Chronic Gastritis



The term "gastritis" was first used in 1728 by the German Physician, Georg Ernst Stahl to describe the inflammation of the inner lining of the stomach- now known to be secondary to mucosal injury (ie, cell damage and regeneration). In the past, many considered gastritis a useful histological finding, but not a disease. This all changed with the discovery of Helicobacter pylori by Robin Warren and Barry Marshall in 1982 leading to the identification, description and classification of a multitude of different gastritides. This article focuses on the pathophysiology, etiology, epidemiology and prognosis of chronic gastritis.[1, 2]

The chronic gastritides are classified on the basis of their underlying cause (eg, H pylori, bile reflux, nonsteroidal anti-inflammatory drugs [NSAIDs], autoimmunity or allergic response) and the histopathologic pattern, which may suggest the cause and the likely clinical course (eg, H pylori–associated multifocal atrophic gastritis). Other classifications are based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis).

It is important to distinguish between gastritis and gastropathy (in which there is cell damage and regeneration, but minimal inflammation); these entities are discussed in this article because they are frequently included in the differential diagnosis of chronic gastritis.

Chemical or reactive gastritis is caused by injury to the gastric mucosa resulting from reflux of bile and pancreatic secretions into the stomach, but it can also be caused by exogenous substances, including NSAIDs, acetylsalicylic acid, chemotherapeutic agents, and alcohol.[3] These chemicals cause epithelial damage, erosions, and ulcers that are followed by regenerative hyperplasia detectable as foveolar hyperplasia, and damage to capillaries, with mucosal edema, hemorrhage, and increased smooth muscle in the lamina propria with minimal or no inflammation.

Because there is minimal or no inflammation in these chemical-caused lesions, gastropathy or chemical gastropathy is a more appropriate description than chemical or reactive gastritis, as proposed by the updated Sydney classification of gastritis.[4] It is important to keep in mind that mixed forms of gastropathy and other types of gastritis, especially H pylori gastritis, may coexist.

There is no universally accepted classification system (including the Sydney system and Olga staging system) that provides an entirely satisfactory description of all of the gastritides and gastropathies.[5] However, an etiologic classification at least provides a direct target toward which therapy can be directed, and for this reason, such a classification is used in this article. In many instances, chronic gastritis is a relatively minor manifestation of diseases that predominantly manifest in other organs or manifest systemically (eg, gastritis in individuals who are immunosuppressed).

H pylori gastritis is a primary infection of the stomach and is the most frequent cause of chronic gastritis, infecting 50% of the global population.[6, 7, 8] Cases of histologically documented chronic gastritis are diagnosed as chronic gastritis of undetermined etiology or gastritis of undetermined type when none of the findings reflect any of the described patterns of gastritis and a specific cause cannot be identified.

For patient education resources, see the Digestive Disorders Center, as well as Gastritis.


The pathophysiology of chronic gastritis complicating a systemic disease, such as hepatic cirrhosis, uremia, or an infection, is described in the articles specifically dealing with these diseases. The pathogenesis of the most common forms of gastritis is described below.

H pylori–associated chronic gastritis

Helicobacter pylori is the leading cause of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma and primary gastric lymphoma.[7, 8, 9] First described by Marshall and Warren in 1983, H pylori is a spiral gram-negative rod that has the ability to colonize and infect the stomach; the lipopolysaccharides on the outer membrane of H pylori are a major component of its ability for colonization and persistence.[9] The bacteria survive within the mucous layer that covers the gastric surface epithelium and the upper portions of the gastric foveolae. The infection is usually acquired during childhood. Once present in the stomach, the bacteria passes through the mucous layer and becomes established at the luminal surface of the stomach causing an intense inflammatory response in the underlying tissue.[2, 9, 10, 11, 12]

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 its 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.[13, 14]

Interaction of H pylori with the surface mucosa results in the release of interleukin (IL)-8, which leads to the recruitment of PMNs and may begin the entire inflammatory process. Gastric epithelial cells express class II molecules, which may increase the inflammatory response by presenting H pylori antigens, leading to the activation of numerous transcription factors, including NF-kB, AP-1 and CREB-1. This in turn leads to further cytokine release and more inflammation. High levels of cytokines, particularly tumor necrosis factor-α (TNF-α)[15] and multiple interleukins (eg, IL-1β, IL-6, IL-8, IL-10, IL-12, IL-17 and IL-18), are detected in the gastric mucosa of patients with H pylori gastritis.[13, 14] Increased frequencies of IL-17a+ and interferon gamma (IFN-γ) cells have been found in the antrum, particularly in individuals with H pylori-induced gastric ulcers.[16]

Leukotriene levels are also quite elevated, especially the level of leukotriene B4, which is synthesized by the host neutrophils and is cytotoxic to the gastric epithelium.[17] This inflammatory response leads to functional changes in the stomach, depending on the areas of the stomach involved. When the inflammation affects the gastric corpus, parietal cells are inhibited, leading to reduced acid secretion. Continued inflammation results in loss of the parietal cells, and the reduction in acid secretion becomes permanent.

Antral inflammation alters the interplay between gastrin and somatostatin secretion, affecting G cells (gastrin-secreting cells) and D cells (somatostatin-secreting cells), respectively. Specifically, gastrin secretion is abnormal in individuals who are infected with H pylori, with an exaggerated meal-stimulated release of gastrin being the most prominent abnormality.[18]

When the infection is cured, neutrophil infiltration of the tissue quickly resolves, with slower resolution of the chronic inflammatory cells. Paralleling the slow resolution of the monocytic infiltrates, meal-stimulated gastrin secretion returns to normal.[19]

Various strains of H pylori exhibit differences in virulence factors, and these differences influence the clinical outcome of H pylori infection. People infected with H pylori strains that secrete the vacuolating toxin A (vacA) are more likely to develop peptic ulcers than people infected with strains that do not secrete this toxin.[20]

Another set of virulence factors is encoded by the H pylori pathogenicity island (PAI). The PAI contains the sequence for several genes and encodes the CAGA gene. Strains that produce CagA protein (CagA+) are associated with a greater risk of development of gastric carcinoma and peptic ulcers. However, infection with CagA- strains also predisposes the person to these diseases.[21, 22, 23, 24]

H pylori-associated chronic gastritis progresses according to the following two main topographic patterns, which have different clinical consequences:

As previously mentioned, 50% of the world's population is infected with H pylori. The overwhelming majority of those infected do not develop significant clinical complications and remain carriers with asymptomatic chronic gastritis. Some individuals who carry additional risk factors may develop peptic ulcers, gastric mucosa–associated lymphoid tissue (MALT) lymphomas, or gastric adenocarcinomas.

An increased duodenal acid load may precipitate and wash out the bile salts, which normally inhibit the growth of H pylori. Progressive damage to the duodenum promotes gastric foveolar metaplasia, resulting in sites for H pylori growth and more inflammation. This cycle renders the duodenal bulb increasingly unable to neutralize acid entering from the stomach until changes in the bulb structure and function are sufficient for an ulcer to develop. H pylori can survive in areas of gastric metaplasia in the duodenum, contributing to the development of peptic ulcers.[11]

MALT lymphomas may develop in association with chronic gastritis secondary to H pylori infection. The stomach usually lacks organized lymphoid tissue, but after infection with H pylori, lymphoid tissue is universally present. Acquisition of gastric lymphoid tissue is thought to be due to persistent antigen stimulation from byproducts of chronic infection with H pylori.[25]

The continuous presence of H pylori results in the persistence of MALT in the gastric mucosa, which eventually may progress to form low- and high-grade MALT lymphomas. MALT lymphomas are monoclonal proliferations of neoplastic B cells that have the ability to infiltrate gastric glands. Gastric MALT lymphomas typically are low-grade T-cell–dependent B-cell lymphomas, and the antigenic stimulus of gastric MALT lymphomas is thought to be H pylori.

Another complication of H pylori gastritis is the development of gastric carcinomas, especially in individuals who develop extensive atrophy and intestinal metaplasia of the gastric mucosa. It is well accepted that a multistep process initiated by H pylori related chronic inflammation of the gastric mucosa progresses to chronic atrophic gastritis, intestinal metaplasia, dysplasia, and finally leading to the development adenocarcinoma. Although the relationship between H pylori and gastritis is constant, only a small proportion of individuals infected with H pylori develop gastric cancer; the exact mechanism for this relationship with gastric carcinogenesis remains unclear, but host genetic background may play a role.[8] The incidence of gastric cancer usually parallels the incidence of H pylori infection in countries with a high incidence of gastric cancer and is consistent with H pylori being the cause of the precursor lesion, chronic atrophic gastritis.[25, 26]

H pylori-related chronic gastritis may also increase the risk of endothelial dysfunction, and thus vascular disease, due to abnormalities in flow-mediated dilation and carotid intima media thickness, as well as elevated levels of soluble vascular cell adhesion molecule-1 (sVCAM-1) and intercellular adhesion molecule-1 (ICAM-1).[27]

Persistence of the organisms and associated inflammation during long-standing infection is likely to permit the accumulation of mutations in the genome of the gastric epithelial cells, leading to an increased risk of malignant transformation and progression to adenocarcinoma. Studies have provided evidence of the accumulation of the mutations in the gastric epithelium secondary to oxidative DNA damage associated with chronic inflammatory byproducts and secondary to deficiency of DNA repair induced by chronic bacterial infection.

Although the role of H pylori in peptic ulcer disease is well established, the role of the infection in non-ulcer or functional dyspepsia remains highly controversial. A recent meta-analysis demonstrates that H pylori eradication therapy is associated with an improvement of dyspeptic symptoms in patients with functional dyspepsia in Asian, European, and American populations.[28] Although this study illustrates that H pylori eradication may be beneficial for symptom relief in some populations, routine H pylori testing and treatment in nonulcer dyspepsia are not currently widely accepted. Therefore, H pylori eradication strategies in patients with nonulcer dyspepsia must be considered on a patient-by-patient basis.

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.[29]

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Granulomatous chronic gastritis. Noncaseating granulomas in the lamina propria. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburg....

Gastritis in patients who are immunosuppressed

Cytomegalovirus (CMV) infection of the stomach is observed in patients with underlying immunosuppression, but it remains unclear whether CMV gastritis promotes the development of gastric carcinoma.[30] Histologically, a patchy, mild inflammatory infiltrate is observed in the lamina propria. Typical intranuclear eosinophilic inclusions and, occasionally, smaller intracytoplasmic inclusions are present in the gastric epithelial cells and in the endothelial or mesenchymal cells in the lamina propria. Severe necrosis may result in ulceration.

Other infectious causes of chronic gastritis in immunosuppressed patients, include the 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.

Autoimmune atrophic gastritis

Autoimmune atrophic gastritis is 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.[31]

The development of chronic atrophic gastritis (sometimes called type A gastritis) limited to corpus-fundus mucosa and marked diffuse atrophy of parietal and chief cells characterizes autoimmune atrophic gastritis. In addition to hypochlorhydria, autoimmune gastritis is associated with serum anti-parietal and anti-IF antibodies that cause IF deficiency, which, in turn, causes decreased availability of cobalamin, eventually leading to pernicious anemia in some patients. Hypochlorhydria induces G-Cell (Gastrin producing) hyperplasia, leading to hypergastrinemia. Gastrin exerts a trophic effect on enterochromaffin-like (ECL) cells and is hypothesized to be one of the mechanisms leading to the development of gastric carcinoid tumors (ECL tumors).[32, 33]

In autoimmune gastritis, autoantibodies are directed against at least 3 antigens, including IF, cytoplasmic (microsomal-canalicular), and plasma membrane antigens. There are two types of IF antibodies, types I and II. Type 1 antibody prevents the attachment of B12 to IF and Type II antibody prevents attachment of the vitamin B12-intrinsic factor complex to ileal receptors.[34]

Cell-mediated immunity also contributes to the disease. T-cell lymphocytes infiltrate the gastric mucosa and contribute to the epithelial cell destruction and resulting gastric atrophy.

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. Although bile reflux may occur in the intact stomach, most of the features associated with bile reflux are typically found in patients with partial gastrectomy, in whom the lesions develop near the surgical stoma.

The mechanisms through which bile alters the gastric epithelium involve the effects of several bile constituents. Both lysolecithin and bile acids can disrupt the gastric mucous barrier, allowing the back diffusion of positive hydrogen ions and resulting in cellular injury. Pancreatic juice enhances epithelial injury in addition to bile acids. In contrast to other chronic gastropathies, minimal inflammation of the gastric mucosa typically occurs in chemical gastropathy.

Chronic noninfectious granulomatous gastritis

Noninfectious diseases are the usual cause of gastric granulomas; these include Crohn disease, sarcoidosis, and isolated granulomatous gastritis. Crohn disease demonstrates gastric involvement in approximately 33% of the cases. Granulomas have also been described in association with gastric malignancies, including carcinoma and malignant lymphoma. Sarcoidlike granulomas may be observed in people who use cocaine, and foreign material is occasionally observed in the granuloma. An underlying cause of chronic granulomatous gastritis cannot be identified in up to 25% of cases. These patients are considered to have idiopathic granulomatous gastritis (IGG).[35]

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.[36, 37, 38, 39, 40]

High anti–H pylori antibody titers have been found in patients with lymphocytic gastritis, and in limited studies, the inflammation disappeared after H pylori was eradicated.[41] However, many patients with lymphocytic gastritis are serologically negative for H pylori. A number of cases may develop secondary to intolerance to gluten and drugs such as ticlopidine.[38, 42]

Eosinophilic gastritis

Large numbers of eosinophils may be observed with parasitic infections such as those caused by Eustoma rotundatum and Anisakis marina. Eosinophilic gastritis can be part of the spectrum of eosinophilic gastroenteritis. Although the gastric antrum is commonly affected and can cause gastric outlet obstruction, this condition can affect any segment of the GI tract and can be segmental.[43] Patients frequently have peripheral blood eosinophilia.

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 the initial radiotherapy. The dose at which 5% of patients develop complications at 5 years, when the entire stomach is irradiated, is estimated to be 50 Gy. Small doses of radiation (up to 15 Gy) cause reversible mucosal damage, whereas higher doses cause irreversible damage with atrophy and ischemic-related ulceration. 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 the fundic glands, mucosal erosions, and capillary hemorrhage. Associated submucosal endarteritis results in mucosal ischemia and secondary ulcer development.[44, 45]

Ischemic gastritis

Ischemic gastritis is believed to result from atherosclerotic thrombi arising from the celiac and superior mesenteric arteries.[46, 47]


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

Noninfectious forms of gastritis include the following:

Some patients have chronic gastritis of undetermined etiology or gastritis of undetermined type (eg, autistic gastritis[56] ).


United States statistics

H pylori is one of the most prevalent bacterial pathogens 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. H pylori prevalence is higher in Hispanics (52%) and black individuals (54%), in contrast to white persons (21%). Overall, the prevalence of H pylori is higher in developing countries and declining in the United States. The incidence of new infections in developing countries ranges from 3%-10% of the population each year, compared to 0.5% in developed countries. Children aged 2-8 years in developing nations acquire the infection at a rate of about 10% per year, whereas in the United States, children become infected at a rate of less than 1% per year. This major difference in the rate of acquisition in childhood is responsible for the differences in the epidemiology between developed countries and developing countries.[19, 57, 58, 59, 60, 61, 62]

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 the acquisition of the infection is associated with large, crowded households and lower socioeconomic status.[63, 64]

Well-defined preventive measures are not established. However, in the United States and in other countries with modern sanitation and clean water supplies, the rate of acquisition has been decreasing since 1950. In fact, the risk of H pylori infection in immigrants to the United States appears to be decreasing with each successive generation born in the United States. The rate of infection in people with several generations of their families living at a high socioeconomic status is in the range of 10%-15%. This is probably the lowest level to which prevalence can decline spontaneously until eradication or vaccination programs are instituted.[63, 65, 66]

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.[67, 68]

Chronic reactive chemical gastropathy is one of the most common and poorly recognized lesions of the stomach.

International statistics

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.[6, 61, 62, 69]

Autoimmune gastritis is a relatively rare disease, most frequently observed in individuals of northern European descent[3, 70] 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.[71, 72, 73]

Age-related demographics

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.[66, 74, 75]

However, this increase in infection prevalence with age is largely apparent rather than real, reflecting a continuing overall decline in the prevalence of H pylori infection. Because the infection is typically acquired in childhood and is life long, the high proportion of older individuals who are infected is the long-term result of infection that occurred in childhood when standards of living were lower. The prevalence will decrease as people who are currently aged 40 years and have a lower rate of infection grow older (a birth cohort phenomenon).

H pylori gastritis is usually acquired during childhood, and complications typically develop later.[76, 77, 78]

Patients with autoimmune gastritis usually present with pernicious anemia, which is typically diagnosed in individuals aged approximately 60 years. However, pernicious anemia can also be detected in children (juvenile pernicious anemia).[79, 80]

Lymphocytic gastritis can be observed in children but is usually detected in late adulthood. On average, patients are aged 50 years.[75]

Eosinophilic gastroenteritis mostly affects people younger than 50 years.[81]

Sex-related demographics

Chronic H pylori-associated gastritis affects both sexes with approximately the same frequency, though some studies have noted a slight male predominance.[82] The female-to-male ratio for autoimmune gastritis has been reported to be 3:1. Lymphocytic gastritis affects men and women at similar rates.[75]

Race-related demographics

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.[59, 60, 65]

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.[31]


The prognosis of chronic gastritis is strongly related to the underlying cause. Chronic gastritis as a primary disease, such as H 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 H pylori infection, such as peptic ulcer or gastric malignancy.[25]

H 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%.[83]

Eradication of H 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 H pylori have been conflicting. Follow-up for as long as several years after H pylori eradication has not demonstrated regression of gastric atrophy in most studies, whereas others report improvement in the extent of atrophy and intestinal metaplasia.[84, 85]

Another important question is whether H 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 H 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 H pylori eradication. This finding supports an intervention approach with eradication of H pylori if the organisms are detected in patients with atrophic gastritis; the goal is to prevent the development of gastric cancer.[86, 87, 88] However, recent reports have shown that gastric cancers can still arise after adequate H pylori therapy.[89, 90]

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.[91, 92]


H pylori infection

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.

Autoimmune gastritis

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.[93]

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 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.[94]

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.[95]

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.[91, 92]

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 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.

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 GVHD have symptoms of nausea, vomiting, and upper abdominal pain without diarrhea.[96]

Physical Examination

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 H pylori–associated gastritis and autoimmune gastritis.

In uncomplicated H 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.

Approach Considerations

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

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:


Magnifying endoscopy is helpful for analyzing the subepithelial microvascular architecture, as well as the mucosal surface microstructure, without tissue biopsy.[97] Using this technique, investigators from the United Kingdom were able to describe the normal gastric microvasculature pattern and identify characteristic patterns in two cases of autoimmune atrophic gastritis.[98]

Upper gastrointestinal (GI) endoscopy is essential for establishing the diagnosis of gastritis. Although some studies have suggested that H 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 H pylori and macroscopic features remains controversial. The endoscopic findings in chronic H 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.[99]


The standard method of determining whether H 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 H 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 H pylori organisms are markedly decreased because intestinal metaplasia creates an unfavorable environment for H pylori. In these cases, other tests (eg, the urea breath test) and serologic indicators of infection may provide evidence for H pylori infection.

Histologic Findings

H pylori–associated gastritis can display different levels of severity. H pylori organisms are found within the gastric mucous layer and frequently accumulate in groups at the apical side of gastric surface cells, occasionally in the lower portions of the gastric foveolae, and rarely within the deeper areas of the mucosa in association with glandular cells (see the images below).

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Helicobacter pylori–caused chronic active gastritis. Genta stain (×20). Multiple organisms (brown) are visibly adherent to gastric surface epithelial ....

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Chronic gastritis associated with Helicobacter pylori infection. Numerous plasma cells are present in the lamina propria.

Patients with typical infections initially develop chronic active gastritis in which H pylori is observed in both the antrum and the corpus (usually in greater numbers in the antrum). Polymorphonuclear leukocytes (PMNs) infiltrate the lamina propria, glands, surface epithelium, and foveolar epithelium, occasionally spilling into the lumen and forming small microabscesses. Lymphoid aggregates and occasional well-developed lymphoid follicles are observed expanding the lamina propria of the mucosa, and occasional lymphocytes permeate the epithelium.

In a disease of longer duration, significant loss of gastric glands is observed, a condition known as gastric atrophy. Gastric atrophy may result from the loss of gastric epithelial cells that were not replaced by appropriate cell proliferation, or it may result from replacement of the epithelium with intestinal-type epithelium (intestinal metaplasia).

In advanced stages of atrophy associated with chronic H pylori infection, both the corpus and the antrum display an extensive replacement by intestinal metaplasia that is associated with the development of hypochlorhydria. With expansion of intestinal metaplasia, the number of H pylori organisms that are detected in the stomach decreases because H pylori is excluded from areas of metaplastic epithelium.

The histologic changes of autoimmune atrophic gastritis vary in different phases of the disease. During an early phase, multifocal diffuse infiltration of the lamina propria by mononuclear cells and eosinophils and focal T-cell infiltration of oxyntic glands with glandular destruction are seen. Focal mucous neck cell hyperplasia (pseudopyloric metaplasia) and hypertrophic changes of parietal cells are also observed.

During the florid phase of the disease, increased lymphocytic inflammation, oxyntic gland atrophy, and focal intestinal metaplasia occur. The end stage is characterized by diffuse involvement of the gastric corpus and fundus by chronic atrophic gastritis associated with little intestinal metaplasia. The antrum is spared.

Granulomatous gastritis predominantly affects the gastric antrum. In early stages, the only findings may be isolated granulomas in the mucosa and submucosa. In later stages of the disease, inflammation extends to the muscularis propria, and fibrosis may be prominent. Granulomas associated with tuberculosis are typically caseating. Poorly formed granulomas can also be observed in syphilitic involvement of the stomach in the tertiary stage of the disease.

Noninfectious causes of gastric granulomas typically result in noncaseating granulomas; such causes include the following:

Crohn disease affecting the stomach consists of patchy inflammation with pit or gland abscesses. Lymphoid aggregates are common. Severe cases may show fissures, ulcers, transmural inflammation, and serosal and submucosal fibrosis. Noncaseating epithelioid granulomas may be observed. Diffuse inflammatory infiltration in the lamina propria and glandular atrophy occur. Gastric involvement is almost invariably synchronous with Crohn disease in the ileum or colon.

Sarcoidosis and isolated granulomas are characterized by bland granulomas with mild associated inflammation. Although sarcoidosis affecting the stomach typically coexists with sarcoidosis involving other organs, isolated granulomatous gastritis only affects the stomach and is a diagnosis of exclusion.

Cytomegalovirus (CMV) infection of the stomach is observed in patients with underlying immunosuppression. Histologically, typical intranuclear eosinophilic inclusions and, occasionally, smaller intracytoplasmic inclusions are found (see the image below). Patchy, mild, inflammatory infiltrate is observed in the lamina propria. Viral inclusions are present in the gastric epithelial cells and in endothelial or mesenchymal cells in the lamina propria. Severe mucosal necrosis may result in severe ulceration.

View Image

Chronic gastritis. Typical cytomegalovirus inclusions in the lamina propria capillary endothelial cells. Image courtesy of Sydney Finkelstein, MD, PhD....

Herpes simplex causes basophilic intranuclear inclusions in epithelial cells. M avium-intracellulare infections are characterized by diffuse infiltration of the lamina propria by histiocytes, which rarely form granulomas (see the image below).

View Image

Chronic gastritis. Mycobacterium avium-intracellulare in the gastric lamina propria macrophages. Image courtesy of Sydney Finkelstein, MD, PhD, Univer....

In cases of gastritis associated with graft versus host disease (GVHD), the stomach is rarely affected. Typical epithelial cell apoptosis and pit or gland dilatation occur. Pit and gland abscesses and nonspecific inflammation of the lamina propria may be observed. In severe disease, glandular atrophy, focal intestinal metaplasia, and severe mucosal denudation may occur.

In eosinophilic gastritis, the mucosa shows intense patchy infiltration by numerous eosinophils, with occasional pit abscesses. The infiltrate typically contains 10-50 eosinophils per high-power field, as well as plasma cells. Mucosal edema, congestion, and necrosis of the surface epithelium with small erosions may be present. Mucosal infiltration by a bandlike eosinophil infiltrate in the lower portion of the lamina propria above the muscularis mucosa characterizes eosinophilic gastroenteritis associated with connective tissue disorders.

In lymphocytic gastritis, the lamina propria and pit epithelium are infiltrated by large numbers of small mature T lymphocytes. Abundant T lymphocytes typically permeate the surface epithelium. A diagnosis can be rendered when 30 or more lymphocytes are observed per 100 consecutive epithelial cells, and performing the counts in biopsies from the gastric corpus is recommended.

In chemical gastropathy, the changes are more prominent in the prepyloric region but may extend to involve the oxyntic mucosa. Histologic changes associated with chronic bile reflux and long-term nonsteroidal anti-inflammatory drug (NSAID) intake include mucosal edema, congestion, fibromuscular hyperplasia in the lamina propria, and pit or foveolar hyperplasia that may create a corkscrew pattern. Cellular proliferation is associated with reactive nuclear features and epithelial reduction of mucin. Epithelial changes occur with a paucity of inflammatory cells.

In radiation gastritis, radiation causes degenerative changes in the epithelial cells and a nonspecific chronic inflammatory infiltrate in the lamina propria. These changes are reversible in a period of a few months. Higher amounts of radiation cause permanent mucosal damage, with atrophy of the fundic glands, mucosal erosions, and capillary hemorrhage. Associated submucosal endarteritis results in mucosal ischemia and secondary ulcer development.

In ischemic gastritis, chronic ischemia may produce superficial erosions and, rarely, deep ulcers. Inflammatory changes are observed in the context of ulcer repair. Ischemic ulcers are more frequently antral and are often surrounded by multiple erosions.

Idiopathic granulomatous gastritis demonstrates histopathology similar to sarcoid involvement of the stomach. Antral narrowing caused by transmural, noncaseating, granulomatous inflammation occurs. Inflammation and fibrosis are usually limited to the mucosa. Idiopathic granulomatous gastritis may represent isolated or limited forms of gastric sarcoid or Crohn disease.

Approach Considerations

Treatment of chronic gastritis can be aimed at a specific etiologic agent, if such an agent is known. For example, the treatment approach for H pylori infection is described in detail below. (See also American College of Gastroenterology Guideline on the Management of Helicobacter pylori Infection.) 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. However, because the disease has a chronic course, treatment is recommended. Some studies have reported successful treatment of exudative lymphocytic gastritis with omeprazole.

Pharmacotherapy for H pylori

At first, specific recommendations for H pylori eradication were limited to peptic ulcer disease. However, the 1997 Digestive Health Initiative (DHI) International Update Conference on H pylori broadened the recommendations for H pylori testing and treatment. H pylori testing and eradication were also recommended after resection of early gastric cancer and for low-grade mucosa-associated lymphoid tissue (MALT) lymphoma. Furthermore, it is now widely accepted that if H pylori is identified as the underlying cause of gastritis, it should be eradicated.

H pylori infection is not easily cured, and research has shown that multidrug therapy is required. As with any bacterial infection, therapy must include antimicrobial agents to which the bacterium is sensitive. Antibiotics that have proven effective against H pylori include clarithromycin, amoxicillin, metronidazole, tetracycline, and furazolidone. Cure rates with single antibiotics have been poor (0%-35%). Monotherapy is associated with the rapid development of antibiotic resistance, especially to metronidazole and clarithromycin. Probiotic supplementation has shown promising results when included in the treatment regimen.[100, 101]

Five 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 (Prometheus Laboratories, San Diego, CA). 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.

Clinical experience has shown that the most effective of these regimens is BMT triple therapy, followed by ranitidine bismuth citrate plus clarithromycin and then by omeprazole plus clarithromycin.

Because higher success rates can be achieved when a third drug is added to the dual therapies, most authorities now recommend triple-drug combinations. This recommendation was confirmed by the FDA’s approval of a combination regimen comprising the proton pump inhibitor (PPI) lansoprazole, clarithromycin, and amoxicillin. The cure rate with this combination exceeds 85%. A 2-drug regimen consisting of lansoprazole plus amoxicillin was also approved, but it yields tremendously variable results and thus is a very poor choice.

In a clinical trial, Rahmani and colleagues evaluated therapy regimens in 100 patients with chronic gastritis who had been infected by H pylori. They found that the combination of triple therapy with coenzyme Q10 (CoQ10) was effective in ameliorating mucosal inflammation and oxidative stress in patients with chronic gastritis.[102]

The most widely used regimens for eradicating H pylori are triple therapies, which are recommended as first-line treatments; quadruple therapies[103] 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 (with indicated adult dosing)

Twice-daily PPI or ranitidine bismuth citrate triple therapies include the following:

Pack kits containing triple therapies are available as a combination of lansoprazole, amoxicillin, and clarithromycin (PrevPac; Takeda Pharmaceuticals America, Deerfield, IL) or a combination of bismuth subsalicylate, tetracycline, and metronidazole (ie, Helidac).

PrevPac contains drug combinations in the dosage recommended as first-line treatment by the Maastricht 2-2000 Consensus Report in Europe.[104] The components are as follows:

The components of Helidac triple therapy are as follows:

Quadruple therapies (with indicated adult dosing)

Quadruple therapy for H pylori infection typically includes the following:

Treatment of H pylori infection in children

Optimal therapy for H pylori infection in childhood is not well established. Treatment has not been studied extensively, and there is no consensus as to the best regimen. However, the benefits of treating the infection in patients with duodenal ulcer are obvious, whereas the benefits of treating children who are asymptomatic remain controversial. Although the literature is replete with contrary recommendations, many authorities now recommend treating all people, adults and children, in whom H pylori infection is demonstrated.

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.

In a study of triple therapy with lansoprazole 0.75 mg/kg plus amoxicillin 25 mg/kg plus clarithromycin 10 mg/kg given twice daily for 7 days, the eradication rate was 87%. A similar study used the same drugs but different dosages—lansoprazole 0.45 mg/kg/day in 2 doses (maximum dose, 15 mg twice daily), amoxicillin 40 mg/kg/day in 2 doses (maximum dose, 1 g twice daily), and clarithromycin 250 mg (for age < 10 y) or 500 mg (for age >10 y) twice daily for 2 weeks. This protocol eradicated bacteria in only 56% of children.

Eradication rates in children have been reported to be as high as 96% with alternative eradication regimens that include amoxicillin, bismuth, and metronidazole.

The adverse effects of the various regimens are similar in children and adults. Bismuth toxicity is not a concern in children receiving H pylori therapy, but salicylate toxicity 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.

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 the findings during endoscopy. For example, 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.

Medication Summary

The most widely used and most efficient regimens for eradicating Helicobacter pylori are triple therapies (recommended as first-line treatment) and quadruple therapies (recommended as second-line treatment).

Amoxicillin (Moxatag)

Clinical Context:  Amoxicillin is an acid-stable semisynthetic penicillin. Its antimicrobial activity is pH-dependent, with the minimal inhibitory concentration (MIC) decreasing as the pH increases.

Clarithromycin (Biaxin)

Clinical Context:  Clarithromycin is a macrolide that binds to bacterial ribosomes and disrupts protein synthesis, leading to bacterial cell death. It is the most acid-stable of the macrolides and has the lowest MIC. Its major metabolite also is active against H pylori.


Clinical Context:  Tetracycline treats infections with gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. It inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s). Its potency is affected in solutions whose pH is less than 2, and it is rapidly destroyed by alkali hydroxide solutions.

Metronidazole (Flagyl)

Clinical Context:  Metronidazole is an imidazole ring-based antibiotic that is active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents. Because the activity of metronidazole is pH-independent, it is theoretically an ideal drug for the gastric environment.

Class Summary

The antibiotics selected have antimicrobial activity against most H pylori strains. Rare resistant strains have been reported.

Omeprazole (Prilosec)

Clinical Context:  Omeprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-adenosine triphosphate (ATP) pump at the secretory surface of gastric parietal cells.

Lansoprazole (Prevacid)

Clinical Context:  Lansoprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump at the secretory surface of gastric parietal cells.

Rabeprazole (AcipHex)

Clinical Context:  Rabeprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump at the secretory surface of gastric parietal cells.

Pantoprazole (Protonix)

Clinical Context:  Pantoprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump at the secretory surface of gastric parietal cells.

Esomeprazole (Nexium)

Clinical Context:  Esomeprazole inhibits gastric acid secretion by inhibiting the H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells.

Class Summary

A substituted benzimidazole (a compound that inhibits gastric acid secretion) is the active ingredient of proton pump inhibitors (PPIs). PPIs do not exhibit anticholinergic or H2 antagonistic activities but suppress acid secretion by specific inhibition of the H+/K+ –adenosine triphosphatase (ATPase) enzyme system on the secretory surface of parietal cells.

Bismuth subsalicylate (Pepto-Bismol, Bismatrol, Diotame)

Clinical Context:  This agent exerts antisecretory and antimicrobial effects. It may also provide anti-inflammatory action.

Class Summary

The components of bismuth-containing therapies have demonstrated in vitro activity against most susceptible strains of H pylori.

What is chronic gastritis?What is the difference between gastritis and gastropathy?What is the classification system for chronic gastritis?Which primary infection leads to chronic gastritis?What is the pathophysiology of chronic gastritis?What is the role of H pylori in the pathogenesis of chronic gastritis?How does the clinical outcome vary by strain of H pylori infection?What are the topographic patterns of chronic gastritis progression?What are complications of H pylori- associated chronic gastritis?What is the pathophysiology of infectious granulomatous gastritis?What is the pathophysiology of chronic gastritis in patients with underlying immunosuppression?What is the pathophysiology of autoimmune atrophic gastritis?What is the pathophysiology of chronic reactive chemical gastropathy?What is the pathophysiology of chronic noninfectious granulomatous gastritis?What is the pathophysiology of lymphocytic gastritis?What is the pathophysiology of eosinophilic gastritis?What is the pathophysiology of radiation gastritis?What is the pathophysiology of ischemic gastritis?What causes infectious forms of chronic gastritis?What causes noninfectious forms of chronic gastritis?What is the prevalence of chronic gastritis in the US?What are the racial predilections of chronic gastritis?How have H pylori preventive measures affected the incidence of chronic gastritis?What is the global prevalence of chronic gastritis?How does the incidence of chronic gastritis vary by age?How does the incidence of chronic gastritis vary by sex?What is the prognosis of chronic gastritis?How does the eradication of H pylori affect the prognosis of chronic gastritis?What are the signs and symptoms of H pylori chronic gastritis?What are the signs and symptoms of autoimmune gastritis?What are the signs and symptoms of granulomatous gastritis?How is idiopathic isolated granulomatous gastritis diagnosed?Which clinical history findings suggest lymphocytic gastritis?What are the signs and symptoms of eosinophilic gastroenteritis?What are the signs and symptoms of gastritis in graft versus host disease (GVHD)?Which physical findings suggest chronic gastritis?What are the differential diagnoses for Chronic Gastritis?How is chronic gastritis diagnosed?What is the role of lab studies in the diagnosis of chronic gastritis?Which test results suggest the diagnosis of autoimmune gastritis?What is the role of endoscopy in the diagnosis of chronic gastritis?What is the role of biopsy in the diagnosis of chronic gastritis?Which histologic findings indicate an infectious chronic gastritis?What are the histologic findings suggestive of noninfectious causes of chronic gastritis?What are the histologic findings characteristic of chronic gastritis in immunosuppressed patients?What are the histologic findings characteristic of herpes simplex, caused chronic gastritis?What are the histologic findings characteristic of chronic gastritis in graft versus host disease (GVHD)?What are the histologic findings characteristic of eosinophilic gastritis?What are the histologic findings characteristic of lymphocytic gastritis?What are the histologic findings characteristic of chemical gastropathy?What are the histologic findings characteristic of radiation gastritis?What are the histologic findings characteristic of ischemic gastritis?What are the histologic findings characteristic of idiopathic granulomatous gastritis?What is the focus of treatment for chronic gastritis?What are the treatment options for H pylori chronic gastritis?What is the most widely used regimen for eradicating H pylori in patients with chronic gastritis?What are the components of triple therapies for treatment of H pylori chronic gastritis?What are the components of PrevPac for treatment of H pylori chronic gastritis?What are the components of Helidac triple therapy for treatment of H pylori chronic gastritis?What are the components of quadruple therapies for treatment of H pylori chronic gastritis?What are the treatment options for H pylori infection in children with chronic gastritis?What is the efficacy of triple therapies for treatment of H pylori chronic gastritis, and what are adverse effects?What is the included in long-term monitoring for patients with chronic gastritis?What is the most widely used regimens for eradicating H pylori?Which medications in the drug class Gastrointestinal Agents, Other are used in the treatment of Chronic Gastritis?Which medications in the drug class Proton Pump Inhibitors are used in the treatment of Chronic Gastritis?Which medications in the drug class Antibiotics are used in the treatment of Chronic Gastritis?


Akiva J Marcus, MD, PhD, Attending Gastroenterologist, West Palm Hospital

Disclosure: Nothing to disclose.


David Greenwald, MD, Professor of Clinical Medicine, Fellowship Program Director, Department of Medicine, Division of Gastroenterology, Montefiore Medical Center, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

Disclosure: Nothing to disclose.


Simmy Bank, MD Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Franco Bazzoli, MD Professor, Department of Internal Medicine and Gastroenterology, University of Bologna, Italy

Franco Bazzoli, MD is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

Maria P Dore, MD Associate Professor, Department of Medicine, Institute of Internal Medicine, University of Sassari, Italy

Maria P Dore, MD is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Tushar Patel, MB, ChB Professor of Medicine, Ohio State University Medical Center

Tushar Patel, MB, ChB is a member of the following medical societies: American Association for the Study of Liver Diseases and American Gastroenterological Association

Disclosure: Nothing to disclose.

Antonia R Sepulveda, MD, PhD Professor of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine; Director of Surgical Pathology, Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania

Antonia R Sepulveda, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Gastroenterological Association, American Society for Investigative Pathology, College of American Pathologists, and United States and Canadian Academy of Pathology

Disclosure: Genentech Honoraria Consulting; Leica Honoraria Consulting

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment


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Granulomatous chronic gastritis. Noncaseating granulomas in the lamina propria. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.

Helicobacter pylori–caused chronic active gastritis. Genta stain (×20). Multiple organisms (brown) are visibly adherent to gastric surface epithelial cells.

Chronic gastritis associated with Helicobacter pylori infection. Numerous plasma cells are present in the lamina propria.

Chronic gastritis. Typical cytomegalovirus inclusions in the lamina propria capillary endothelial cells. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.

Chronic gastritis. Mycobacterium avium-intracellulare in the gastric lamina propria macrophages. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.

Helicobacter pylori–caused chronic active gastritis. Genta stain (×20). Multiple organisms (brown) are visibly adherent to gastric surface epithelial cells.

Chronic gastritis associated with Helicobacter pylori infection. Numerous plasma cells are present in the lamina propria.

Granulomatous chronic gastritis. Noncaseating granulomas in the lamina propria. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.

Chronic gastritis. Mycobacterium avium-intracellulare in the gastric lamina propria macrophages. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.

Chronic gastritis. Typical cytomegalovirus inclusions in the lamina propria capillary endothelial cells. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.

Chronic gastritis. Chemical gastropathy. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.

Lymphocytic chronic gastritis. Gastric epithelium is studded with numerous lymphocytes (left). Intraepithelial lymphocytes are T-cell lymphocytes shown by immunoreactivity to CD3 (brown stain, right).