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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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 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.

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.

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.

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.

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.

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 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.

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.

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.