Gastritis
EPIDEMIOLOGY
PATHOPHYSIOLOGY
TREATMENT
CLINICAL PRESENTATION
DIAGNOSIS
US STATISTICS
H pylori is one most prevalent bacterial pathogen in humans and in the United States approximately 30-35% of adults are infected, but the prevalence of infection in minority groups and immigrants from developing countries is much higher
SOCIOECONOMIC
Socioeconomic differences are the most important predictor of the prevalence of the infection in any group. Higher standards of living are associated with higher levels of education and better sanitation, thus the prevalence of infection is lower. Epidemiologic studies of H pylori-associated chronic gastritis have shown that acquisition of the infection is associated with large, crowded households and lower socioeconomic status.
INTERNATIONALLY
Lymphocytic gastritis has an incidence of between 0.83% and 2.5% in patients undergoing endoscopy and of 4-5% in those with chronic gastritis. The disease has been reported in various parts of the world but more commonly in Europe, and it appears to be less common in the United States. [59, 60]
Chronic reactive chemical gastropathy is one of the most common and poorly recognized lesions of the stomach
An estimated 50% of the world population is infected with H pylori; consequently, chronic gastritis is extremely frequent. H pylori infection is highly prevalent in Asia and in developing countries, and multifocal atrophic gastritis and gastric adenocarcinomas are more prevalent in these areas.
Autoimmune gastritis is a relatively rare disease, most frequently observed in individuals of northern European descent and black people. The prevalence of pernicious anemia, resulting from autoimmune gastritis, has been estimated at 127 cases per 100,000 population in the United Kingdom, Denmark, and Sweden. The frequency of pernicious anemia is increased in patients with other immunologic diseases, including Graves disease, myxedema, thyroiditis, vitiligo and hypoparathyroidism
Age is the most important variable relating to the prevalence of H pylori infection, with persons born before 1950 having a notably higher rate of infection than those born after 1950. For example, roughly 50% of people older than 60 years are infected, compared with 20% of people younger than 40 years
Race
H pylori -associated chronic gastritis appears to be more common among Asian and Hispanic people than in people of other races. In the United States, H pylori infection is more common among black, Native American, and Hispanic people than among white people, a difference that has been attributed to socioeconomic factors.
Autoimmune gastritis is more frequent in individuals of northern European descent and in black people, and it is less frequent in southern European and Asian people.
SEX: Chronic H pylori- associated gastritis affects both sexes with approximately the same frequency, though some studies have noted a slight male predominance. The female-to-male ratio for autoimmune gastritis has been reported to be 3:1. Lymphocytic gastritis affects men and women at similar rates
Infectious granulomatous gastritis: Granulomatous gastritis (see the image below) is a rare entity. Tuberculosis may affect the stomach and cause caseating granulomas. Fungi, including cryptococcus, can also cause caseating granulomas and necrosis, a finding that is usually observed in patients who are immunosuppressed. Granulomatous gastritis has also been associated with H pylori infection
Immunosuppressed patients: Cytomegalovirus (CMV) infection of the stomach.Herpes simplex virus (HSV), which causes basophilic intranuclear inclusions in epithelial cells. Mycobacterial infections involving Mycobacterium avium-intracellulare are characterized by diffuse infiltration of the lamina propria by histiocytes, which rarely form granulomas.
H pylori–associated chronic gastritis:
Helicobacter pylori is the leading cause of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma and primary gastric lymphoma.
The presence of H pylori is associated with tissue damage and the histologic finding of both an active and a chronic gastritis. The host response to H pylori and bacterial products is composed of T and B lymphocytes, denoting chronic gastritis, followed by infiltration of the lamina propria and gastric epithelium by polymorphonuclear leukocytes (PMNs) that eventually phagocytize the bacteria. The presence of PMNs in the gastric mucosa is diagnostic of active gastritis
Chronic reactive chemical gastropathy:Chronic reactive chemical gastritis is associated with long-term intake of aspirin or NSAIDs. It also develops when bile-containing intestinal contents reflux into the stomach.
Autoimmune atrophic gastritis: associated with serum anti-parietal and anti–intrinsic factor (IF) antibodies. The gastric corpus undergoes progressive atrophy, IF deficiency occurs, and patients may develop pernicious anemia
Lymphocytic gastritis:Lymphocytic gastritis is a type of chronic gastritis characterized by dense infiltration of the surface and foveolar epithelium by T lymphocytes and associated chronic infiltrates in the lamina propria. Because its histopathology is similar to that of celiac disease, lymphocytic gastritis has been proposed to result from intraluminal antigens
Chronic noninfectious granulomatous gastritis:
Noninfectious diseases are the usual cause of gastric granulomas; Crohn disease, sarcoidosis, and isolated granulomatous gastritis.
Eosinophilic gastritis
Large numbers of eosinophils may be observed with parasitic infections such as those caused by Eustoma rotundatum and Anisakis marina.In some cases, especially in children, eosinophilic gastroenteritis can result from food allergy, usually to milk or soy protein. Eosinophilic gastroenteritis can also be found in some patients with connective tissue disorders, including scleroderma, polymyositis, and dermatomyositis
Radiation gastritis:
Radiation gastritis usually occurs 2-9 mo after initial radiotherapy. Reversible changes consist of degenerative changes in the epithelial cells and nonspecific chronic inflammatory infiltrate in the lamina propria. Higher amounts of radiation cause permanent mucosal damage, with atrophy of fundic glands, mucosal erosions, and capillary hemorrhage. Associated submucosal endarteritis results in mucosal ischemia and secondary ulcer development
Ischemic gastritis
believed to result from atherosclerotic thrombi arising from the celiac and superior mesenteric arteries
Acute H pylori infection usually is not detected clinically, but persistence of the organism causes H 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 H pylori gastritis, which include peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma.
The clinical manifestations of autoimmune gastritis are primarily related to the deficiency in 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 deficiency affects the hematologic, gastrointestinal (GI), and neurologic systems.
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.
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.
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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 mostly affects middle-aged or elderly patients. It may be associated with chronic H 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.
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.
Graft versus host disease (GVHD) follows allogeneic bone marrow transplantation or transfusions, especially in patients who are immunocompromised. Patients with isolated gastric GVHD have symptoms of nausea, vomiting, and upper abdominal pain without diarrhea.
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
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 H pylori infection in the presence of peptic ulcers may result in ulcer recurrence and complications
Laboratory Studies: 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.
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.
Upper gastrointestinal (GI) endoscopy is essential for establishing the diagnosis of gastritis w/ w/o biopsy.
Magnifying endoscopy is helpful for analyzing the subepithelial microvascular architecture, as well as the mucosal surface microstructure
Long-Term Monitoring
If a patient was treated for H 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.
Follow-up may be individualized, depending on findings during endoscopy. If dysplasia is found at endoscopy, increased surveillance is necessary. For patients with atrophic gastritis or dysplasia, follow-up endoscopy is recommended after 6 months
Pharmacotherapy for H pylori
Treatment of chronic gastritis can be aimed at a specific etiologic agent, if such an agent is known.When gastritis represents gastric involvement of a systemic disease, treatment is directed toward the primary disease.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.
H pylori infection is not easily cured, and research has shown that multidrug therapy is requiredFive regimens are approved by the US Food and Drug Administration (FDA) for the treatment of H pylori infection..
One is a version of the traditional bismuth-metronidazole-tetracycline (BMT) triple therapy, which is commercially available as Helidac. The antibiotics and bismuth are provided in a convenient dose pack that is thought to enhance compliance.
Three different combinations using clarithromycin have been approved, including 2 dual therapies consisting of 500 mg of clarithromycin 3 times daily plus either omeprazole or ranitidine bismuth citrate. The cure rates reported in the packaging literature suggest that the 3 combinations are similarly effective.
The most widely used regimens for eradicating H pylori are triple therapies, which are recommended as first-line treatments; quadruple therapies are recommended as second-line treatment when triple therapies fail. With either type of regimen, the best results are achieved by administering therapy for 10-14 days, though some studies have limited the duration of treatment to 7 days. The accepted definition of cure is that no evidence of H pylori exists for 4 or more weeks after ending the antimicrobial therapy.
Do not administer antibiotic therapy if the patient does not have a confirmed infection, and be sure to assess the results of the therapy carefully. Manage cases of subsequent H pylori eradication failure on a case-by-case basis, and base antibiotic selection on pretreatment antibiotic sensitivity test results.
Triple therapies ADULT
Twice-daily PPI or ranitidine bismuth citrate triple therapies include the following:
Lansoprazole 30 mg, omeprazole 20 mg, or ranitidine bismuth citrate 400 mg orally twice daily
Clarithromycin 500 mg orally twice daily
Amoxicillin 1000 mg or metronidazole 500 mg orally twice daily
Quadruple therapies ADULT
PPI (lansoprazole 30 mg or omeprazole 20 mg) orally twice daily
Tetracycline HCl 500 mg orally 4 times daily
Bismuth subsalicylate 120 mg orally 4 times daily
Metronidazole 500 mg orally 3 times daily
Treatment of H pylori infection in children
Optimal therapy for H pylori infection in childhood is not well established.Isolated studies have shown eradication efficiencies with triple therapies, ranging from 56-87% of the cases. In children, clarithromycin and metronidazole H pylori resistance is a problem in several countries, resulting in less efficient eradication regimens.
Eradication rates in children have been reported to be as high as 96% with alternative eradication regimens that include amoxicillin, bismuth, and metronidazole
Bismuth toxicity is not a concern in children receiving H pylori therapy, but salicylate ingestion from the use of bismuth subsalicylate is. Inform parents of the presence of subsalicylate. Ideally, children younger than 16 years should not receive salicylate-containing compounds, because of the risk of Reye syndrome
Medications
*The most widely used and most efficient regimens for eradicating Helicobacter pylori are triple therapies and quadruple therapies*
Antibiotics
Proton Pump Inhibitors
Gastrointestinal Agents