AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Acute gastritis is a term covering a broad spectrum of entities that induce inflammatory changes in the gastric mucosa. The 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 2 categories: erosive (eg, superficial erosions, deep erosions, hemorrhagic erosions) and nonerosive (generally caused by Helicobacter pylori).

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.

Pathophysiology

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 the exposure to a variety of agents or factors. This is referred to as reactive gastritis. These agents/factors include nonsteroidal anti-inflammatory medications (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 oral or 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 on 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 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.

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 ulcersand80%ofduodenal 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 gastric epithelial cells. It also has several adhesions 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.

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 because of 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 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 progresses to peritonitis and death.

Viral infections can cause gastritis. Cytomegalovirus (CMV) is a common viral cause of gastritis. It is usually encountered in individuals who are immunocompromised, including those with cancer, immunosuppression, transplants, and AIDS. 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.

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.

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.

Sex

No sexual predilection exists.

Age

Gastritis affects all age groups. The incidence of H pylori infection increases with age.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• Gnawing or burning epigastric distress, occasionally accompanied by nausea and/or vomiting. The pain may improve or worsen with eating.
• 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 NSAIDs, especially at high doses

Physical

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.

Causes

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.

• 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)
• Viral infections (eg, CMV)
• Fungal infections
• • Candidiasis
  • Histoplasmosis
  • Phycomycosis
• Parasitic infection (eg, anisakidosis)
• Acute stress (shock)
• Radiation
• Allergy and food poisoning
• Bile: The reflux of bile (an alkaline medium 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.
• Direct trauma

DIFFERENTIALS

Section 4 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Hyperplastic gastropathy/Menetrier disease
Granulomatous gastropathy
Pregnancy

WORKUP

Section 5 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• A number of laboratory tests are usually ordered.
• • CBC count to assess for anemia, as acute gastritis can cause gastrointestinal bleeding
  • Liver and kidney function tests
  • Gallbladder and pancreatic function tests
  • Pregnancy test
  • Stool for blood

Imaging Studies

• 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. They usually are 1-3 mm in size. 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.

Other Tests

• 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.
  • • 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 an 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.
  • • The first test is the rapid urease test (RUT). It is performed by placing a gastric biopsy specimen, obtained on 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 a bacterial culture 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.
• 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.

Procedures

• Endoscopy
• • 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.

Histologic Findings

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 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 nonnecrotizing granulomas containing the organisms. The diagnosis of histoplasmosis requires a positive culture result from a 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 pigments 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 histology of radiation-induced gastritis include nuclear karyorrhexis and cytoplasmic eosinophilia of the gastric pit epithelium in 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.

TREATMENT

Section 6 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

• 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.
• Administer fluids and electrolytes as required, particularly if the patient is vomiting.
• Discontinue the use of drugs known to cause gastritis (eg, NSAIDs, alcohol).

Surgical Care

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.

Consultations

Consult a gastroenterologist in complicated cases.

MEDICATION

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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 period 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. No effective antiviral therapy exists for the treatment of human cytomegalovirus (HCMV) infection, though 2 agents (ie, ganciclovir, foscarnet) have been shown to be virostatic. 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.

Drug Category: Antacids

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.

Drug Category: H2 blockers

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. When used alone, they are frequently used as antisecretory drugs in H pylori therapy regimens. 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.

Drug Category: Proton pump inhibitors

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.

Drug Category: Antibiotics

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 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 of 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.

Drug Category: Antidiarrheal agents

Used in combination with antibiotics and proton pump inhibitors/H2 receptor antagonists to eradicate H pylori.

FOLLOW-UP

Section 8 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
• References

Transfer

• No specifications

Complications

• Bleeding from an erosion or ulcer
• Gastric outlet obstruction due to edema limiting the adequate transfer of food from the stomach to the small intestine
• Dehydration from vomiting
• Renal insufficiency as a result of dehydration

Prognosis

• Gastritis generally clears spontaneously.
• With treatment, the mortality rate of phlegmonous gastritis is 64%.

Patient Education

• Explain the disease to the patient.
• Encourage cessation of smoking and alcohol consumption.
• Warn patients of the potential effects of noxious drugs and chemical agents.
• For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education article Gastritis.

MISCELLANEOUS

Section 9 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Early diagnosis is not made often.

MULTIMEDIA

Section 10 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Acute gastritis with superficial erosions.
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Media file 2:  Mucosal erythema and edema consistent with acute gastritis.
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REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Andersen LP. Colonization and infection by Helicobacter pylori in humans. Helicobacter. Nov 2007;12 Suppl 2:12-5. [Medline].
• Beers M, Berkow R, eds. Gastritis. In: The Merck Manual of Diagnosis and Therapy. 18^th ed. 2006:Section 3, Chapter 23. [Full Text].
• Feldman. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 7^th ed. 2002:810-823.
• Ford A, Delaney B, Forman D. Eradication therapy for peptic ulcer disease in Helicobacter pylori positive patients. Cochrane Database Syst Rev. 2004;CD003840.
• Gelfand DW, Ott DJ, Chen MY. Radiologic evaluation of gastritis and duodenitis. AJR Am J Roentgenol. Aug 1999;173(2):357-61. [Medline].
• Gisbert JP, Pajares JM. Diagnosis of Helicobacter pylori infection by stool antigen determination: a systematic review. Am J Gastroenterol. Oct 2001;96(10):2829-38. [Medline].
• Haruma K. Helicobacter heilmannii: a spiral shaped organism other than Helicobacter pylori. Intern Med. Mar 1999;38(3):217-8. [Medline].
• Iwakiri Y, Kabemura T, Yasuda D, et al. A case of acute phlegmonous gastritis successfully treated with antibiotics. J Clin Gastroenterol. Mar 1999;28(2):175-7. [Medline].
• Kasper DL, Braunwald E, Fauci A, et al. Gastritis. In: Harrison's Principles of Internal Medicine: Companion Handbook. 16^th ed. McGraw-Hill: 2006:Part 12, Chapter 274.
• Richieri JP, Pol B, Payan MJ. Acute necrotizing ischemic gastritis: clinical, endoscopic and histopathologic aspects. Gastrointest Endosc. Aug 1998;48(2):210-2. [Medline].
• Soltermann A, Koetzer S, Eigenmann F, et al. Correlation of Helicobacter pylori virulence genotypes vacA and cagA with histological parameters of gastritis and patient's age. Mod Pathol. Aug 2007;20(8):878-83. [Medline]. [Full Text].
• Srivastava A, Lauwers GY. Pathology of non-infective gastritis. Histopathology. Jan 2007;50(1):15-29. [Medline].
• Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med. Oct 10 2002;347(15):1175-86. [Medline].
• Yamamoto T, Matsumoto J, Shiota K, et al. Helicobacter heilmannii associated erosive gastritis. Intern Med. Mar 1999;38(3):240-3. [Medline].

Article Last Updated: Jul 30, 2008