Gastritis

Definition

Gastritis commonly refers to inflammation of the lining of the stomach, but the term is often used to encompass a variety of symptoms resulting from stomach lining inflammation, as well as symptoms of burning or discomfort. True gastritis comes in several forms and is diagnosed using a combination of tests. In the 1990s scientists discovered that the main cause of true gastritis is infection from a bacterium called Helicobacter pylori (H. pylori).

Description

Gastritis should not be confused with common symptoms of upper abdominal discomfort. Gastritis has been associated with resulting ulcers, particularly peptic ulcers. In some cases, chronic gastritis can lead to more serious complications.

Nonerosive Helicobacter pylori (H. pylori) gastritis

The main cause of true gastritis is H. pylori infection. H. pylori is indicated in an average of 90% of persons with chronic gastritis. This form of nonerosive gastritis is the result of infection with the H. pylori bacterium, a microorganism whose outer layer is resistant to the normal effects of stomach acid in breaking down bacteria. This resistance means that the bacterium may rest in the stomach for long periods of times, even years, and eventually cause symptoms of gastritis or ulcers when other factors are introduced, such as the ingestion of nonsteroidal antiinflammatory drugs (NSAIDs). It also seems to be activated in people with a genetic predisposition. Study of the role of H. pylori in development of gastritis and peptic ulcers has disproved the former belief that stress led to most stomach and duodenal ulcers. This understanding has resulted in improved treatment and reduction of stomach ulcers. H. pylori is most likely transmitted between humans, although the specific routes of transmission were still under study in 2001. Studies are also underway to determine the role of H. pylori and resulting chronic gastritis in the development of gastric cancer.

Erosive and hemorrhagic gastritis

After H. pylori, the second most common cause of chronic gastritis is the use of NSAIDs. These commonly used pain killers, including aspirin, fenoprofen, ibuprofen, and naproxen—among others—can lead to gastritis and peptic ulcers. Other forms of erosive gastritis are those due to ingestion of alcohol and corrosive agents, or due to such trauma as ingestion of foreign bodies.

Other forms of gastritis

Clinicians differ on the classification of the less common and specific forms of gastritis, particularly since there is so much overlap with H. pylori in development of chronic gastritis and complications of gastritis. Other types of gastritis that may be diagnosed include:

  • Acute stress gastritis. This is the most serious form of gastritis and usually occurs in persons who are critically ill, such as those in intensive care. Stress erosions may develop suddenly as a result of severe trauma or stress to the stomach lining.
  • Atrophic gastritis. This is the result of chronic gastritis that is leading to atrophy (a decrease in size and wasting away) of the gastric lining. Gastric atrophy is the final stage of chronic gastritis and may be a precursor of gastric cancer.
  • Superficial gastritis. This is a term often used to describe the initial stages of chronic gastritis.
  • Uncommon forms of gastritis. These are nonspecific forms of gastritis that include granulomatous, eosinophilic, and lymphocytic gastritis.

Causes and symptoms

Nonerosive H. pylori gastritis

H. pylori gastritis is caused by infection from the H. pylori bacterium. It is believed that most infection occurs in childhood. The route of its transmission was still under study in 2001 and clinicians assume there may be more than one route for the bacterium to enter a body. Its prevalence and distribution differ in nations around the world. The presence of H. pylori has been detected in between 86% and 99% of persons with chronic superficial gastritis. However, physicians are still learning about the link between H. pylori and chronic gastritis and peptic ulcers, since many persons with H. pylori infection do not develop symptoms of gastritis or peptic ulcers. H. pylori is also seen in approximately 90% to 100% of people with duodenal ulcers.

Symptoms of H. pylori gastritis include abdominal pain and reduced acid secretion in the stomach. However, the majority of people with H. pylori infection suffer no symptoms, even though the infection may lead to ulcers and resulting problems. Ulcer symptoms include dull, gnawing pain, often two to three hours after meals, and pain in the middle of the night when the stomach is empty.

Erosive and hemorrhagic gastritis

The most common cause of this form of gastritis is use of NSAIDs. Other causes may be alcoholism, or stress from surgery or critical illness. The role of NSAIDs in development of gastritis and peptic ulcers depends upon the dosage level. Although even low doses of aspirin or other NSAIDs may cause some gastric upset, such low doses generally will not lead to gastritis. However, as many as 10%–30% of persons on higher and more frequent doses of NSAIDs, such as those with chronic arthritis, may develop gastric ulcers. As of 2001, studies were underway to determine the role of H. pylori in gastritis and ulcers among persons using NSAIDs.

Individuals with erosive gastritis may also experience no symptoms. When symptoms do occur, they may include anorexia nervosa, gastric pain, nausea, and vomiting.

Other forms of gastritis

Less common forms of gastritis may result from a number of generalized diseases, or from complications of chronic gastritis. Any number of mechanisms may cause various less common forms of gastritis that may differ slightly in their presentation, symptoms, and clinical signs. However, they all have in common inflammation of the gastric mucosa.

Diagnosis

Nonerosive H. pylorigastritis

H. pylori gastritis is easily diagnosed through the use of the urea breath test. This test detects the active presence of H. pylori infection. Other serological tests, which may be readily available in a physician's office, may be used to detect H. pylori infection. Newly developed versions offer rapid diagnosis. The choice of test will depend upon cost, availability, and the physician's experience, since nearly all of the available tests have an accuracy rate of 90% or better. Endoscopy, or the examination of the stomach area using a hollow tube inserted through the mouth, may be ordered to confirm diagnosis. A biopsy of the gastric lining may also be ordered.

Erosive or hemorrhagic gastritis

The patient's clinical history may be particularly important in the diagnosis of this type of gastritis, since its cause is most often the result of chronic use of NSAIDs, alcohol, or other erosive substances.

Other forms of gastritis

Gastritis that has developed to the stage of duodenal or gastric ulcers usually requires endoscopy for diagnosis. The endoscopy allows a physician to perform a biopsy for possible malignancy and for H. pylori. Sometimes, an upper gastrointestinal x-ray study with barium is ordered. Some diseases, such as Zollinger-Ellison syndrome, an ulcerative disease of the upper gastrointestinal tract, may show large mucosal folds in the stomach and duodenum on radiographs or in endoscopy. Other tests check for changes in gastric function.

Treatment

H. pylori gastritis

The discovery of H. pylori's role in development of gastritis and ulcers has led to improved treatment of chronic gastritis. In particular, relapse rates for duodenal and gastric ulcers have been reduced with successful treatment of H. pylori infections. Since the infection can be treated with antibiotics, the bacterium can be completely eliminated up to 90% of the time.

Although H. pylori can be successfully treated, the treatment can be inconvenient, and relies heavily on the patient's compliance. As of 2001 studies were underway to identify the best treatment method based on simplicity, personal cooperation, and results. No single antibiotic had been found at that time that would eliminate H. pylori, so a combination of antibiotics is prescribed to treat the infection.

DUAL THERAPY. Dual therapy involves the use of an antibiotic and a proton pump inhibitor. Proton pump inhibitors are medications that help reduce stomach acid by halting the mechanism that pumps acid into the stomach. This combination also helps promote healing of ulcers or inflammation. Dual therapy has not been proven to be as effective as triple therapy, but may be ordered for some people who are unable to consistently comply with the use of a larger number of medications, and who will therefore more likely follow the two-week course of therapy.

TRIPLE THERAPY. As of 2001, triple therapy was the preferred treatment for persons with H. pylori gastritis. It is estimated that triple therapy successfully treats between 80% and 95% of H. pylori cases. This treatment regimen usually involves a two-week course of three drugs. An antibiotic such as amoxicillin or tetracycline, and a second antibiotic such as clarithromycin or metronidazole, are used in combination with bismuth subsalicy-late, a substance found in the over-the-counter medication Pepto-Bismol, that helps protect the lining of the stomach from acid. Physicians are experimenting with various combinations of drugs and times of treatment to balance side effects with effectiveness. Side effects of triple therapy are not serious, but may cause enough discomfort that people are not inclined to follow the treatment regimen.

OTHER TREATMENT THERAPIES. Scientists have experimented with quadruple therapy, which adds an antisecretory drug—one that suppresses gastric secretion—to the standard triple therapy protocol. One study showed this therapy to be effective with only a one-week course of treatment in more than 90% of patients. Short-course therapy was attempted with triple therapy involving antibiotics and a proton pump inhibitor, and seemed effective in eliminating H. pylori in one week for more than 90% of patients. The goal is to develop the most effective therapy combination that can work in a treatment period of one week or less.

MEASURING H. PYLORI TREATMENT EFFECTIVENESS. In order to ensure that H. pylori has been eradicated from the gatrointestinal tract, physicians will test persons following treatment. The breath test is, once again, the preferred method.

Treatment of erosive gastritis

Since few people with this form of gastritis show symptoms, treatment may depend upon severity of symptoms. When symptoms do occur, patients may be treated with therapy similar to that for H. pylori, especially since some studies have demonstrated a link between H. pylori and NSAIDs in causing gastric ulcers. Avoidance of NSAIDs will most likely be prescribed.

Other forms of gastritis

Specific treatment will depend upon the cause and type of gastritis. These may include prednisone or antibiotics.


KEY TERMS


Duodenal—Refers to the duodenum, or the first part of the small intestine.

Gastric—Relating to the stomach.

Mucosa—The mucous membrane, or the thin layer of tissue that lines many body cavities and passages.

Ulcer—A break in the skin or mucous membrane. It can fester and create exudate like a sore.


Critically ill persons at high risk for bleeding may be treated with preventive drugs to reduce risk of acute stress gastritis. If stress gastritis does occur, the patient is treated with a constant infusion of a drug to stop bleeding. Sometimes surgery is recommended, but must be weighed against the possibility of surgical complications or death. Once torrential bleeding occurs in acute stress gastritis, mortality rates can exceed 60%.

Alternative treatment

Alternative forms of treatment for gastritis and ulcers should be used cautiously and in conjunction with conventional medical care, particularly now that scientists have confirmed the role of H. pylori in gastritis and ulcers. Such alternative treatments as diet, nutritional supplements, herbal medicine, and Ayurvedic medicine can help address gastritis symptoms. It is believed that zinc, vitamin A, and beta-carotene aid in the stomach lining's ability to repair and regenerate itself. Herbs thought to stimulate the immune system and reduce inflammation include echinacea (Echinacea spp.) and goldenseal (Hydrastis canadensis). Ayurvedic medicine involves meditation. There are also certain herbs and nutritional supplements aimed at helping to treat ulcers.

Prognosis

The discovery of H. pylori has improved the prognosis for persons with gastritis and ulcers. Since treatment exists with the potential to eradicate the infection, recurrence is much less common. As of 2001, people requiring treatment for H. pylori were those at high risk because of such factors as NSAIDs use, or those with ulcers and other complicating factors or symptoms. Research will continue into the most effective treatment of H. pylori, especially in light of the bacterium's resistance to certain antibiotics. Regular treatment of persons with gastric and duodenal ulcers has been recommended, since H. pylori plays such a consistently high role in development of ulcers. It is believed that H. pylori also plays a role in the eventual development of serious gastritis complications and cancer. Detection and treatment of H. pylori infection may help reduce occurrence of these diseases. The prognosis for persons with acute stress gastritis is less encouraging, with a 60% or higher mortality rate among those experiencing heavy bleeding.

Health care team roles

A family physician or internist usually makes a diagnosis of gastritis, prescribes treatment, and provides follow-up testing to ascertain the effectiveness of the prescribed treatment regimen. Surgeons occasionally remove a portion of stomach when gastritis is caused by factors other than H. pylori or by cancer. Nurses play an important role in patient education, particularly in relation to medication, diet, prevention, compliance with treatment, and treatment side effects.

Prevention

The widespread detection and treatment of H. pylori as a preventive measure in gastritis has been discussed but not resolved. Until more is known about the routes by which H. pylori is spread, specific prevention recommendations cannot be made. Erosive gastritis from NSAIDs can be prevented by discontinuing the use of these drugs. In 1998 an education campaign was launched to educate people, particularly an aging population of arthritis sufferers, about the risk of ulcers from NSAIDs and alternative drugs. As of 2001 the success of this campaign had not been evaluated.

Resources

BOOKS

Brandt, Lawrence J., and Frederick Daum. Clinical Practice of Gastroenterology. New York: Churchill Livingstone, 1999.

Burton Goldberg Group. Alternative Medicine: The Definitive Guide. Puyallup, WA: Future Medicine Publishing, Inc.,1994.

Debas, Haile, and Susan Orloff. "Peptic Ulcer Disease: Surgical Therapy." In Cecil Textbook of Medicine, 21st ed. Ed. Lee Goldman and J. Claude Bennett. Philadelphia: W.B. Saunders, 2000, 680-684.

Friedman, Lawrence S., and Walter L. Peterson. "Peptic Ulcer and Related Disorders." In Harrison's Principles of Internal Medicine, 14th ed. Ed. Anthony S. Fauci, et al. New York: McGraw-Hill, 1998, 1596-1616.

Graham, David Y., Robert M. Genta, and Michael F. Dixon. Gastritis. Philadelphia: Lippincott Williams & Wilkins, 1999.

Graham, Donald Y. "Peptic Ulcer Disease: Medical Therapy." In Cecil Textbook of Medicine, 21st ed. Ed. Lee Goldman and J. Claude Bennett. Philadelphia: W.B. Saunders, 2000, 675-678.

Graham, Donald Y. "Complications of Peptic Ulcer." In Cecil Textbook of Medicine, 21st ed. Ed. Lee Goldman and J. Claude Bennett. Philadelphia: W.B. Saunders, 2000, 678-680.

Greeley, George H. Gastrointestinal Endocrinology. Totowa, NJ: Humana Press, 1998.

Herbst, John J. "Primary (Peptic) Ulcers." In Nelson Textbook of Pediatrics, 16th ed. Ed. Richard E. Behrman et al., Philadelphia: Saunders, 2000, 1148-1149.

Herbst, John J. "Secondary or Stress (Peptic) Ulcer Disease." In Nelson Textbook of Pediatrics, 16th ed. Ed. Richard E. Behrman et al., Philadelphia: Saunders, 2000, 1149-1150.

Herbst, John J. "Ulcer Disease." In Nelson Textbook of Pediatrics, 16th ed. Ed. Richard E. Behrman et al., Philadelphia: Saunders, 2000, 1147-1148.

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Mobley, Harry L.T., George L. Mendz, and Stuart L. Hazell. Helicobacter Pylori: Physiology and Genetics. Washington, DC: American Society for Microbiology, 2001.

Soll, Andrew H., and Jon Isenberg. "Peptic Ulcer Disease: Epidemiology, Pathophysiology, Clinical Manifestations and Diagnosis." In Cecil Textbook of Medicine, 21st ed. Ed. Lee Goldman and J. Claude Bennett. Philadelphia:W.B. Saunders, 2000, 671-675.

Soll, Andrew H. "Gastritis and Helicobacter Pylori." In Cecil Textbook of Medicine, 21st ed. Ed. Lee Goldman and J. Claude Bennett. Philadelphia: W.B. Saunders, 2000, 668-671.

Yamada, Tadataka, David H. Alpers, and Loren Laine. Textbook of Gastroenterology, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 1999.

PERIODICALS

Bartolome Resano R, B. Martinez, Echeverria A. Martinez, Penuela J. Martinez, Abadia A. Isturiz, Flamarique F. Olcoz, and Cativiela J. del Cazo. "Gastritis Caused by Helicobacter Heilmannii." Gastroenterology and Hepatology 24, no. 4 (2001): 202-204.

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Finn L.S., and D.L. Christie. "Helicobacter Pylori and Meckel's Diverticula." Journal of Pediatric Gastroenterology and Nutrition 32, no. 2 (2001): 150-155.

Gold B.D. "New Approaches to Helicobacter Pylori Infection in Children." Current Gastroenterology Reports 3, no. 3(2001): 235-247.

Moshkowitz M., S. Brill, F.M. Konikoff, M. Averbuch, N. Arber, and Z. Halpern. "Additive Deleterious Effect of Smoking on Gastroduodenal Pathology and Clinical Course in Helicobacter Pylori-Positive Dyspeptic Patients." Israel Medical Association Journal 2, no. 12(2000): 892-895.

Orihara T, H. Wakabayashi, A. Nakaya, K. Fukuta, S. Makimoto, K. Naganuma, A. Entani, and A. Watanabe. "Effect of Helicobacter Pylori Eradication on Gastric Mucosal Phospholipid Content and its Fatty Acid Composition." Journal of Gastroenterology and Hepatology 16, no. 3 (2001): 269-275.

Parente F., R. Negrini, V. Imbesi, G. Maconi, M. Sainaghi, L. Vago, and G.B. Porro. "Presence of Gastric Autoantibodies Impairs Gastric Secretory Function in Patients with Helicobacter Pylori-Positive Duodenal Ulcer." Scandinavian Journal of Gastroenterology 36, no. 5 (2001): 474-478.

Podolski, J.L. "Recent Advances In Peptic Ulcer Disease: H. Pylori Infection and its Treatement." Gastroenterology Nursing 19, no. 4: 128-136.

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Spaziani E., M. Catani, A. Mingoli, P. Del Duca, A. Di Filippo, R. De Milito, P. Siciliano, M. Chiaretti, and R. Corsi. "Duodenal Ulcer and Helicobacter Pylori." Minerva Medicine 92, no. 1 (2001): 1-5.

Urakami Y., and T. Sano. "Endoscopic Duodenitis, Gastric Metaplasia and Helicobacter Pylori." Journal of Gastroenterology and Hepatology 16, no. 5 (2001): 513-518.

Xia H.H., B.C. Yu Wong, N.J. Talley, and S.K. Lam. #x201C;Helicobacter Pylori Infection—Current Treatment Practice." Expert Opinion in Pharmacotherapy 2, no. 2(2001): 253-266.

ORGANIZATIONS

American College of Gastroenterology. 4900 B South 31st Street, Arlington VA 22206. (703) 820-7400. <http://www.acg.gi.org>.

National Digestive Diseases Information Clearinghouse (NDDIC). 2 Information Way, Bethesda, MD 20892-3570. <http://www.niddk.nih.gov>.

OTHER

American Academy of Family Physicians. <http://www.aafp.org/afp/991201ap/2555.html>.

American Academy of Pediatrics. <http://www.aap.org/policy/gastro.htm>.

American College of Gastroenterology. <http://www.acg.org>.

Centers for Disease Control and Prevention. <http://www.cdc.gov/ncidod/dvrd/gastro.htm>.

Health Answers. <http://www.healthanswers.com>.

Medical College of Wisconsin. <http://healthlink.mcw.edu/article/923884638.html>.

Merck Manual. <http://www.merck.com/pubs/mmanual/section3/chapter23/23a.htm>.

National Digestive Diseases Clearinghouse. <http://www.niddk.nih.gov/health/digest/summary/gastritis/ga... >.

National Library of Medicine. <http://www.nlm.nih.gov/medlineplus/ency/article/000240.htm.,> and <http://www.nlm.nih.gov/medlineplus/ency/article/000232.htm.,> and <http://www.nlm.nih.gov/medlineplus/ency/article/001150.htm>.

Rush University College of Medicine. <http://www.rush.edu/worldbook/articles/007000a/007000014.ht... >.

University of Maryland College of Medicine. <http://umm.drkoop.com/conditions/ency/article/001150.htm>.

L. Fleming Fallon, Jr., M.D., Dr.P.H.