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Gastritis

Gastritis

Definition

Gastritis commonly refers to inflammation of the lining of the stomach, but the term is often used to cover a variety of symptoms resulting from this 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 most gastritis is infection by a bacterium called Helicobacter pylori.

Description

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

Nonerosive H. pylori gastritis

Under current theory, the main cause of true gastritis is H. pylori infection, which is found in an average of 90% of patients with chronic gastritis. H. pylori is a bacterium whose outer layer is resistant to the normal effects of stomach acid in breaking down bacteria. The resistance of H. pylori means that the bacterium may remain 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 presence of specific genes or the use of nonsteroidal anti-inflammatory drugs (NSAIDs). Studies of the role of H. pylori in the development of gastritis and peptic ulcers have disproved the former belief that stress leads to most stomach and duodenal ulcers. The newer findings have resulted in improved treatment and reduction of stomach ulcers. H. pylori is most likely transmitted between humans, although the specific routes of transmission are still under study. Studies were also underway to determine the role of H. pylori and resulting chronic gastritis in the development of gastric cancers.

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, can lead to gastritis and peptic ulcers. Other forms of erosive gastritis are caused by alcohol or corrosive agents, or by injuries to the stomach tissues from the 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. It usually occurs in critically ill patients, such as those in intensive care. Stress erosions may develop suddenly as a result of severe trauma or stresses on the stomach lining.
  • Atrophic gastritis. This form of gastritis results from chronic gastritis. It is characterized by atrophy, or 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 term is often used to describe the initial stages of chronic gastritis.
  • Uncommon specific forms of gastritis include granulomatous, eosiniphilic, and lymphocytic gastritis.

Causes & 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. Clinicians think that there may be more than one route for the bacterium. Its prevalence and distribution differs in nations around the world. The presence of H. pylori has been detected in 8699% of patients with chronic superficial gastritis. Physicians are still learning about the link of H. pylori to chronic gastritis and peptic ulcers, since many patients with H. pylori infection do not develop symptoms or peptic ulcers. H. pylori is also seen in 90100% of patients with duodenal ulcers.

The symptoms of H. pylori gastritis include abdominal pain and reduced acid secretion in the stomach. The majority of patients with H. pylori infection, however, suffer no symptoms, even though the infection may lead to ulcers and resulting symptoms. 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 the 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 on the dose level. Although even low doses of aspirin or other nonsteroidal anti-inflammatory drugs may cause some gastric upset, low doses generally will not lead to gastritis. However, as many as 1030% of patients on higher and more frequent doses of NSAIDs, such as those with chronic arthritis, may develop gastric ulcers. Patients with H. pylori already present in the stomach who are treated with NSAIDs are much more susceptible to ulcers and other gastrointestinal effects of these pain killers.

Patients with erosive gastritis may also show 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 and they may differ slightly in their symptoms and clinical signs. However, they all have inflammation of the gastric mucosa in common. Research recently found that severe gastritis may occur rarely as a result of infectious mononucleosis .

Diagnosis

Nonerosive H. pylori gastritis

H. pylori gastritis is easily diagnosed through the use of the urea breath test. This test detects 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. New stool antigen tests were developed and made available in 2002. The choice of test will depend on 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 the diagnosis. A biopsy of the gastric lining also may 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, alcoholism, or abuse of other substances.

Other forms of gastritis

Gastritis that has developed to the stage of duodenal or gastric ulcers usually requires endoscopy for diagnosis. It allows the 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 ulcer 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

Some alternative treatments for gastritis follow mainstream medical practice in distinguishing between gastritis and other digestive disorders; others treat all disorders originating in the stomach in similar fashion.

Dietary supplements

Of all the alternative treatments for gastritis, dietary supplements of various types are the most likely to have been tested in clinical research. Some alternative practitioners have used the following supplements:

  • Capsaicin. Capsaicin is the active ingredient in chili peppers. One study in human subjects indicates that capsaicin offers some protection against gastritis caused by aspirin.
  • Antioxidants. Vitamin C and beta-carotene given in combination appear to be beneficial to most patients with chronic atrophic gastritis.
  • Amino acids. Several studies indicate that cysteine speeds healing in bleeding gastritis related to NSAIDs and in atrophic gastritis. Glutamine appears to protect against the development of stress-related gastritis.
  • Vitamins. Preliminary research suggests that large doses of vitamin A may reduce or eliminate erosive gastritis. Vitamin B12 is helpful for patients with prenicious anemia related to atrophic gastritis.
  • Gamma oryzanol. In one study, 87% of patients with various types of gastritis reported at least some improvement from a daily dose of 300 mg of gamma oryzanol.

Herbal therapy

Herbs that have been recommended for gastritis include:

  • Licorice . Licorice is a traditional remedy for stomach inflammation. It also appears to inhibit the growth of H. pylori. People who gain water weight or develop high blood pressure as side effects of taking licorice can be treated with licorice that has had the glycyrrhizin removed.
  • Goldenseal. This herb contains berberine, a compound with antibiotic properties. There is some evidence that berberine is active against H. pylori.
  • Chamomile . Chamomile contains apigenin, a bioflavonoid that inhibits H. pylori, and chamazulene, a compound that counteracts free radicals.
  • Marsh mallow and slippery elm . These herbs have demulcent properties, which means that they soothe irritated mucous membranes.
  • Echinacea and geranium. These herbs are recommended by some practitioners for their antiseptic and analgesic (pain-relieving) properties.

Naturopathic practitioners also advise patients with gastritis to eat certain categories of food separately. Patients are advised to eat protein foods by themselves or with green leafy vegetables; to eat fruits alone; and to avoid combining proteins and starches.

Acupuncture/acupressure

One source recommends applying gentle pressure to a point on the abdomen known as CV (conception vessel) 12, midway between the navel and the breastbone. Pressure should be applied when the stomach is empty. Trained acupuncturists treat stomach problems by releasing energy from the spleen and from other energy points associated with digestion.

Yoga

The Bow Pose is recommended by some teachers of yoga for stomach disorders because it puts pressure on a number of acupoints on the abdomen associated with the digestive process and with the stomach meridian.

Chinese herbal medicine

The Chinese traditionally use a tea made from ginger (Zingiber officinale ) as a stomachic, to improve digestive functions.

Reflexology

A trained reflexologist will gently massage the stomach reflexes located on the hands and feet. On the hands, the stomach reflexes are on the palms, below the pads of the middle and index fingers. On the feet, the stomach reflexes are located on the sole just below the pad of the big toe.

Allopathic treatment

H. pylori gastritis

The discovery of H. pylori's role in the development of gastritis and ulcers has led to improved treatment of chronic gastritis. Since the infection can be treated with antibiotics, the bacterium can be completely eliminated up to 90% of the time. The treatment, however, may be uncomfortable for patients and relies heavily on patient compliance. No single antibiotic has been found that would eliminate H. pylori on its own, so various combinations of antibiotics have been prescribed to treat the infection.

TRIPLE THERAPY. As of early 1998, triple therapy was the preferred treatment for patients with H. pylori gastritis. This treatment regimen usually involves a two-week course of three drugs. An antibiotic such as amoxicillin or tetracycline, and another antibiotic such as clarithromycin or metronidazole are used in combination with bismuth subsalicylate, a substance that helps protect the lining of the stomach from acid. However, this treatment often fails due to poor patient compliance and quadruple therapy is required.

DUAL THERAPY. Dual therapy involves the use of an antibiotic and a proton pump inhibitor. Proton pump inhibitors help reduce stomach acid by halting the mechanism that pumps acid into the stomach. Dual therapy has not been proven to be as effective as triple therapy, but may be ordered for some patients who can more comfortably handle the use of fewer drugs.

OTHER TREATMENTS. Scientists have experimented with quadruple therapy, which adds an antisecretory drug, or one that suppresses gastric secretion, to the standard triple therapy. One study showed this therapy to be effective with only a week's course of treatment in more than 90% of patients. The goal is to develop the most effective therapy combination that can work in one week of treatment or less.

Treatment of erosive gastritis

Patients with erosive gastritis may be given treatments similar to those for H. pylori, especially since some studies have demonstrated a link between H. pylori and NSAIDs in causing ulcers. The patient will most likely be advised to avoid NSAIDs.

Other forms of gastritis

Specific treatment will depend on the cause and type of gastritis. These may include prednisone or antibiotics. Critically ill patients at high risk for bleeding may be treated with preventive drugs to reduce the risk of acute stress gastritis. Sometimes surgery is recommended, but is weighed against the possibility of surgical complications or death. Once heavy bleeding occurs in acute stress gastritis, mortality is as high as 60%.

Expected results

The results expected from alternative treatments for gastritis include accelerated healing from some of the dietary therapies, and some symptomatic relief from acupressure , yoga, and reflexology .

The discovery of H. pylori has improved the prognosis for patients with gastritis and ulcers. Since treatment exists to eradicate the infection, recurrence is much less common. The prognosis for patients with acute stress gastritis is much poorer, with a 60% or higher mortality rate among those bleeding heavily. Recent studies have shown that infection with H. pylori and resulting gastritis may lead to such complications as chronic gastritis or as serious as gastric adenoma, a form of stomach cancer.

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 through which H.pylori is spread, specific prevention recommendations are not available. It was estimated in late 2002 that the organism was present in 80% of middle-aged adults in developing countries and about 20% of those in industrialized countries. Erosive gastritis from NSAIDs can be prevented with cessation of use of these drugs. An education campaign was launched in 1998 to educate patients, particularly an aging population of arthritis sufferers, about the risk of developing ulcers from NSAIDs and alternative drugs.

Resources

BOOK

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

Gach, Michael Reed and Carolyn Marco. Acu-Yoga: Self Help Techniques to Relieve Tension. Tokyo and New York: Japan Publications, Inc., 1998.

LaMont, J. Thomas. Gastrointestinal Infections, Diagnosis and Management. New York: Marcel Dekker, Inc. 1997.

Murray, Michael, N.D., and Joseph Pizzorno, N.D. Encyclopedia of Natural Medicine. Rocklin, CA: Prima Publishing, 1991.

PERIODICALS

Graham, David Y. "NSAIDs, Helicobacter Pylori, and Pandora's Box." The New England Journal of Medicine (December 26, 2002):2162.

"Helicobacter Pylori Infection." Internal Medicine Alert (December 15, 2002):179182.

"Severe Gastritis May Occasionally Result from Infectious Mononucleosis." Gastroenterology Week (June 23, 2003):20.

ORGANIZATION

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

OTHER

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

Rebecca J. Frey, PhD

Teresa G. Odle

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Gastritis

Gastritis

Definition

Gastritis commonly refers to inflammation of the lining of the stomach, but the term is often used to cover a variety of symptoms resulting from stomach lining inflammation and 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. It has been associated with resulting ulcers, particularly peptic ulcers. And in some cases, chronic gastritis can lead to more serious complications.

Nonerosive H. pylori gastritis

The main cause of true gastritis is H. pylori infection. H. pylori is indicated in an average of 90% of patients with chronic gastritis. This form of nonerosive gastritis is the result of infection with Helicobacter pylori bacterium, a microorganism whose outer layer is resistant to the normal effects of stomach acid in breaking down bacteria.

The resistance of H. pylori 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 presence of specific genes or ingestion of nonsteroidal anti-inflammatory drugs (NSAIDS). Study of the role of H. pylori in development of gastritis and peptic ulcers has disproved the former belief that stress lead to most stomach and duodenal ulcers and 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 early 1998. Studies were also underway to determine the role of H. pylori and resulting chronic gastritis in development of gastric cancer.

Erosive and hemorrhagic gastritis

After H. pylori, the second most common cause of chronic gastritis is use of nonsteroidal anti-inflammatory drugs. 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 alcohol and corrosive agents or due to trauma such 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-the most serious form of gastritis which usually occurs in critically ill patients, 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 is the result of chronic gastritis which is leading to atrophy, or decrease in size and wasting away, of the gastric lining. Gastric atrophy is the final stage of chronic gastritis and may be a precursor to gastric cancer.
  • Superficial gastritis is a term often used to describe the initial stages of chronic gastritis.
  • Uncommon specific forms of gastritis include granulomatous, eosiniphilic 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 1998 and clinicians guessed that there may be more than one route for the bacterium. Its prevalence and distribution differs in nations around the world. The presence of H. pylori has been detected in 86-99% of patients with chronic superficial gastritis. However, physicians are still learning about the link of H. pylori to chronic gastritis and peptic ulcers, since many patients with H. pylori infection do not develop symptoms or peptic ulcers. H. pylori is also seen in 90-100% of patients with duodenal ulcers.

Symptoms of H. pylori gastritis include abdominal pain and reduced acid secretion in the stomach. However, the majority of patients with H. pylori infection suffer no symptoms, even though the infection may lead to ulcers and resulting symptoms. 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 on the dose level. Although even low doses of aspirin or other nonsteroidal anti-inflammatory drugs may cause some gastric upset, low doses generally will not lead to gastritis. However, as many as 10-30% of patients on higher and more frequent doses of NSAIDS, such as those with chronic arthritis, may develop gastric ulcers. In 1998, studies were underway to understand the role of H. pylori in gastritis and ulcers among patients using NSAIDS.

Patients with erosive gastritis may also show 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 and they may differ slightly in their symptoms and clinical signs. However, they all have in common inflammation of the gastric mucosa.

Diagnosis

Nonerosive H. pylori gastritis

H. pylori gastritis is easily diagnosed through the use of the urea breath test. This test detects 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 on 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

Clinical history of the patient 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, alcoholism, or other substances.

Other forms of gastritis

Gastritis that has developed to the stage of duodenal or gastric ulcers usually requires endoscopy for diagnosis. It allows the 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 ulcer 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 has been reduced with successful treatment of H. pylori infection. 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 may be uncomfortable for patients and relies heavily on patient compliance. In 1998, studies were underway to identify the best treatment method based on simplicity, patient cooperation and results. No single antibiotic had been found which would eliminate H. pylori on its own, so a combination of antibiotics has been prescribed to treat the infection.

DUAL THERAPY. Dual therapy involves the use of an antibiotic and a proton pump inhibitor. Proton pump inhibitors help reduce stomach acid by halting the mechanism that pumps acid into the stomach. This 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 patients who can more comfortably handle the use of less drugs and will therefore more likely follow the two-week course of therapy.

TRIPLE THERAPY. As of early 1998, triple therapy was the preferred treatment for patients with H. pylori gastritis. It is estimated that triple therapy successfully eliminates 80-95% of H. pylori cases. This treatment regimen usually involves a two-week course of three drugs. An antibiotic such as amoxicillin or tetracycline, and another antibiotic such as clarithomycin or metronidazole are used in combination with bismuth subsalicylate, a substance found in the over-the-counter medication, Pepto-Bismol, which helps protect the lining of the stomach from acid. Physicians were experimenting with various combinations of drugs and time of treatment to balance side effects with effectiveness. Side effects of triple therapy are not serious, but may cause enough discomfort that patients are not inclined to follow the treatment.

OTHER TREATMENT THERAPIES. Scientists have experimented with quadruple therapy, which adds an antisecretory drug, or one which suppresses gastric secretion, to the standard triple therapy. One study showed this therapy to be effective with only a week's 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 one week of treatment or less.

MEASURING H. PYLORI TREATMENT EFFECTIVENESS. In order to ensure that H. pylori has been eradicated, physicians will test patients following treatment. The breath test is the preferred method to check for remaining signs of H. pylori.

Treatment of erosive gastritis

Since few patients with this form of gastritis show symptoms, treatment may depend on 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 ulcers. Avoidance of NSAIDS will most likely be prescribed.

Other forms of gastritis

Specific treatment will depend on the cause and type of gastritis. These may include prednisone or antibiotics. Critically ill patients 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 constant infusion of a drug to stop bleeding. Sometimes surgery is recommended, but is weighed with the possibility of surgical complications or death. Once torrential bleeding occurs in acute stress gastritis, mortality is as high as greater than 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. Alternative treatments can help address gastritis symptoms with diet and nutritional supplements, herbal medicine and ayurvedic medicine. 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 patients with gastritis and ulcers. Since treatment exists to eradicate the infection, recurrence is much less common. As of 1998, the only patients requiring treatment for H. pylori were those at high risk because of factors such as NSAIDS use or for 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 patients 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 patients with acute stress gastritis is much poorer, with a 60 percent or higher mortality rate among those bleeding heavily.

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 through which H. pylori is spread, specific prevention recommendations are not available. Erosive gastritis from NSAIDS can be prevented with cessation of use of these drugs. An education campaign was launched in 1998 to educate patients, particularly an aging population of arthritis sufferers, about risk for ulcers from NSAIDS and alternative drugs.

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 which lines body cavities and passages.

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

Resources

PERIODICALS

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

ORGANIZATIONS

National Digestive Diseases Information Clearinghouse. 2 Information Way, Bethesda, MD 20892-3570. (800) 891-5389. http://www.niddk.nih.gov/health/digest/nddic.htm.

OTHER

American College of Gastroenterology Page. http://www.acg.org.

HealthAnswers.com. http://www.healthanswers.com.

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gastritis

gastritis (gas-try-tis) n. inflammation of the lining (mucosa) of the stomach. acute g. gastritis in which vomiting occurs, caused by ingesting excess alcohol or other irritating or corrosive substances. atrophic g. gastritis in which the stomach lining is atrophied. chronic g. gastritis that is usually caused by the bacterium Helicobacter pylori but may be associated with smoking and chronic alcoholism or be caused by bile entering the stomach from the duodenum. It has no definite symptoms, but the patient is liable to develop gastric ulcers or stomach cancer.

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gastritis

gastritis Inflammation of the mucosal lining of the stomach; may result from infection or excessive alcohol consumption. Atrophic gastritis is the progressive loss of gastric secretion with increasing age.

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gastritis

gas·tri·tis / gaˈstrītis/ • n. Med. inflammation of the lining of the stomach.

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Gastritis

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 anti-inflammatory 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 trauma such 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. The role of H. pylori in gastritis and ulcers among persons using NSAIDs is being studied.

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. pylori gastritis

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. 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. Triple therapy is 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 subsalicylate, 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. 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. Alternative treatments such as diet, nutritional supplements, herbal medicine, and Ayurvedic medicine can help address gastritis symptoms. It is believed that zinc, vitamin A, and betacarotene 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.

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.

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. People requiring treatment for H. pylori were those at high risk because of factors such 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.

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: 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, p. 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: 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, p. 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.

LaMont, J. Thomas. Gastrointestinal Infections, Diagnosis and Management. Marcel Dekker, Inc., 1997.

Mobley, Harry L.T., George L. Mendz, and Stuart L. Hazell. Helicobacter Pylori: Physiology and Genetics. Washington: 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., 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.

Choe Y.H., T.S. Hwang, H.J. Kim, S.H. Shin, S.U. Song, and M.S. Choi. "A Possible Relation of the Helicobacter Pylori pfr Gene to Iron Deficiency Anemia? Helicobacter 6, no. 1 (2001): 55-59.

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.

Schowengerdt C.G. "Standard Acid Reflux Testing Revisited." Digestive Disease Science 46, no. 3 (2001): 603-605.

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. "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/gastritis.htm〉.

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

Rush University College of Medicine. 〈http://www.rush.edu/worldbook/articles/007000a/007000014.html〉.

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

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Gastritis

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.

LaMont, J. Thomas. Gastrointestinal Infections, Diagnosis and Management. Marcel Dekker, Inc., 1997.

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.

Choe Y.H., T.S. Hwang, H.J. Kim, S.H. Shin, S.U. Song, and M.S. Choi. "A Possible Relation of the Helicobacter Pylori pfr Gene to Iron Deficiency Anemia." Helicobacter 6, no. 1 (2001): 55-59.

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.

Schowengerdt C.G. "Standard Acid Reflux Testing Revisited." Digestive Disease Science 46, no. 3 (2001): 603-605.

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/gastritis.htm>.

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.html>.

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

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

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