affected area may be the most effective form of treatment.
Consult a gastroenterologist in complicated cases.
Administer medical therapy as needed, depending on the cause and the pathological findings.
No specific therapy exists for acute gastritis, except for cases caused by H pylori. The American College of Gastroenterology guidelines suggest that the current evidence does not support the notion that treating H pylori worsens gastroesophageal reflux disease (GERD). For patients who need eradication of H pylori, this should not be a concern.[7] In patients with persistent H pylori infection despite appropriate initial treatment, combination therapy with a proton pump inhibitor (PPI), levofloxacin, and amoxicillin for 10 days appears to be more effective and better tolerated than a combination of a PPI, bismuth, tetracycline, and metronidazole. However this has not been validated in the US literature.[7, 8, 9, 10]
Administer fluids and electrolytes as required, particularly if the patient is vomiting.
Discontinue the use of drugs known to cause gastritis (eg, NSAIDs, alcohol). A long-term prospective study found that patients with arthritis who were older than 65 years and regularly took low-dose aspirin were at an increased risk for dyspepsia severe enough to necessitate the discontinuation of NSAIDs.[11] This suggests that better management of NSAID use should be discussed with older patients in order to reduce NSAID-associated upper GI events.
There has been a growing concern in recent years regarding the interaction between PPIs and clopidogrel. A decrease in the antiplatelet activity of clopidogrel with a possible increase in adverse cardiac events is postulated. Pharmacokinetically it has been shown that omeprazole and lansoprazole interact significantly with clopidogrel, and that omeprazole, rabeprazole, and esomeprazole interact with prasugrel. Pantoprazole has been shown to have the least interaction and thus, pantoprazole with low CYP2C19-inhibiting properties appears to be the safest PPI to be used with clopidogrel until more concrete evidence is available.[7, 12]
H pylori eradication testing can be performed 4 weeks after completing therapy. It is carried out using either the rapid urease breath testing or stool antigen testing. However, it is not cost effective and is not always done. The current recommendation is that patients with ulcers from H pylori, MALT lymphoma, history of gastric cancer, and those with no improvement of symptoms despite treatment must be checked for resolution of H pylori infection.[7]
Specific treatment is dependent on the etiology of gastritis.
According to the Centers for Disease Control and Prevention (CDC), the treatment of tuberculosis consists of a 2-month course of daily isoniazid, rifampin, and pyrazinamide, followed by 4 months of daily isoniazid along with rifampin. See Tuberculosis.
Medical management generally is ineffective in treating phlegmonous gastritis. Several drugs are available for the treatment of cytomegalovirus (CMV) infection. These include ganciclovir, valganciclovir, foscarnet, and cidofovir. It should be noted that the majority of immunocompetent individuals recover from CMV infection without any therapeutic intervention. See Cytomegalovirus.
The treatment of C albicans includes a variety of agents, including nystatin, oral clotrimazole, itraconazole, fluconazole, amphotericin B, and ketoconazole. See Candidiasis.
The treatment of disseminated histoplasmosis includes a variety of agents, including amphotericin B, itraconazole, and fluconazole. They have all been determined to be effective. See Histoplasmosis.
No drugs are available to treat anisakidosis. Endoscopic removal may be necessary.
Clinical Context:
Drug combination that neutralizes gastric acidity and increases pH of the stomach and duodenal bulb. Aluminum ions inhibit smooth-muscle contraction and inhibit gastric emptying. Magnesium/aluminum antacid mixtures are used to avoid bowel function changes.
Used for general prophylaxis. Antacids containing aluminum and magnesium can help relieve symptoms of gastritis by neutralizing gastric acids. These agents are inexpensive and safe.
Clinical Context:
Inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentration.
This class includes drugs whose mechanism of action is competitive inhibition of histamine at the histamine 2 (H2) receptor. Histamine plays an important role in gastric acid secretion, thereby making H2 blockers effective suppressors of basal gastric acid output and acid output stimulated by food and the neurological system. There are different drugs with different potencies and half-lives (eg, cimetidine, ranitidine, famotidine, nizatidine). Cimetidine will be discussed below as a representative of this class of drugs.
Proton pump inhibitors are potent inhibitors of the proton (acid) pump (ie, the enzyme H+,K+-ATPase), located in the apical secretory membrane of the gastric acid secretory cells (parietal cell). Proton pump inhibitors can completely inhibit acid secretion and have a long duration of action. They are the most effective gastric acid blockers. Omeprazole will be discussed as a representative of this class of drugs.
Clinical Context:
Interferes with the synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.
Clinical Context:
Inhibits bacterial growth, possibly by blocking the dissociation of peptidyl t-RNA from ribosomes and causing arrest of RNA-dependent protein synthesis.
Bacterial infections also can cause gastritis. The most common causative organism is H pylori. A number of therapeutic regimens are effective against H pylori. Single antimicrobial agents generally are not recommended because of the potential development of resistance.
Dual therapy includes a proton pump inhibitor plus amoxicillin (no longer recommended because eradication rates are only 30-80%) or a proton pump inhibitor plus clarithromycin (eradication rate of roughly 71%). Adding a second antimicrobial agent is recommended for successful eradication.
Triple regimens are preferred in clinical practice. One drug is a proton pump inhibitor or a bismuth-based drug, the second drug is clarithromycin, and the third drug is amoxicillin or metronidazole. Quadruple therapy regimens (ie, 2 antibiotics, bismuth, antisecretory agent) generally are effective; however, because more drugs are prescribed and taken, increased adverse effects and decreased patient compliance can occur. This regimen is used in the event that triple therapy fails.
The decision as to which medications to use is based on the following 4 criteria: (1) the different toxicities of the various medications, (2) the relative costs of each medication and regimen, (3) the emergence of antimicrobial-resistant bacteria, and (4) the level of patient compliance.
What is acute gastritis?What are the symptoms of acute gastritis?How is acute gastritis diagnosed?What is the incidence of acute gastritis?What causes acute gastritis?What is the pathophysiology of acute erosive gastritis?What is the pathophysiology of acute bacterial gastritis?What is the pathophysiology of reactive gastropathy?What is the prevalence of Helicobacter heilmannii in acute gastritis?What are rare causes of gastritis?What is phlegmonous gastritis?Which organisms cause viral gastritis?Which organisms cause fungal gastritis?How is parasitic gastritis transmitted?What is the pathophysiology of ulcero-hemorrhagic gastritis?What is the association between gastritis and inflammatory bowel disease?Which disorders are associated with eosinophilic gastritis?What is the etiology of acute gastritis?What are the prevalence of acute gastritis?What is the prognosis of acute gastritis?What is the mortality or morbidity in acute gastritis?What are possible complications of acute gastritis?What information about acute gastritis should patients be given?What are the symptoms of acute gastritis?What should be the focus of clinical history for acute gastritis?Which physical findings are suggestive acute gastritis?What should be considered in the differential diagnosis of suspected gastritis?What are the differential diagnoses for Acute Gastritis?What is the role of lab testing in the workup of acute gastritis?What are the radiologic signs of acute gastritis?What is the significance of a radiographic finding of nodularity in the workup of acute gastritis?Which imaging findings are indicate of acute gastritis?Which lab tests are used to identify H pylori in the workup of acute gastritis?What is the role of endoscopy in the workup of acute gastritis?What other conditions may be diagnosed in an endoscopic evaluation for acute gastritis?Which endoscopic findings suggest acute gastritis indicate?What is the role of histologic exam in the workup of acute gastritis?Which histologic features help determine etiology of acute gastritis?What is the role of surgery in the treatment of acute gastritis?When should medical therapy be administered for acute gastritis?What are the treatment options for acute gastritis?How is acute gastritis treated?What long-term monitoring is needed following treatment for acute gastritis?What is the basis of treatment selection for acute gastritis?Which medications in the drug class Antidiarrheal agents are used in the treatment of Acute Gastritis?Which medications in the drug class Antibiotics are used in the treatment of Acute Gastritis?Which medications in the drug class Proton pump inhibitors are used in the treatment of Acute Gastritis?Which medications in the drug class H2 blockers are used in the treatment of Acute Gastritis?Which medications in the drug class Antacids are used in the treatment of Acute Gastritis?
Mohammad Wehbi, MD, Associate Professor of Medicine, Associate Program Director, Department of Gastroenterology, Emory University School of Medicine; Section Chief of Gastroenterology, Atlanta Veterans Affairs Medical Center
Disclosure: Nothing to disclose.
Coauthor(s)
Gwendolyn Sarver,
Disclosure: Nothing to disclose.
Kamil Obideen, MD, Assistant Professor of Medicine, Division of Digestive Diseases, Emory University School of Medicine; Consulting Staff, Division of Gastrointestinal Endoscopy, Atlanta Veterans Affairs Medical Center
Disclosure: Nothing to disclose.
Sunil Dacha, MBBS, MD, House Staff, Division of Digestive Disease, Emory University School of Medicine
Disclosure: Nothing to disclose.
Vincent W Yang, MD, PhD, R Bruce Logue Professor, Director, Division of Digestive Diseases, Department of Medicine, Professor of Hematology and Oncology, Winship Cancer Institute, Emory University School of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Waqar A Qureshi, MD, FRCP(UK), FACP, FACG, FASGE, Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
Disclosure: Nothing to disclose.
Acknowledgements
Nicole M Griglione, MD Fellow in Gastroenterology, Department of Medicine, Emory University School of Medicine
Nicole M Griglione, MD is a member of the following medical societies: American Medical Association and Illinois State Medical Society
Disclosure: Nothing to disclose.
Richard H Snyder, MD Vice-Chair, Program Director, Department of Medicine, Norfolk General Hospital; Clinical Associate Professor, Department of Internal Medicine, East Virginia Medical School
Richard H Snyder, MD is a member of the following medical societies: American College of Physicians
Beers M, Berkow R, eds. Gastritis. The Merck Manual of Diagnosis and Therapy. 18th ed. 2006. Section 3, Chapter 23.
Lee EL, Feldman M. Gastritis and other gastropathies. Feldman M, Friedman LS, Sleisenger MH, eds. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 7th ed. Philadelphia: Saunders; 2002. 810-27.
Kasper DL, Braunwald E, Fauci A, et al. Gastritis. Harrison's Principles of Internal Medicine: Companion Handbook. 16th ed. McGraw-Hill: 2006. Part 12, Chapter 274.
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