Chronic gastritis

Chronic gastritis is a long lasting condition in which the stomach lining known as the mucosa is inflamed, or swollen. If chronic gastritis is not treated, it may last for years or even a lifetime. The stomach lining contains glands that produce stomach acid and an enzyme called pepsin. The stomach acid breaks down food and pepsin digests protein. A thick layer of mucus coats the stomach lining and helps prevent the acidic digestive juice from dissolving the stomach tissue. When the stomach lining is inflamed, it produces less acid and fewer enzymes. However, the stomach lining also produces less mucus and other substances that normally protect the stomach lining from acidic digestive juice.

Chronic gastritis can be erosive or nonerosive:

• Erosive gastritis can cause the stomach lining to wear away, causing erosions—shallow breaks in the stomach lining—or ulcers—deep sores in the stomach lining.
• Nonerosive gastritis causes inflammation in the stomach lining; however, erosions or ulcers do not accompany nonerosive gastritis.

Causes of chronic gastritis

Chronic gastritis may be caused by either infectious or noninfectious conditions. Infectious forms of gastritis include the following:

• Chronic gastritis caused by Helicobacter pylori infection – This is the most common cause of chronic gastritis ¹
• Gastritis caused by Helicobacter heilmannii infection ²
• Granulomatous gastritis associated with gastric infections in mycobacteriosis, syphilis, histoplasmosis, mucormycosis, South American blastomycosis, anisakiasis, or anisakidosis
• Chronic gastritis associated with parasitic infections -Strongyloides species, schistosomiasis, or Diphyllobothrium latum
• Gastritis caused by viral (eg, CMV or herpesvirus) infection ³

Helicobacter pylori infection

Helicobacter pylori is a type of bacteria—organisms that may cause an infection. Helicobacter pylori infection:

• causes most cases of gastritis
• typically causes nonerosive gastritis
• may cause acute or chronic gastritis

Helicobacter pylori infection is common, particularly in developing countries, and the infection often begins in childhood. Many people who are infected with Helicobacter pylori never have any symptoms. Adults are more likely to show symptoms when symptoms do occur.

Researchers are not sure how the Helicobacter pylori infection spreads, although they think contaminated food, water, or eating utensils may transmit the bacteria. Some infected people have Helicobacter pylori in their saliva, which suggests that infection can spread through direct contact with saliva or other body fluids.

Noninfectious forms of chronic gastritis include the following:

• Autoimmune gastritis: This is a chronic inflammatory disease characterized by chronic atrophic gastritis and associated with raised serum anti-parietal and anti-intrinsic factor antibodies. The loss of parietal cells results in a reduction of gastric acid secretion, which is necessary for the absorption of inorganic iron. Therefore, iron deficiency is commonly a finding in patients with autoimmune gastritis. Iron deficiency in these patients usually precedes vitamin B12 deficiency. The disease is common in young women.
• Chemical gastropathy- usually related to chronic bile reflux, nonsteroidal anti-inflammatory drug (NSAID) and aspirin intake ⁴
• Uremic gastropathy
• Chronic noninfectious granulomatous gastritis ⁵ – This may be associated with Crohn disease, sarcoidosis, granulomatosis with polyangiitis (Wegener granulomatosis), foreign bodies, cocaine use, isolated granulomatous gastritis, chronic granulomatous disease of childhood, eosinophilic granuloma, allergic granulomatosis and vasculitis, plasma cell granulomas, rheumatoid nodules, tumoral amyloidosis and granulomas associated with gastric carcinoma, gastric lymphoma, or Langerhans cell histiocytosis
• Lymphocytic gastritis, including gastritis associated with celiac disease (also called collagenous gastritis) ⁶. About 16% of patients with celiac disease have lymphocytic gastritis, which improves after a gluten-free diet, but there does not appear to be an association between lymphocytic gastritis and Helicobacter pylori ⁶. Chronic gastritis, whether active or inactive, does not appear to be affected by a gluten-free diet ⁶
• Eosinophilic gastritis: This is another rare cause of gastritis. The disease could be part of the eosinophilic gastrointestinal disorders which is characterized by the absence of known causes of eosinophilia (not secondary to an infection, systematic inflammatory disease, or any other causes to explain the eosinophilia).
• Radiation injury to the stomach
• Graft-versus-host disease (GVHD)
• Ischemic gastritis:  This is rare and associated with high mortality ⁷
• Gastritis secondary to drug therapy (NSAIDs and aspirin)
• Ménétrier disease: This disease is characterized by- (1) Presence of large gastric mucosal folds in the body and fundus of the stomach, (2) Massive foveolar hyperplasia of surface and glandular mucous cells, (3) Protein-losing gastropathy, hypoalbuminemia, and edema in 20 to 100% of patients, and (4) reduced gastric acid secretion because of loss of parietal cells ⁸.

Some patients have chronic gastritis of undetermined cause or gastritis of undetermined type (eg, autistic gastritis) ⁹.

Chronic gastritis prevention

People may be able to reduce their chances of getting gastritis by preventing Helicobacter pylori infection. No one knows for sure how Helicobacter pylori infection spreads, so prevention is difficult. To help prevent infection, health care providers advise people to:

• wash their hands with soap and water after using the bathroom and before eating
• eat food that has been washed well and cooked properly
• drink water from a clean, safe source

Chronic gastritis symptoms

Some people who have gastritis have pain or discomfort in the upper part of the abdomen—the area between the chest and hips. However, many people with gastritis do not have any signs and symptoms. The relationship between gastritis and a person’s symptoms is not clear. The term “gastritis” is sometimes mistakenly used to describe any symptoms of pain or discomfort in the upper abdomen.

When symptoms are present, they may include

• upper abdominal discomfort or pain
• nausea
• vomiting

Helicobacter pylori infection

Acute Helicobacter pylori infection usually is not detected clinically, but persistence of the organism causes Helicobacter pylori chronic gastritis, which is usually asymptomatic but may manifest as epigastric pain, nausea, vomiting, anorexia, early satiety or weight loss. Symptoms may occur with the development of complications of chronic Helicobacter pylori gastritis, which include peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma.

Autoimmune gastritis

The clinical manifestations of autoimmune gastritis are primarily related to the deficiency in vitamin B12 or cobalamin, which is not adequately absorbed because of intrinsic factor (IF) deficiency resulting from severe gastric parietal cell atrophy. The disease has an insidious onset and progresses slowly. Cobalamin (vitamin B12) deficiency affects the hematologic, gastrointestinal (GI), and neurologic systems ¹⁰.

The most significant hematologic manifestation is megaloblastic anemia, but on rare occasions, purpura due to thrombocytopenia may develop. Symptoms of anemia include weakness, light-headedness, vertigo, tinnitus, palpitations, angina and symptoms of congestive heart failure.

There are many gastrointestinal manifestations of cobalamin (vitamin B12) deficiency. Patients sometimes report having soreness of the tongue- called glossitis. Anorexia with moderate weight loss that is occasionally associated with diarrhea may result from malabsorption associated with megaloblastic changes of the small intestinal epithelial cells ¹¹.

Neurologic manifestations result from demyelination, followed by axonal degeneration and neuronal death. Affected sites include the peripheral nerves, posterior and lateral columns of the spinal cord, and cerebrum. Signs and symptoms include numbness and paresthesias in the extremities, weakness, and ataxia. Sphincter disturbances may occur. Mental function disturbances range from mild irritability to severe dementia or psychosis. Neurologic disease may occur in a patient with hematocrit and red cell parameters within the reference range ¹².

As previously mentioned, patients with pernicious anemia have an increased frequency of gastric polyps and gastric carcinoid, in addition to an increase in the frequency of gastric adenocarcinoma ¹³.

Granulomatous gastritis

In multisystemic diseases, specific symptoms related to gastric involvement may be minor. Caseating granulomas secondary to tuberculosis may be found in the absence of lung disease in patients who are malnourished, immunosuppressed, or alcoholic.

Patients with Crohn disease and gastric involvement may report abdominal pain, nausea, and vomiting. Gastric involvement in Crohn disease is almost invariably associated with intestinal disease, and intestinal manifestations predominate.

Sarcoidosis of the stomach is usually associated with granulomatous inflammation in other locations, especially the lungs, hilar nodes, or salivary glands. About 10% of patients with sarcoid involvement of the stomach are asymptomatic. Patients who are symptomatic present with gastric ulcers, hemorrhage, pyloric stricture, and gastric outlet obstruction.

Idiopathic isolated granulomatous gastritis

The diagnosis of idiopathic isolated granulomatous gastritis is established only when known entities associated with granulomas are excluded. Patients who are symptomatic usually are older than 40 years at presentation and have epigastric pain, weight loss, and vomiting secondary to pyloric obstruction.

Lymphocytic gastritis

Lymphocytic gastritis mostly affects middle-aged or elderly patients. It may be associated with chronic Helicobacter pylori infection, gluten-sensitive enteropathy, and Menetrier disease. It may represent a hypersensitivity reaction involving the gastric body. Lymphocytic gastritis has been described as complicating MALT lymphoma and gastric carcinoma.

Eosinophilic gastroenteritis

Some patients with eosinophilic gastroenteritis have underlying connective tissue disorders. Those with predominant mucosal involvement may report nausea, vomiting, and abdominal pain related to the ingestion of specific foods. Those with involvement of the muscularis propria and resulting thickening and rigidity may present with outlet obstruction symptoms. Many patients have a history of allergy, peripheral eosinophilia, asthma, eczema, or food sensitivity. Some respond to removal of these items from the diet, and steroid treatment is often helpful.

Gastritis in graft versus host disease

Graft versus host disease (GVHD) follows allogeneic bone marrow transplantation or transfusions, especially in patients who are immunocompromised. Patients with isolated gastric graft versus host disease have symptoms of nausea, vomiting, and upper abdominal pain without diarrhea ¹⁴.

Chronic gastritis complications

The complications of chronic gastritis may include:

• Peptic ulcers. Peptic ulcers are sores involving the lining of the stomach or duodenum, the first part of the small intestine. NSAID use and H. pylori gastritis increase the chance of developing peptic ulcers.
• Atrophic gastritis. Atrophic gastritis happens when chronic inflammation of the stomach lining causes the loss of the stomach lining and glands. Chronic gastritis can progress to atrophic gastritis.
• Anemia. Erosive gastritis can cause chronic bleeding in the stomach, and the blood loss can lead to anemia. Anemia is a condition in which red blood cells are fewer or smaller than normal, which prevents the body’s cells from getting enough oxygen. Red blood cells contain hemoglobin, an iron-rich protein that gives blood its red color and enables the red blood cells to transport oxygen from the lungs to the tissues of the body. Research suggests that H. pylori gastritis and autoimmune atrophic gastritis can interfere with the body’s ability to absorb iron from food, which may also cause anemia.
• Vitamin B12 deficiency and pernicious anemia. People with autoimmune atrophic gastritis do not produce enough intrinsic factor. Intrinsic factor is a protein made in the stomach and helps the intestines absorb vitamin B12. The body needs vitamin B12 to make red blood cells and nerve cells. Poor absorption of vitamin B12 may lead to a type of anemia called pernicious anemia.
• Growths in the stomach lining. Chronic gastritis increases the chance of developing benign, or noncancerous, and malignant, or cancerous, growths in the stomach lining. Chronic H. pylori gastritis increases the chance of developing a type of cancer called gastric mucosa-associated lymphoid tissue (MALT) lymphoma.

Chronic gastritis diagnosis

The diagnosis of chronic gastritis can only be established on histologic grounds. Therefore, histologic assessment of endoscopic biopsies is essential. Identification of the underlying cause of chronic gastritis and assessment of specific complications can require several laboratory tests.

Failure to diagnose the underlying cause of chronic gastritis correctly may result in unnecessary morbidity. Failure to identify and treat Helicobacter pylori infection in the presence of peptic ulcers may result in ulcer recurrence and complications.

A health care provider diagnoses chronic gastritis based on the following:

• medical history
• physical exam
• upper GI endoscopy
• other tests

Medical history

Taking a medical history may help the health care provider diagnose chronic gastritis. He or she will ask the patient to provide a medical history. The history may include questions about chronic symptoms and travel to developing countries.

Physical exam

The physical examination contributes relatively little to the assessment and management of chronic gastritis. However, some findings are specifically associated with the particular complications of Helicobacter pylori–associated gastritis and autoimmune gastritis.

In uncomplicated Helicobacter pylori–associated atrophic gastritis, clinical findings are few and nonspecific. Epigastric tenderness may exist. If gastric ulcers coexist, guaiac-positive stool may result from occult blood loss. Bad breath (ie, halitosis) and abdominal pain or discomfort may occur, with bloating associated with bacterial overgrowth syndrome.

Physical findings may result from the development of pernicious anemia and neurologic complications in patients with autoimmune atrophic gastritis. With severe cobalamin deficiency, the patient is pale and has slightly icteric skin and eyes. The pulse is rapid, and the heart may be enlarged. Auscultation usually reveals a systolic flow murmur.

Laboratory studies

Atrophic gastritis may be assessed by measuring the ratio of pepsinogen I (PGI, PGA) to pepsinogen II (PGII, PGC) in the serum. PGI and PGII are synthesized and secreted by gastric chief cells. After being secreted into the gastric lumen, they are converted into proteolytic active pepsins. The level of PGI in the serum decreases as gastric chief cells are lost during gastric atrophy, resulting in a decreased PGI/PGII ratio. Gastric carcinoma occurs, especially the intestinal type, usually in association with severe atrophic gastritis.

Measuring the levels of PGI and PGII and the PGI/PGII ratio in the serum is useful in screening for atrophic gastritis and gastric cancer in regions with a high incidence of these diseases. Pepsinogen determination is especially useful in epidemiologic studies; however, the reported sensitivity and specificity of the assay are relatively low (84.6% and 73.5%, respectively).

A rapid urease test should be done on gastric biopsy tissue. Bacterial culture of gastric biopsy tissue is usually performed in the research setting or to assess antibiotic susceptibility in patients in whom first-line eradication therapy fails.

The following test results suggest the diagnosis of autoimmune gastritis:

• Antiparietal and anti–intrinsic factor (IF) antibodies in the serum
• Achlorhydria, both basal and stimulated, and hypergastrinemia
• Low serum cobalamin (vitamin B-12) levels (< 100 pg/mL)
• Possible abnormal result on Schilling test (this can be corrected by intrinsic factor)

Upper Gastrointestinal Endoscopy

Upper gastrointestinal (GI) endoscopy is essential for establishing the diagnosis of gastritis. Although some studies have suggested that Helicobacter pylori infection can be determined on the basis of unique endoscopic features, particularly the presence of antral nodularity, whether there is a specific relation between Helicobacter pylori and macroscopic features remains controversial. The endoscopic findings in chronic Helicobacter pylori infection may include areas of intestinal metaplasia.

Multiple biopsy specimens should be obtained. Tissue sampling from the gastric antrum, incisura, and corpus is essential to establish the topography of gastritis and to identify atrophy and intestinal metaplasia, which usually is patchy. It is recommended that biopsy samples of the gastric body and those from the antrum and incisura be submitted in separate containers for pathologic evaluation.

Endoscopic findings in granulomatous gastritis include mucosal nodularity with cobblestoning, multiple aphthous ulcers, linear or serpiginous ulcerations, thickened antral folds, antral narrowing, hypoperistalsis, and duodenal strictures. Extensive gastric involvement may resemble linitis plastica.

Endoscopic findings in lymphocytic gastritis include enlarged folds and aphthoid erosions, with the appearance of small, heaped-up, volcanolike mounds pocked with a central crater. This endoscopic pattern has also been described as varioliform gastritis.

The endoscopic findings of reflux and chemical gastropathy are those of a gastric mucosa that is red or has red streaks with areas of apparent hemorrhage.

A meta-analysis has shown that for individuals who undergo endoscopy for dyspepsia, the most common finding is erosive esophagitis (though the prevalence was lower when the Rome criteria were used to define dyspepsia), followed by peptic ulcers ¹⁵.

Biopsy

The standard method of determining whether Helicobacter pylori is the underlying cause of gastritis is histologic identification of the organism. Histologic examination is also used to evaluate the degree and distribution of gastritis. Obtain at least 2 biopsies from the gastric antrum, 2 from the corpus, and 1 from the incisura.

Special stains to identify Helicobacter pylori (eg, Warthin-Starry, Giemsa, or Genta) or immunohistochemistry may be necessary when the organisms are not observed and chronic gastritis is obvious.

At late stages of infection with extensive atrophic gastritis, the numbers of Helicobacter pylori organisms are markedly decreased because intestinal metaplasia creates an unfavorable environment for Helicobacter pylori. In these cases, other tests (eg, the urea breath test) and serologic indicators of infection may provide evidence for Helicobacter pylori infection.

Blood tests

A health care provider may use blood tests to check for anemia or H. pylori. A health care provider draws a blood sample during an office visit or at a commercial facility and sends the sample to a lab for analysis.

Stool test

A health care provider may use a stool test to check for blood in the stool, another sign of bleeding in the stomach, and for H. pylori infection. A stool test is an analysis of a sample of stool. The health care provider will give the patient a container for catching and storing the stool. The patient returns the sample to the health care provider or a commercial facility that will send the sample to a lab for analysis.

Urea breath test

A health care provider may use a urea breath test to check for H. pylori infection. The patient swallows a capsule, liquid, or pudding that contains urea—a waste product the body produces as it breaks down protein. The urea is “labeled” with a special carbon atom. If Helicobacter pylori are present, the bacteria will convert the urea into carbon dioxide. After a few minutes, the patient breathes into a container, exhaling carbon dioxide. A nurse or technician will perform this test at a health care provider’s office or a commercial facility and send the samples to a lab. If the test detects the labeled carbon atoms in the exhaled breath, the health care provider will confirm an Helicobacter pylori infection in the gastrointestinal tract.

Chronic gastritis treatment

Treatment of chronic gastritis can be aimed at treating the underlying cause. When chronic gastritis represents gastric involvement of a systemic disease, treatment is directed toward the primary disease.

Depending on the cause of chronic gastritis, a health care provider may recommend additional treatments.

• Treating Helicobacter pylori infection with antibiotics is important, even if a person does not have symptoms from the infection. Curing the infection often cures the gastritis and decreases the chance of developing complications, such as peptic ulcer disease, MALT lymphoma, and gastric cancer. A triple-therapy of clarithromycin/proton-pump inhibitor/amoxicillin for 14 to 21 days is considered the first line of treatment. Clarithromycin is preferred over metronidazole because the recurrence rates with clarithromycin are far less compared to a triple-therapy using metronidazole ¹⁶. However, in areas where clarithromycin resistance is known, metronidazole is the option of choice. Quadruple bismuth containing therapy would be of benefit, particularly if using metronidazole ¹⁷. If a patient was treated for Helicobacter pylori infection, confirm that the organism has been eradicated. Evaluate eradication at least 4 weeks after the beginning of treatment. Eradication may be assessed by means of noninvasive methods such as the urea breath test or the stool antigen test.
• Avoiding the cause of reactive gastritis can provide some people with a cure. For example, if prolonged NSAID use is the cause of the gastritis, a health care provider may advise the patient to stop taking the NSAIDs, reduce the dose, or change pain medications.
• Health care providers may prescribe medications to prevent or treat stress gastritis in a patient who is critically ill or injured. Medications to protect the stomach lining include sucralfate (Carafate), H2 blockers, and proton pump inhibitors (PPIs). Treating the underlying illness or injury most often cures stress gastritis.
• Health care providers may treat people with pernicious anemia due to autoimmune atrophic gastritis with vitamin B12 injections

Some entities manifested by chronic gastritis do not have well-established treatment protocols. For example, in lymphocytic gastritis, some cases of spontaneous healing have been reported. However, because the disease has a chronic course, treatment is recommended. Some studies have reported successful treatment of exudative lymphocytic gastritis with omeprazole.

Chronic gastritis prognosis

The prognosis of chronic gastritis is strongly related to the underlying cause. Chronic gastritis as a primary disease, such as Helicobacter pylori-associated chronic gastritis, may progress as an asymptomatic disease in some patients, whereas other patients may report dyspeptic symptoms. The clinical course may be worsened when patients develop any of the possible complications of Helicobacter pylori infection, such as peptic ulcer or gastric malignancy ¹⁸.

Helicobacter pylori gastritis is the most frequent cause of MALT lymphoma- occurring in 0.1% of those infected. Patients with chronic atrophic gastritis may have a 12- to 16-fold increased risk of developing gastric carcinoma, compared with the general population. Approximately 10% of infected persons develop peptic ulcer and the lifetime risk of gastric cancer is in the range of 1%-3% ¹⁹.

Eradication of Helicobacter pylori results in rapid cure of the infection with disappearance of the neutrophilic infiltration of the gastric mucosa. Disappearance of the lymphoid component of gastritis might take several months after treatment. Data on the evolution of atrophic gastritis after eradication of Helicobacter pylori have been conflicting. Follow-up for as long as several years after Helicobacter pylori eradication has not demonstrated regression of gastric atrophy in most studies, whereas others report improvement in the extent of atrophy and intestinal metaplasia ²⁰.

Another important question is whether Helicobacter pylori eradication in a patient with atrophic gastritis reduces the risk of gastric cancer development. Unfortunately, the data up to now has been mixed. A prospective study in a Japanese population reported that Helicobacter pylori eradication in patients with endoscopically resected early gastric cancer resulted in the decreased appearance of new early cancers, whereas intestinal-type gastric cancers developed in the control group without Helicobacter pylori eradication. This finding supports an intervention approach with eradication of Helicobacter pylori if the organisms are detected in patients with atrophic gastritis; the goal is to prevent the development of gastric cancer ²¹. However, recent reports have shown that gastric cancers can still arise after adequate Helicobacter pylori therapy ²².

In patients with autoimmune gastritis, the major effects are consequent to the loss of parietal and chief cells and include achlorhydria, hypergastrinemia, loss of pepsin and pepsinogen, anemia, and an increased risk of gastric neoplasms. The prevalence of gastric neoplasia in patients with pernicious anemia, is reported to be about 1%-3% for adenocarcinoma and 1%-7% for gastric carcinoid ¹³.

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