Definition
Gastritis is inflammation of the gastric mucosa. It is a group of disorders, not a single disease entity. These disorders are distinguished by clinical features, histologic findings, anatomic distribution, and etiology.
* Erosive and hemorrhagic gastritis is generally associated with alcoholism, nonsteroidal anti-inflammatory drug (NSAID) injury, stress lesions in critically ill patients (e.g., intensive care unit [ICU] disease), trauma (e.g., nasogastric tube suction, retching, radiation, chemotherapy), and surgery (e.g., postgastrectomy).
* Nonerosive, nonspecific gastritis is generally associated with infectious etiologies (e.g., Helicobactor pylori), aging, gastric or duodenal ulcers, autoimmune diseases (e.g., pernicious anemia, lymphocytic gastritis), and reactive gastropathies (e.g., postgastrectomy).
* Distinctive gastritis is generally associated with bacterial (e.g., syphilis, tuberculosis), viral (e.g., cytomegalovirus), fungal (e.g., Candida), and parasitic (e.g., cryptosporidiosis) infections; with chronic systemic inflammatory diseases (e.g., Crohn's disease, sarcoidosis), as well as with unknown localized disease of unknown causes (e.g., Menetrier's disease).
Etiology
* NSAID use
* Alcohol and tobacco
* Reflux injury (e.g., bile)
* Trauma (e.g., surgery, radiation, vomiting, foreign body)
* Bacterial infections (e.g., H. pylori, Treponema pallidum, Mycobacterium tuberculosis)
* Autoimmune etiologies (e.g., pernicious anemia)
* Viral, fungal, and parasitic infections
* Systemic disease (e.g., Crohn's disease, sarcoidosis, graft-versus-host disease)
* Unknown causes (e.g., Menetrier's disease or other hypertrophic gastropathies)
* Stress lesions
Risk Factors
For erosive and hemorrhagic gastritis:
* Exposure to ulcerogenic drugs
* Alcoholism
* Severe illness or trauma
For nonerosive gastritis:
* Colonization with H. pylori in early childhood
* Familial contact infected with H. pylori
* Latino or African-American ancestry
* Institutionalized individuals
* Low socioeconomic status
* Gastroenterologists (person-to-person transmission, especially from endoscopy)
* Age over 60 years
* History of pernicious anema or gastric lymphoma
Signs and Symptoms
Most patients are asymptomatic; even gastric erosions and hemorrhages are not usually associated with abdominal pain. Symptomatic patients often have other gastrointestinal conditions, and gastritis is diagnosed as an incidental histologic finding. Presenting complaints may include the following.
* Dyspepsia
* Anorexia
* Abdominal pain often aggravated by eating
* Nausea with/without vomiting
* Gastrointestinal bleeding (e.g., hematemesis, melena)
Differential Diagnosis
* Nonulcerative dyspepsia
* Peptic ulcer disease
* Gastroesophageal reflux
* Gastric cancer
* Gastroenteritis
* Celiac disease
* Functional gastrointestinal disorder
* Pancreatic disease
Diagnosis
Physical Examination
Unremarkable physical presentation unless the patient presents with abdominal pain, bleeding, vomiting, and anorexia, where the patient looks ill, pale, and in severe cases, cachectic (malnourished) or dehydrated.
Laboratory Tests
Usually unremarkable unless the patient presents with pernicious anemia. Blood or breath tests, as well as tissue examination, can detect H. pylori (the major cause of nonerosive gastritis).
* Histologic studies using the following stains: hematoxylin and eosin, modified Giemsa, Warthin-Starry, Gram
* Serologic studies using enzyme-linked immunosorbent assay (ELISA)
* Histologic studies using the rapid urease test (H. pylori produces increased quantities of urease)
* Urea carbon breath test using 13C- and 14C-labeled urea, given orally; it is hydrolyzed by the urease produced by H. pylori, creating ammonia and CO2; CO2 in patient's breath then measured
* Serologic studies using polymerase chain reaction (PCR)
Pathology/Pathophysiology
For erosive and hemorrhagic gastritis:
* Erosions (breaks in the mucosa that do not extend beyond the muscularis mucosae) that appear as multiple lesions surrounded by erythema
* Hemorrhagic lesions that appear as bright red streaks or petechiae
* Epithelial abnormalities and hyperplasia
* Minimal inflammation
For nonerosive gastritis:
* Clumps of mononuclear cells and neutrophils
* Foveolar hypoplasia (abnormal pit epithelium)
* Intestinal metaplasia (epithelial cells resemble intestinal epithelium)
* Mucus gland metaplasia (fundus replaced by mucus glands)
* Endocrine cell hyperplasia
* H. pylori organisms
Imaging
Imaging studies such as an upper GI series are used to rule out conditions that mimic gastritis such as gastroesophageal reflux or gastric malignancy.
Other Diagnostic Procedures
Endoscopy with biopsy is the gold standard for diagnosing gastritis (several suspected areas must be biopsied because of patchy and irregular distribution). A complete blood count will detect anemia, and a guaiac test of stool or vomitus will detect gastrointestinal bleeding.
Treatment Options
Treatment Strategy
No specific treatment is required for gastritis even with atrophic changes in asymptomatic individuals; however, treat associated conditions in symptomatic patients.
Drug Therapies
To treat H. pylori infection: triple-drug therapy (for two weeks) to prevent antibiotic resistance, Pepto-Bismol, 2 tablets every six hours; metronidazole, 250 mg every eight hours; and tetracycline, 500 mg every eight hours; use amoxicillin (500 mg every eight hours) if tetracycline is not tolerated. Treatment of asymptomatic H. pylori infections is controversial; at present H. pylori is only treated if associated with duodenal and gastric ulcers and MALT lymphoma.
To treat peptic ulcer disease: triple-drug therapy (for one week) to reduce acid production omeprazole, 20 mg bid; clarithromycin, 250 mg bid; and metronidazole, 500 mg bid.
Complementary and Alternative Therapies
Nutritional and herbal support help to heal gastric mucosa, fight infection, and reduce recurrence. In addition, mind-body techniques such as meditation, progressive muscle relaxation, tai chi, yoga, and stress management may reduce the frequency and severity of symptoms and enhance healing.
Nutrition
* Avoid dairy, caffeine, alcohol, and sugar. Coffee, even decaffeinated, should be eliminated because of irritating oils.
* Eliminate any known food allergens.
* Include sulphur-containing foods such as garlic, onions, broccoli, cabbage, brussel sprouts, and cauliflower in the diet. Sulphur is a precursor to glutathione which provides antioxidant protection to the gastric mucosa. N-acetylcysteine (200 mg bid between meals) is also a precursor to glutathione.
* Vitamin C (1,000 mg tid) decreases nitrosamines which are linked to stomach cancer.
* Zinc (30 to 50 mg/day) enhances healing.
* To treat pernicious anemia: lifelong regular parenteral vitamin B12
Herbs
Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.
* DGL (deglycyrrhizinated licorice), 250 mg qid 15 to 20 minutes before meals and one to two hours after last meal, increases circulation and healing to gastric mucosa. This preparation has the hypertensive factor in licorice root removed making it safe to take long-term and in cases of hypertension.
* Powders of slippery elm (Ulmus fulva) and marshmallow root (Althea officinalis) may be taken singly or together, 1 tsp. bid to tid, to decrease inflammation and encourage healing.
* Ginger root tea (Zingiber officinale) is a warming carminative that increases circulation and enhances digestion. Drink 2 to 3 cups/day with meals.
* For H. pylori, bismuth subcitrate (120 mg qid for eight weeks) may be helpful in eradicating H. pylori and reducing recurrence. It is poorly absorbed, which decreases the likelihood of side effects; however, it is associated with neurotoxicity if used long-term. Patient may still need antibiotics if H. pylori has not resolved after eight weeks.
Homeopathy
An experienced homeopath should assess individual constitutional types and severity of disease to select correct remedy and potency. Consider three remedies, Nux vomica, Arsenicum album, and Lycopodium.
Acupuncture
Acupuncture may help in reducing stress and improving digestive function.
Massage
Therapeutic massage can alleviate stress and increase sense of well-being.
Patient Monitoring
Symptomatic individuals must be treated and followed with repeat endoscopy or gastroscopy if symptoms persist.
Other Considerations
Prevention
Patients must be advised of the risks of continued alcohol, tobacco, and NSAID use. A high-fiber diet is recommended to decrease the incidence of digestive problems. H. pylori should be eradicated in symptomatic individuals.
Complications/Sequelae
* Epidemiolgic studies have linked the presence of H. pylori with the development of gastric cancer (a three- to six-fold increased risk).
* Chronic gastritis may lead to atrophic gastritis, gastric atrophy, and gastric metaplasia, which may result in gastric cancer.
* Acid-suppressive therapy alone may indirectly increase the risk of gastric cancer by increasing the development of gastric atrophy
* GI bleeding may result from advanced mucosal erosion/ulceration.
Prognosis
If the etiology of the gastritis is properly identified, most cases are successfully treated. Gastritis resulting from H. pylori infection may clear initially but require repeated treatment.
Pregnancy
Do not use bismuth subcitrate in pregnancy.
References
Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:427.
Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998: 941-943,1610-1614.
Murray MT, Pizzorno JE. Encyclopedia of Natural Medicine. 2nd ed. Rocklin, Calif: Prima Publishing; 1998:522-523.
Sklar M, ed. Gastoenterologic problems. Clin Geriatr Med. 1991;7:235-238.
Sleisenger MH, Fordtran JS, Scharschmidt BF, et al. Gastrointestinal Disease. 5th ed. Philadelphia, Pa: WB Saunders Co; 1993:545-564.







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