- Author: Akiva J Marcus, MD, PhD; Chief Editor: BS Anand, MD more...
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 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. 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. 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. 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. 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.
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. 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 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, 7, 8, 9]
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.[10, 11]
Interaction of H pylori with the surface mucosa results in the release of interleukin (IL)-8, which leads to 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) 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.[10, 11]
Leukotriene levels are also quite elevated, especially the level of leukotriene B4, which is synthesized by host neutrophils and is cytotoxic to gastric epithelium. This inflammatory response leads to functional changes in the stomach, depending on the areas of the stomach involved. When inflammation affects the gastric corpus, parietal cells are inhibited, leading to reduced acid secretion. Continued inflammation results in loss of 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.
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.
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.
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.[17, 18, 19, 20]
H pylori- associated chronic gastritis progresses according to the following 2 main topographic patterns, which have different clinical consequences:
Antral predominant gastritis – This is characterized by inflammation and is mostly limited to the antrum; individuals with peptic ulcers usually demonstrate this pattern
Multifocal atrophic gastritis – This is characterized by the involvement of the corpus and gastric antrum with progressive development of gastric atrophy (loss of the gastric glands) and partial replacement of gastric glands by an intestinal-type epithelium (intestinal metaplasia); individuals who develop gastric carcinoma and gastric ulcers usually demonstrate this pattern.
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 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.
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.
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 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.[21, 22]
Persistence of the organisms and associated inflammation during long-standing infection is likely to permit the accumulation of mutations in the gastric epithelial cells’ genome, leading to an increased risk of malignant transformation and progression to adenocarcinoma. Studies have provided evidence of the accumulation of 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 improvement of dyspeptic symptoms in patients with functional dyspepsia in Asian, European, and American populations. 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.
Gastritis in patients who are immunosuppressed
Cytomegalovirus (CMV) infection of the stomach is observed in patients with underlying immunosuppression. 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.
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).[26, 27]
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.
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).
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.[30, 31, 32, 33, 34]
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. 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.[32, 36]
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. 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 usually occurs 2-9 mo after initial radiotherapy. The dose at which 5 percent of patients develop complications at five 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 fundic glands, mucosal erosions, and capillary hemorrhage. Associated submucosal endarteritis results in mucosal ischemia and secondary ulcer development.[38, 39]
Ischemic gastritis is believed to result from atherosclerotic thrombi arising from the celiac and superior mesenteric arteries.[40, 41]
Chronic gastritis may be caused by either infectious or noninfectious conditions. Infectious forms of gastritis include the following:
Chronic gastritis caused by H pylori infection – This is the most common cause of chronic gastritis.
Gastritis caused by Helicobacter heilmannii infection 
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 
Noninfectious forms of gastritis include the following:
Chemical gastropathy- usually related to chronic bile reflux, NSAID and aspirin intake 
Chronic noninfectious granulomatous gastritis [29, 45, 46] – This may be associated with Crohn disease, sarcoidosis, 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) [30, 31, 32, 33, 47]
Radiation injury to the stomach
Graft-versus-host disease (GVHD)
Ischemic gastritis 
Gastritis secondary to drug therapy (NSAIDs and aspirin)
Some patients have chronic gastritis of undetermined etiology or gastritis of undetermined type (eg, autistic gastritis ).
United States 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. H pylori prevalence is higher in Hispanics (52%), 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 percent 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.[15, 49, 50, 51, 52, 53, 54]
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.[55, 56]
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 decrease 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.[57, 55, 58]
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.[6, 53, 54, 61]
Autoimmune gastritis is a relatively rare disease, most frequently observed in individuals of northern European descent[3, 62] 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.[63, 64, 65]
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.[58, 66, 67]
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.[68, 69, 70]
Patients with autoimmune gastritis usually present with pernicious anemia, which is typically diagnosed in individuals aged approximately 60 years. However, pernicious anemia can be detected in children (juvenile pernicious anemia).[71, 72]
Lymphocytic gastritis can be observed in children but is usually detected in late adulthood. On average, patients are aged 50 years.
Eosinophilic gastroenteritis mostly affects people younger than 50 years.
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.
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.[51, 52, 57]
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.
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.
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%.
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.[76, 77]
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.[78, 79, 80] However, recent reports have shown that gastric cancers can still arise after adequate H pylori therapy.[81, 82]
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.[83, 84]
Szabo IL, Cseko K, Czimmer J, Mozsik G. Diagnosis of gastritis – Review from early pathological evaluation to present day management. Mozsik G, ed. Current Topics in Gastritis - 2012. Rijeka, Croatia: In Tech; 2012. Chap 1. [Full Text].
Warren JR, Marshall B. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet. 1983 Jun 4. 1(8336):1273-5. [Medline].
Gao L, Weck MN, Stegmaier C, Rothenbacher D, Brenner H. Alcohol consumption and chronic atrophic gastritis: population-based study among 9,444 older adults from Germany. Int J Cancer. 2009 Dec 15. 125(12):2918-22. [Medline].
Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol. 1996 Oct. 20(10):1161-81. [Medline].
Sepulveda AR, Patil M. Practical approach to the pathologic diagnosis of gastritis. Arch Pathol Lab Med. 2008 Oct. 132(10):1586-93. [Medline].
Pounder RE, Ng D. The prevalence of Helicobacter pylori infection in different countries. Aliment Pharmacol Ther. 1995. 9 Suppl 2:33-9. [Medline].
McColl KE. Clinical practice. Helicobacter pylori infection. N Engl J Med. 2010 Apr 29. 362(17):1597-604. [Medline].
NIH Consensus Conference. Helicobacter pylori in peptic ulcer disease. NIH Consensus Development Panel on Helicobacter pylori in Peptic Ulcer Disease. JAMA. 1994 Jul 6. 272(1):65-9. [Medline].
Shiotani A, Nurgalieva ZZ, Yamaoka Y, Graham DY. Helicobacter pylori. Med Clin North Am. 2000 Sep. 84(5):1125-36, viii. [Medline].
Wilson KT, Crabtree JE. Immunology of Helicobacter pylori: insights into the failure of the immune response and perspectives on vaccine studies. Gastroenterology. 2007 Jul. 133(1):288-308. [Medline].
Zalewska-Ziob M, Adamek B, Strzelczyk JK, et al. TNF-alpha expression in gastric mucosa of individuals infected with different virulent Helicobacter pylori strains. Med Sci Monit. 2009 Jun. 15(6):BR166-71. [Medline].
Wallace JL. Gastric ulceration: critical events at the neutrophil--endothelium interface. Can J Physiol Pharmacol. 1993 Jan. 71(1):98-102. [Medline].
Graham DY, Opekun A, Lew GM, Evans DJ Jr, Klein PD, Evans DG. Ablation of exaggerated meal-stimulated gastrin release in duodenal ulcer patients after clearance of Helicobacter (Campylobacter) pylori infection. Am J Gastroenterol. 1990 Apr. 85(4):394-8. [Medline].
Graham DY, Go MF, Lew GM, Genta RM, Rehfeld JF. Helicobacter pylori infection and exaggerated gastrin release. Effects of inflammation and progastrin processing. Scand J Gastroenterol. 1993 Aug. 28(8):690-4. [Medline].
Gao L, Weck MN, Nieters A, Brenner H. Inverse association between a pro-inflammatory genetic profile and Helicobacter pylori seropositivity among patients with chronic atrophic gastritis: enhanced elimination of the infection during disease progression?. Eur J Cancer. 2009 Nov. 45(16):2860-6. [Medline].
Wang SY, Shen XY, Wu CY, et al. Analysis of whole genomic expression profiles of Helicobacter pylori related chronic atrophic gastritis with IL-1B-31CC/-511TT genotypes. J Dig Dis. 2009 May. 10(2):99-106. [Medline].
Paniagua GL, Monroy E, Rodriguez R, et al. Frequency of vacA, cagA and babA2 virulence markers in Helicobacter pylori strains isolated from Mexican patients with chronic gastritis. Ann Clin Microbiol Antimicrob. 2009 Apr 30. 8:14. [Medline]. [Full Text].
Antonio-Rincon F, Lopez-Vidal Y, Castillo-Rojas G, et al. Pathogenicity island cag, vacA and IS605 genotypes in Mexican strains of Helicobacter pylori associated with peptic ulcers. Ann Clin Microbiol Antimicrob. 2011 May 13. 10:18. [Medline]. [Full Text].
Conteduca V, Sansonno D, Lauletta G, Russi S, Ingravallo G, Dammacco F. H pylori infection and gastric cancer: state of the art (review). Int J Oncol. 2013 Jan. 42(1):5-18. [Medline].
Uemura N, Okamoto S, Yamamoto S, et al. Helicobacter pylori infection and the development of gastric cancer. N Engl J Med. 2001 Sep 13. 345(11):784-9. [Medline].
Zhao B, Zhao J, Cheng WF, et al. Efficacy of Helicobacter pylori eradication therapy on functional dyspepsia: a meta-analysis of randomized controlled studies with 12-month follow-up. J Clin Gastroenterol. 2014 Mar. 48(3):241-7. [Medline].
Delgado JS, Landa E, Ben-Dor D. Granulomatous gastritis and Helicobacter pylori infection. Isr Med Assoc J. 2013 Jun. 15(6):317-8. [Medline].
Neumann WL, Coss E, Rugge M, Genta RM. Autoimmune atrophic gastritis--pathogenesis, pathology and management. Nat Rev Gastroenterol Hepatol. 2013 Sep. 10(9):529-41. [Medline].
Hung OY, Maithel SK, Willingham FF, Farris AB 3rd, Kauh JS. Hypergastrinemia, type 1 gastric carcinoid tumors: diagnosis and management. J Clin Oncol. 2011 Sep 1. 29(25):e713-5. [Medline].
Gilligan CJ, Lawton GP, Tang LH, West AB, Modlin IM. Gastric carcinoid tumors: the biology and therapy of an enigmatic and controversial lesion. Am J Gastroenterol. 1995 Mar. 90(3):338-52. [Medline].
Conn DA. Detection of type I and type II antibodies to intrinsic factor. Med Lab Sci. 1986 Apr. 43(2):148-51. [Medline].
Ectors NL, Dixon MF, Geboes KJ, Rutgeerts PJ, Desmet VJ, Vantrappen GR. Granulomatous gastritis: a morphological and diagnostic approach. Histopathology. 1993 Jul. 23(1):55-61. [Medline].
Wu TT, Hamilton SR. Lymphocytic gastritis: association with etiology and topology. Am J Surg Pathol. 1999 Feb. 23(2):153-8. [Medline].
Wolber R, Owen D, DelBuono L, Appelman H, Freeman H. Lymphocytic gastritis in patients with celiac sprue or spruelike intestinal disease. Gastroenterology. 1990 Feb. 98(2):310-5. [Medline].
Lambert R, Andre C, Moulinier B, Bugnon B. Diffuse varioliform gastritis. Digestion. 1978. 17(2):159-67. [Medline].
Makinen JM, Niemela S, Kerola T, Lehtola J, Karttunen TJ. Epithelial cell proliferation and glandular atrophy in lymphocytic gastritis: effect of H pylori treatment. World J Gastroenterol. 2003 Dec. 9(12):2706-10. [Medline].
Ruget O, Burtin P, Cerez H, Cales P, Boyer J. Chronic diarrhea associated with villous atrophy and lymphocytic gastritis, caused by ticlopidine. Gastroenterol Clin Biol. 1992. 16(3):290. [Medline].
Sheikh RA, Prindiville TP, Pecha RE, Ruebner BH. Unusual presentations of eosinophilic gastroenteritis: case series and review of literature. World J Gastroenterol. 2009 May 7. 15(17):2156-61. [Medline]. [Full Text].
Sell A, Jensen TS. Acute gastric ulcers induced by radiation. Acta Radiol Ther Phys Biol. 1966 Aug. 4(4):289-97. [Medline].
Flobert C, Cellier C, Landi B, et al. [Severe hemorrhagic gastritis of radiation origin]. Gastroenterol Clin Biol. 1998 Feb. 22(2):232-4. [Medline].
Quentin V, Dib N, Thouveny F, L'Hoste P, Croue A, Boyer J. Chronic ischemic gastritis: case report of a difficult diagnosis and review of the literature. Endoscopy. 2006 May. 38(5):529-32. [Medline].
Chambon JP, Bianchini A, Massouille D, Perot C, Lancelevee J, Zerbib P. Ischemic gastritis: a rare but lethal consequence of celiac territory ischemic syndrome. Minerva Chir. 2012 Oct. 67(5):421-8. [Medline].
Singhal AV, Sepulveda AR. Helicobacter heilmannii gastritis: a case study with review of literature. Am J Surg Pathol. 2005 Nov. 29(11):1537-9. [Medline].
Hasegawa Y, Goto A, Nishimura S, Sukawa Y, Fujii K, Suzuki K. Cytomegalovirus gastritis after treatment with rituximab. Endoscopy. 2009 Jul. 41(S 02):E199. [Medline].
Genta RM. Differential diagnosis of reactive gastropathy. Semin Diagn Pathol. 2005 Nov. 22(4):273-83. [Medline].
Shapiro JL, Goldblum JR, Petras RE. A clinicopathologic study of 42 patients with granulomatous gastritis. Is there really an "idiopathic" granulomatous gastritis?. Am J Surg Pathol. 1996 Apr. 20(4):462-70. [Medline].
Maeng L, Lee A, Choi K, Kang CS, Kim KM. Granulomatous gastritis: a clinicopathologic analysis of 18 biopsy cases. Am J Surg Pathol. 2004 Jul. 28(7):941-5. [Medline].
Leung ST, Chandan VS, Murray JA, Wu TT. Collagenous gastritis: histopathologic features and association with other gastrointestinal diseases. Am J Surg Pathol. 2009 May. 33(5):788-98. [Medline].
Rosenberg JJ. Helicobacter pylori. Pediatr Rev. 2010 Feb. 31(2):85-6; discussion 86. [Medline].
Everhart JE, Kruszon-Moran D, Perez-Perez GI, Tralka TS, McQuillan G. Seroprevalence and ethnic differences in Helicobacter pylori infection among adults in the United States. J Infect Dis. 2000 Apr. 181(4):1359-63. [Medline].
Everhart JE. Recent developments in the epidemiology of Helicobacter pylori. Gastroenterol Clin North Am. 2000 Sep. 29(3):559-78. [Medline].
Nabwera HM, Nguyen-Van-Tam JS, Logan RF, Logan RP. Prevalence of Helicobacter pylori infection in Kenyan schoolchildren aged 3-15 years and risk factors for infection. Eur J Gastroenterol Hepatol. 2000 May. 12(5):483-7. [Medline].
Sathar MA, Gouws E, Simjee AE, Mayat AM. Seroepidemiological study of Helicobacter pylori infection in South African children. Trans R Soc Trop Med Hyg. 1997 Jul-Aug. 91(4):393-5. [Medline].
Dattoli VC, Veiga RV, da Cunha SS, Pontes-de-Carvalho LC, Barreto ML, Alcantara-Neves NM. Seroprevalence and potential risk factors for Helicobacter pylori infection in Brazilian children. Helicobacter. 2010 Aug. 15(4):273-8. [Medline]. [Full Text].
Tsai CJ, Perry S, Sanchez L, Parsonnet J. Helicobacter pylori infection in different generations of Hispanics in the San Francisco Bay Area. Am J Epidemiol. 2005 Aug 15. 162(4):351-7. [Medline].
Lin DB, Lin JB, Chen CY, Chen SC, Chen WK. Seroprevalence of Helicobacter pylori infection among schoolchildren and teachers in Taiwan. Helicobacter. 2007 Jun. 12(3):258-64. [Medline].
Rubio CA, Befritz R, Eriksson B, Christensson B, Duvander A, Larsson B. The topographic distribution of lymphocytic gastritis in gastrectomy specimens. APMIS. 1991 Sep. 99(9):815-9. [Medline].
Jaskiewicz K, Price SK, Zak J, Louwrens HD. Lymphocytic gastritis in nonulcer dyspepsia. Dig Dis Sci. 1991 Aug. 36(8):1079-83. [Medline].
Tanih NF, Dube C, Green E, et al. An African perspective on Helicobacter pylori: prevalence of human infection, drug resistance, and alternative approaches to treatment. Ann Trop Med Parasitol. 2009 Apr. 103(3):189-204. [Medline].
Gao L, Weck MN, Raum E, Stegmaier C, Rothenbacher D, Brenner H. Sibship size, Helicobacter pylori infection and chronic atrophic gastritis: a population-based study among 9444 older adults from Germany. Int J Epidemiol. 2010 Feb. 39(1):129-34. [Medline].
Boelaert K, Newby PR, Simmonds MJ, et al. Prevalence and relative risk of other autoimmune diseases in subjects with autoimmune thyroid disease. Am J Med. 2010 Feb. 123(2):183.e1-9. [Medline].
Laberge G, Mailloux CM, Gowan K, et al. Early disease onset and increased risk of other autoimmune diseases in familial generalized vitiligo. Pigment Cell Res. 2005 Aug. 18(4):300-5. [Medline].
de Vega Santos T, Zamarron Moreno A, Pascual de Pablo E, Lopez Lopez C. [Pernicious anemia and primary hyperparathyroidism]. Rev Clin Esp. 1995 Mar. 195(3):200-1. [Medline].
Asaka M, Kimura T, Kudo M, et al. Relationship of Helicobacter pylori to serum pepsinogens in an asymptomatic Japanese population. Gastroenterology. 1992 Mar. 102(3):760-6. [Medline].
Sugiyama T, Nishikawa K, Komatsu Y, et al. Attributable risk of H pylori in peptic ulcer disease: does declining prevalence of infection in general population explain increasing frequency of non-H pylori ulcers?. Dig Dis Sci. 2001 Feb. 46(2):307-10. [Medline].
O'Donohoe JM, Sullivan PB, Scott R, Rogers T, Brueton MJ, Barltrop D. Recurrent abdominal pain and Helicobacter pylori in a community-based sample of London children. Acta Paediatr. 1996 Aug. 85(8):961-4. [Medline].
Lindkvist P, Asrat D, Nilsson I, et al. Age at acquisition of Helicobacter pylori infection: comparison of a high and a low prevalence country. Scand J Infect Dis. 1996. 28(2):181-4. [Medline].
Gold BD, Colletti RB, Abbott M, et al. Helicobacter pylori infection in children: recommendations for diagnosis and treatment. J Pediatr Gastroenterol Nutr. 2000 Nov. 31(5):490-7. [Medline].
Hall CA, Beebe RT. Early onset of pernicious anaemia in two siblings: genetic and autoimmune aspects. Br J Haematol. 1973 Dec. 25(6):751-6. [Medline].
Annibale B, Lahner E, Fave GD. Diagnosis and management of pernicious anemia. Curr Gastroenterol Rep. 2011 Dec. 13(6):518-24. [Medline].
Min KU, Metcalfe DD. Eosinophilic gastroenteritis. Immunol Allergy Clin North Am. 1991. 11:799-813.
Ndip RN, Malange AE, Akoachere JF, MacKay WG, Titanji VP, Weaver LT. Helicobacter pylori antigens in the faeces of asymptomatic children in the Buea and Limbe health districts of Cameroon: a pilot study. Trop Med Int Health. 2004 Sep. 9(9):1036-40. [Medline].
Wang F, Meng W, Wang B, Qiao L. Helicobacter pylori-induced gastric inflammation and gastric cancer. Cancer Lett. 2014 Apr 10. 345(2):196-202. [Medline].
Iacopini F, Consolazio A, Bosco D, et al. Oxidative damage of the gastric mucosa in Helicobacter pylori positive chronic atrophic and nonatrophic gastritis, before and after eradication. Helicobacter. 2003. 8(5):503-12. [Medline].
Warren JR. Gastric pathology associated with Helicobacter pylori. Gastroenterol Clin North Am. 2000 Sep. 29(3):705-51. [Medline].
Macintyre G, Kooi C, Wong F, Anderson R. On the membrane cytopathology of mouse hepatitis virus infection as probed by a semi-permeable translation-inhibiting drug. Adv Exp Med Biol. 1990. 276:67-72. [Medline].
Ito M, Takata S, Tatsugami M, et al. Clinical prevention of gastric cancer by Helicobacter pylori eradication therapy: a systematic review. J Gastroenterol. 2009. 44(5):365-71. [Medline].
Fukase K, Kato M, Kikuchi S, et al. Effect of eradication of Helicobacter pylori on incidence of metachronous gastric carcinoma after endoscopic resection of early gastric cancer: an open-label, randomised controlled trial. Lancet. 2008 Aug 2. 372(9636):392-7. [Medline].
Kamada T, Hata J, Sugiu K, et al. Clinical features of gastric cancer discovered after successful eradication of Helicobacter pylori: results from a 9-year prospective follow-up study in Japan. Aliment Pharmacol Ther. 2005 May 1. 21(9):1121-6. [Medline].
Yamamoto K, Kato M, Takahashi M, et al. Clinicopathological analysis of early-stage gastric cancers detected after successful eradication of Helicobacter pylori. Helicobacter. 2011 Jun. 16(3):210-6. [Medline].
Toh BH, van Driel IR, Gleeson PA. Pernicious anemia. N Engl J Med. 1997 Nov 13. 337(20):1441-8. [Medline].
Stabler SP. Clinical practice. Vitamin B12 deficiency. N Engl J Med. 2013 Jan 10. 368(2):149-60. [Medline].
Arvanitakis C. Functional and morphological abnormalities of the small intestinal mucosa in pernicious anemia--a prospective study. Acta Hepatogastroenterol (Stuttg). 1978 Aug. 25(4):313-8. [Medline].
Kumar N. Neurologic aspects of cobalamin (B12) deficiency. Handb Clin Neurol. 2014. 120:915-26. [Medline].
Ross WA, Ghosh S, Dekovich AA, Liu S, Ayers GD, Cleary KR. Endoscopic biopsy diagnosis of acute gastrointestinal graft-versus-host disease: rectosigmoid biopsies are more sensitive than upper gastrointestinal biopsies. Am J Gastroenterol. 2008 Apr. 103(4):982-9. [Medline].
Tahara T, Shibata T, Nakamura M, et al. Gastric mucosal pattern by using magnifying narrow-band imaging endoscopy clearly distinguishes histological and serological severity of chronic gastritis. Gastrointest Endosc. 2009 Aug. 70(2):246-53. [Medline].
Anagnostopoulos GK, Ragunath K, Shonde A, Hawkey CJ, Yao K. Diagnosis of autoimmune gastritis by high resolution magnification endoscopy. World J Gastroenterol. 2006 Jul 28. 12(28):4586-7. [Medline].
Ford AC, Marwaha A, Lim A, Moayyedi P. What is the prevalence of clinically significant endoscopic findings in subjects with dyspepsia? Systematic review and meta-analysis. Clin Gastroenterol Hepatol. 2010 Oct. 8(10):830-7, 837.e1-2. [Medline].
Graham DY, Belson G, Abudayyeh S, Osato MS, Dore MP, El-Zimaity HM. Twice daily (mid-day and evening) quadruple therapy for H pylori infection in the United States. Dig Liver Dis. 2004 Jun. 36(6):384-7. [Medline].
Malfertheiner P, Megraud F, O'Morain C, et al for the European Helicobacter Pylori Study Group (EHPSG). Current concepts in the management of Helicobacter pylori infection--the Maastricht 2-2000 Consensus Report. Aliment Pharmacol Ther. 2002 Feb. 16(2):167-80. [Medline].
Oberhuber G, Hirsch M, Stolte M. High incidence of upper gastrointestinal tract involvement in Crohn's disease. Virchows Arch. 1998 Jan. 432(1):49-52. [Medline].
Shkolnik LE, Shin RD, Brabeck DM, Rothman RD. Symptomatic gastric sarcoidosis in a patient with pulmonary sarcoidosis in remission. BMJ Case Rep. 2012 Jul 13. 2012:[Medline].
Weck MN, Gao L, Brenner H. Helicobacter pylori infection and chronic atrophic gastritis: associations according to severity of disease. Epidemiology. 2009 Jul. 20(4):569-74. [Medline].