Acute and Chronic Gastritis Due to Helicobacter Pylori

16/10/2014 Acute and chronic gastritis due to Helicobacter pylori

http://www.uptodate.com/contents/acute-and-chronic-gastritis-due-to-helicobacter-pylori?topicKey=GAST%2F31&elapsedTimeMs=1&source=search_re 1/8

Official reprint from UpToDate www.uptodate.com 2014 UpToDate

AuthorsPamela J Jensen, MDMark Feldman, MD, MACP, AGAF,FACG

Section EditorJ Thomas Lamont, MD

Deputy EditorShilpa Grover, MD, MPH

Acute and chronic gastritis due to Helicobacter pylori

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Sep 2014. | This topic last updated: May 11, 2013.

INTRODUCTION Injury to the gastric mucosa is associated with epithelial cell damage and regeneration. The term gastritis is used to denote inflammation associated withmucosal injury. However, epithelial cell injury and regeneration are not always accompanied by mucosal inflammation. This distinction has caused considerable confusion sincegastritis is often used to describe endoscopic or radiologic characteristics of the gastric mucosa rather than specific histologic findings. Epithelial cell damage and regenerationwithout associated inflammation is referred to as "gastropathy" [1,2]. (See "Classification and diagnosis of gastritis and gastropathy".)

The causes, natural history, and therapeutic implications of gastropathy differ from gastritis:

Gastropathy is usually caused by irritants such as drugs (eg, nonsteroidal antiinflammatory agents), alcohol, bile, circulatory failure, and chronic congestion.

Gastritis is usually due to infectious agents (such as Helicobacter pylori [H. pylori]) and autoimmune and hypersensitivity reactions.

Most classification systems distinguish acute, short-term from chronic, long-term disease. The terms acute and chronic are also used to describe the type of inflammatory cellinfiltrate. Acute ("active") inflammation is usually associated with neutrophilic infiltration, while chronic inflammation is usually characterized by mononuclear cells, chieflylymphocytes, plasma cells and macrophages. A practical clinicopathologic framework for the classification of gastritis and gastropathy based upon these factors can be proposed(table 1) [1].

Acute and chronic gastritis due to H. pylori will be reviewed here [3,4]. Although described separately, most patients with H. pylori infection will show features of both acute andchronic gastritis. The other forms of gastritis and gastropathy and other issues related to H. pylori are discussed separately. (See "Classification and diagnosis of gastritis andgastropathy" and "Indications and diagnostic tests for Helicobacter pylori infection" and "Treatment regimens for Helicobacter pylori" and "Association between Helicobacter pyloriinfection and gastrointestinal malignancy" and "Association between Helicobacter pylori infection and duodenal ulcer" and "Helicobacter pylori and gastroesophageal reflux disease"and "Pathophysiology of and immune response to Helicobacter pylori infection".)

HELICOBACTER PYLORI GASTRITIS

Acute Helicobacter pylori gastritis The ability of H. pylori to cause acute gastritis was demonstrated most clearly after healthy volunteers ingested the organisms anddeveloped a mild illness (consisting of epigastric pain, nausea, and vomiting without fever) associated with acute inflammatory changes on gastric biopsy [5,6]. Acute infection wasalso demonstrated in volunteers undergoing gastric secretory studies who were inadvertently infected by contaminated equipment [7-9]. These cases also demonstrated that acuteinfection is associated with the development of hypochlorhydria, a phenomenon that was suspected to be caused by an infectious agent and was referred to as "epidemichypochlorhydria." (See "Pathophysiology of and immune response to Helicobacter pylori infection".)

Despite the high prevalence of chronic H. pylori gastritis, few examples of spontaneous acute infection have been recognized [10-12]. This is not surprising since the majority ofpatients who develop dyspeptic complaints (which may signal acute infection) are not immediately investigated; furthermore, the initial infection occurring in the community probablyproduces few or no symptoms in the majority of individuals.

Endoscopic and histopathologic features The endoscopic appearance of acute H. pylori gastritis is variable and, in severe cases, can resemble lymphoma or carcinoma.Early after infection, H. pylori gastritis preferentially involves the gastric antrum. Histologic changes of acute H. pylori gastritis include intense neutrophilic infiltration of the mucousneck region and lamina propria. When severe, pit abscesses occur, along with mucin loss, erosion of the juxtaluminal cytoplasm, and desquamation of surface foveolar cells. Boththe neutrophils and the bacteria are responsible for destruction of the epithelium. Acute gastritis almost always evolves into active chronic gastritis unless treated with appropriateantibiotics.

Chronic Helicobacter pylori gastritis Chronic H. pylori gastritis affects two-thirds of the world's population and is one of the most common chronic inflammatory disorders ofhumans [13]. The major clinical associations with chronic H. pylori gastritis are peptic ulcer disease and, less commonly, gastric cancer and MALT lymphoma. (See appropriatetopic reviews.) An association between chronic H. pylori infection and dyspepsia remains controversial. (See "Functional dyspepsia in adults".)

H. pylori organisms reside primarily in the unstirred layer of gastric mucus, adjacent to epithelial cells at the mucosal surface and in gastric pits (picture 1A-B) [14]. Gastric glandsare usually not involved. The epithelial localization reflects the affinity of H. pylori organisms for gastric mucous cells [15,16]. H. pylori organisms do not attach to small intestinal orother gastric epithelial cell types. The organisms are uncommonly found in the lamina propria, except possibly in patients with AIDS [17]. (See "Pathophysiology of and immuneresponse to Helicobacter pylori infection".)

The organisms can be detected in both the antrum and the body of the stomach in the majority of infected patients. The following represents the approximate frequency of H. pylorilocalization within the stomach, based upon the collective experience of several investigators [18]:

Antrum and body 80 percentAntrum only 8 percentBody only 10 percent

The first two patterns are associated with H. pylori and the last pattern is associated with H. pylori infection, modified by PPIs or marked atrophy and intestinal metaplasia. Theusual natural history of H. pylori gastritis is of an antral predominant early stage of infection with only minimal corpus involvement. This stage is associated with exaggerated gastrinrelease and reduced somatostatin release, precipitating an increase in acid secretion, enough to cause duodenal ulcers in some patients [19].

With continued inflammation, gastrin producing (G) cells and acid producing parietal cells are gradually lost, precipitating a fall in acid secretion and the development of atrophy withintestinal metaplasia [20]. These changes facilitate the proximal migration of the bacteria, leading to corpus gastritis [21]. Thus, the natural history of H. pylori gastritis is of diffuseantral inflammation spreading to the corpus, resulting in an atrophic front of advancing corpus injury with concomitant reduction in acid secretion. This scenario is accelerated withlow acid secretion states such as chronic therapy with PPIs. However, this evolution is not inevitable since it can be modified by treatment.

Patients in whom H. pylori colonization is heaviest in the gastric body may differ from those with antral predominant infection. Duodenal ulcers are typically associated with antralpredominant gastritis, little or no atrophy, and normal or increased acid secretion. By contrast, gastric ulcers and gastric cancer are typically associated with extensive gastritis,widespread intestinal metaplasia and hypochlorhydria [22].

Histopathologic diagnosis of Helicobacter pylori In current practice, noninvasive testing (eg, serology or stool antigen assay) is generally used to establish the diagnosis ofH. pylori infection. (See "Indications and diagnostic tests for Helicobacter pylori infection".) A major role for histopathology is in the following indications:

Diagnosing H. pylori infection in patients taking a proton pump inhibitor (PPI), as PPIs can reduce the sensitivity of some of the noninvasive assays. This effect that may bedue to the antimicrobial activity of these drugs [23].To establish gastritis.To detect associated abnormalities such as intestinal metaplasia and mucosa-associated lymphoid tissue (MALT) lymphoma.

The variable distribution of H. pylori in the stomach, and the attenuated growth observed during treatment with PPIs has implications for optimal sites and the number of biopsyspecimens that should be obtained to establish the diagnosis of H. pylori. In one study, the combination of four biopsy sites (lesser and greater curvature of the mid antrum, lesserand greater curvature of the mid body) was found to be optimal for the detection of H. pylori and the assessment of the extent of atrophic gastritis [24].

A definitive histopathologic diagnosis of H. pylori infection depends upon the demonstration of the typical spiral shaped bacilli on a biopsy specimen. During treatment, H. pyloribacteria may lose their typical spiral shape and assume new forms, including U-shaped, rod-like, and coccoid forms. The coccoid forms appear as round basophilic dots, 0.4 to 1.2



m in diameter. Proton pump inhibitors and other hypochlorhydric states facilitate survival of non-H. pylori bacteria, such that the presence of gastric organisms (including cocci)does not confirm the presence of Helicobacter infection [25]. In such cases, the distinction requires immunohistochemistry for H. pylori.

Staining Although it is frequently possible to identify H. pylori in standard hematoxylin and eosin preparations, this type of staining is unreliable and is not advised [26,27]. Avariety of better staining methods for H. pylori are available [28,29]:

The quick Giemsa method (eg, Diff-Quik) is easy to use, inexpensive, and gives consistent results. It is the preferred method in many laboratories [28].

Immunostaining techniques are also available, and are highly sensitive and reliable (picture 2) [29]. They have a particular advantage in patients partially treated for H. pylorigastritis, a setting that can result in atypical (including coccoid) forms, which may mimic bacteria or cell debris on hematoxylin and eosin preparations.

Silver stains (such Warthin-Starry and Genta methods), which were crucial to the original demonstration of H. pylori, [30] are expensive and the results are not always reliable[28].

Mucosal changes The inflammatory changes in chronic H. pylori gastritis have been well described [31]. Acute and chronic inflammatory cells are concentrated in the upperpart of the mucosa, beginning just below the surface epithelium and giving the appearance of superficial gastritis, particularly in oxyntic mucosa. This pattern is so characteristic thatthe observer can suspect H. pylori gastritis even at the lowest magnifications.

The chronic inflammatory elements in H. pylori gastritis primarily consist of lymphocytes and plasma cells, scattered macrophages, and often increased eosinophils [31]. Lymphoidfollicles are frequently present. They represent an immune response to the bacteria and their presence provides a useful marker for H. pylori infection (see 'Significance of lymphoidfollicles' below). Similarly, a prominence of plasma cells is a valuable clue to H. pylori infection.

The acute (active) inflammatory component consists of neutrophilic infiltration of the surface and foveolar epithelium and the lamina propria, usually in scattered foci, with thefrequent presence of small pit abscesses.

The intensity of the inflammation varies among patients and sometimes from specimen to specimen in the same patient. Active inflammation is somewhat more common in antralthan in oxyntic H. pylori infection [32]. Although casual observation reveals no obvious relation between the numbers of organisms and the severity of the acute or chronicinflammation, a correlation with active gastritis has been described [33].

Significance of lymphoid follicles Lymphoid follicles represent an immune response to the organism, and are composed of aggregates of lymphocytes and otherlymphoid cells associated with a central germinal center made up of larger, paler mononuclear cells. They appear within one week after the onset of acute H. pylori infection, and areuncommon in non-H. pylori-infected gastric mucosa [8,34]. The number of lymphoid follicles correlates with the titer of serum IgG anti-H. pylori antibodies [35].

Lymphoid follicles accompanying H. pylori gastritis are involved in the genesis of primary gastric lymphoma [36,37]. The pathogenesis may involve stimulation of B cells with theability for unsuppressed proliferation by activated T cells within the follicles. (See "Association between Helicobacter pylori infection and gastrointestinal malignancy".)

Mucosal histopathology after eradication The acute inflammation associated with chronic H. pylori gastritis improves dramatically after eradication of the organisms withantibiotics.

Neutrophils disappear rapidly; the persistence of even small numbers of neutrophils may be predictive of relapse [38].

Lymphocytes and eosinophils decrease more slowly, and some chronic inflammation can be seen after one year. Lymphoid follicles are the slowest to disappear, and usuallyremain present throughout the stomach for more than one year [38].

Intestinal metaplasia and atrophy usually do not resolve by one year [39]. However, eradication may help prevent the development of further gastric atrophy and intestinalmetaplasia [40].

Fibrosis and architectural distortion, including foveolar hyperplasia, may persist long after H. pylori infection is eliminated and, in our experience, often resembles chemicalgastropathy.

Iron deficiency anemia Iron deficiency anemia (without evidence of blood loss from the gastrointestinal tract or other sources) has been described in association with H. pylorigastritis and may respond to eradication of H. pylori infection [41]. The pathogenesis is incompletely understood, but may relate to the organism's dependence upon iron as a growthfactor or the presence of H. pylori-associated gastric atrophy [42,43].

HELICOBACTER HEILMANNII Infectious agents other than H. pylori have been associated with gastritis. One such agent is Helicobacter heilmannii (formerly Gastrospirillumhominis). H. heilmannii is an uncommon zoonotic infection that has been associated with gastritis (typically mild), duodenal ulcers, acute gastric mucosal lesions, mucosa-associated lymphoid tissue lymphoma, and gastric carcinoma. The organism is twice as long as H. pylori (5 to 9 microns) and has five to seven tight spirals. Immunohistochemicalstains for H. pylori also react with H. heilmannii. Treatment is similar [44-48].

INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces arewritten in plain language, at the 5 to 6 grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best forpatients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed.These articles are written at the 10 to 12 grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient educationarticles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient information: H. pylori infection (The Basics)" and "Patient information: Gastritis (The Basics)" and "Patient information: Upper endoscopy (TheBasics)")

Beyond the Basics topics (see "Patient information: Helicobacter pylori infection and treatment (Beyond the Basics)" and "Patient information: Upper endoscopy (Beyond theBasics)")

SUMMARY AND RECOMMENDATIONS

Helicobacter pylori (H. pylori) is almost always accompanied by gastritis and the diagnosis should be suspect in its absence.

H. pylori gastritis typically begins as a diffuse antral gastritis, which subsequently spreads to the gastric corpus if untreated. Changes of chronic active gastritis may beassociated with intestinal metaplasia (atrophy). (See 'Chronic Helicobacter pylori gastritis' above.)

Chronic use of proton pump inhibitors (PPIs) may facilitate proximal migration of the organisms leading to corpus gastritis. (See 'Chronic Helicobacter pylori gastritis' above.)

Acute inflammation disappears rapidly with treatment, but the chronic inflammation, including lymphoid follicles, can persist for years. (See 'Significance of lymphoid follicles'above.)

Four different biopsy sites are recommended for the optimal detection of H. pylori. (See 'Histopathologic diagnosis of Helicobacter pylori' above.)

Immunohistochemistry may be necessary for the detection of H. pylori organisms in patients on antibiotic, chronic PPI therapy or with other hypochlorhydric states thatpredispose to gastric bacterial overgrowth. (See 'Staining' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis,

th th

th th



Houston 1994. Am J Surg Pathol 1996; 20:1161.2. Carpenter HA, Talley NJ. Gastroscopy is incomplete without biopsy: clinical relevance of distinguishing gastropathy from gastritis. Gastroenterology 1995; 108:917.3. Yardley JH, Hendrix TR. Gastritis, duodenitis, and associated ulcerative lesions. In: Textbook of Gastroenterology, Yamada T, Alpers DH, Owyang C, et al (Eds), Lippincott,

Philadelphia 1995. p.1456.4. Yardley JH, Hendrix TR. Gastritis, duodenitis, and associated ulcerative lesions. In: Textbook of Gastroenterology, 3rd ed, Yamada T, Alpers DH, Owyang C, Powell DW,

Silverstein FE (Eds), Lippincott, Philadelphia 1999.5. Marshall BJ, Armstrong JA, McGechie DB, Glancy RJ. Attempt to fulfil Koch's postulates for pyloric Campylobacter. Med J Aust 1985; 142:436.6. Morris A, Nicholson G. Ingestion of Campylobacter pyloridis causes gastritis and raised fasting gastric pH. Am J Gastroenterol 1987; 82:192.7. Ramsey EJ, Carey KV, Peterson WL, et al. Epidemic gastritis with hypochlorhydria. Gastroenterology 1979; 76:1449.8. Graham DY, Alpert LC, Smith JL, Yoshimura HH. Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydria. Am J Gastroenterol 1988; 83:974.9. Gledhill T, Leicester RJ, Addis B, et al. Epidemic hypochlorhydria. Br Med J (Clin Res Ed) 1985; 290:1383.

10. Salmeron M, Desplaces N, Lavergne A, Houdart R. Campylobacter-like organisms and acute purulent gastritis. Lancet 1986; 2:975.11. Frommer DJ, Carrick J, Lee A, Hazell SL. Acute presentation of Campylobacter pylori gastritis. Am J Gastroenterol 1988; 83:1168.12. Rocha GA, Queiroz DM, Mendes EN, et al. Helicobacter pylori acute gastritis: histological, endoscopical, clinical, and therapeutic features. Am J Gastroenterol 1991;

86:1592.13. Odze RD, Goldblum JR. Inflammatory disorders of the stomach. In: Surgical Pathology of the GI Tract, Liver, Biliary Tract, and Pancreas, Lash RH, Lauwers GY, et al. (Eds),

Saunders, Philadelphia 2009. p.285.14. Hazell SL, Lee A, Brady L, Hennessy W. Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important

factors in colonization of the gastric epithelium. J Infect Dis 1986; 153:658.15. Noach LA, Rolf TM, Tytgat GN. Electron microscopic study of association between Helicobacter pylori and gastric and duodenal mucosa. J Clin Pathol 1994; 47:699.16. Falk P, Roth KA, Born T, et al. An in vitro adherence assay reveals that Helicobacter pylori exhibits cell lineage-specific tropism in the human gastric epithelium. Proc Natl

Acad Sci U S A 1993; 90:2035.17. Meiselman MS, Miller-Catchpole R, Christ M, Randall E. Campylobacter pylori gastritis in the acquired immunodeficiency syndrome. Gastroenterology 1988; 95:209.18. Paull G, Yardley JH. Pathology of C pylori-associated gastric and esophageal lesions. In: Campylobacter Pylori in Gastritis and Peptic Ulcer Disease, Blaser MJ (Ed), Igaku-

Shoin, New York 1989. p.73.19. Graham DY, Opekun A, Lew GM, et al. Helicobacter pylori-associated exaggerated gastrin release in duodenal ulcer patients. The effect of bombesin infusion and urea

ingestion. Gastroenterology 1991; 100:1571.20. Vnnen H, Vauhkonen M, Helske T, et al. Non-endoscopic diagnosis of atrophic gastritis with a blood test. Correlation between gastric histology and serum levels of

gastrin-17 and pepsinogen I: a multicentre study. Eur J Gastroenterol Hepatol 2003; 15:885.21. Gutierrez O, Kim JG, Akamatsu T, et al. Geographic differences in the distribution of intestinal metaplasia in duodenal ulcer patients. Am J Gastroenterol 2001; 96:666.22. Correa P. Human gastric carcinogenesis: a multistep and multifactorial process--First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention.

Cancer Res 1992; 52:6735.23. Jonkers D, Stobberingh E, Stockbrgger R. Omeprazole inhibits growth of gram-positive and gram-negative bacteria including Helicobacter pylori in vitro. J Antimicrob

Chemother 1996; 37:145.24. Satoh K, Kimura K, Taniguchi Y, et al. Biopsy sites suitable for the diagnosis of Helicobacter pylori infection and the assessment of the extent of atrophic gastritis. Am J

Gastroenterol 1998; 93:569.25. El-Zimaity H. How to interpret biopsies for "gastritis". Path Case Rev 2008; 13:157.26. Agbamu DA. Staining for Helicobacter pylori: an E-mail survey. Hum Pathol 1997; 28:635.27. Molyneux AJ, Harris MD. Helicobacter pylori in gastric biopsies--should you trust the pathology report? J R Coll Physicians Lond 1993; 27:119.28. Madan E, Kemp J, Westblom TU, et al. Evaluation of staining methods for identifying Campylobacter pylori. Am J Clin Pathol 1988; 90:450.29. Ashton-Key M, Diss TC, Isaacson PG. Detection of Helicobacter pylori in gastric biopsy and resection specimens. J Clin Pathol 1996; 49:107.30. Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984; 1:1311.31. Karttunen T, Niemel S, Lehtola J, et al. Campylobacter-like organisms and gastritis: histopathology, bile reflux, and gastric fluid composition. Scand J Gastroenterol 1987;

22:478.32. Johnston BJ, Reed PI, Ali MH. Prevalence of Campylobacter pylori in duodenal and gastric mucosa--relationship to inflammation. Scand J Gastroenterol Suppl 1988; 142:69.33. Wyatt JI, Rathbone BJ, Heatley RV. Local immune response to gastric Campylobacter in non-ulcer dyspepsia. J Clin Pathol 1986; 39:863.34. Genta RM, Hamner HW, Graham DY. Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy. Hum Pathol 1993;

24:577.35. Fox JG, Correa P, Taylor NS, et al. Campylobacter pylori-associated gastritis and immune response in a population at increased risk of gastric carcinoma. Am J Gastroenterol

1989; 84:775.36. Isaacson PG, Spencer J. Is gastric lymphoma an infectious disease? Hum Pathol 1993; 24:569.37. Wotherspoon AC, Ortiz-Hidalgo C, Falzon MR, Isaacson PG. Helicobacter pylori-associated gastritis and primary B-cell gastric lymphoma. Lancet 1991; 338:1175.38. Genta RM, Lew GM, Graham DY. Changes in the gastric mucosa following eradication of Helicobacter pylori. Mod Pathol 1993; 6:281.39. van der Hulst RW, van der Ende A, Dekker FW, et al. Effect of Helicobacter pylori eradication on gastritis in relation to cagA: a prospective 1-year follow-up study.

Gastroenterology 1997; 113:25.40. Sung JJ, Lin SR, Ching JY, et al. Atrophy and intestinal metaplasia one year after cure of H. pylori infection: a prospective, randomized study. Gastroenterology 2000; 119:7.41. Yakoob J, Jafri W, Abid S. Helicobacter pylori infection and micronutrient deficiencies. World J Gastroenterol 2003; 9:2137.42. Cardenas VM, Mulla ZD, Ortiz M, Graham DY. Iron deficiency and Helicobacter pylori infection in the United States. Am J Epidemiol 2006; 163:127.43. Annibale B, Marignani M, Monarca B, et al. Reversal of iron deficiency anemia after Helicobacter pylori eradication in patients with asymptomatic gastritis. Ann Intern Med

1999; 131:668.44. Goddard AF, Logan RP, Atherton JC, et al. Healing of duodenal ulcer after eradication of Helicobacter heilmannii. Lancet 1997; 349:1815.45. al-Himyary AJ, Zabaneh RI, Zabaneh SS, Barnett S. Gastrospirillum hominis in acute gastric erosion. South Med J 1994; 87:1147.46. Morgner A, Bayerdrffer E, Meining A, et al. Helicobacter heilmannii and gastric cancer. Lancet 1995; 346:511.47. Morgner A, Lehn N, Andersen LP, et al. Helicobacter heilmannii-associated primary gastric low-grade MALT lymphoma: complete remission after curing the infection.

Gastroenterology 2000; 118:821.48. Okiyama Y, Matsuzawa K, Hidaka E, et al. Helicobacter heilmannii infection: clinical, endoscopic and histopathological features in Japanese patients. Pathol Int 2005; 55:398.

Topic 31 Version 11.0



GRAPHICS

Classification of gastritides and gastropathies

Acute formsAcute hemorrhagic and erosive gastropathy

Acute Helicobacter pylori gastritis

Uncommon acute infectious gastritides

Common formsHelicobacter pylori gastritis

Chemical gastropathy

Aspirin and other nonsteroidal antiinflammatory drugs

Bile reflux

Alcohol

Others (?)

Metaplastic atrophic gastritis

Autoimmune

Environmental

Chronic gastritis/gastropathy of indeterminate type

Uncommon formsPostantrectomy atrophic gastritis

Eosinophilic gastritis

Infectious gastritis

Bacterial, other than Helicobacter pylori

Helicobacter heilmannii

Phlegmonous

Mycobacterial

Syphilitic

Viral

Parasitic

Fungal

Crohn disease

Sarcoidosis

Isolated granulomatous gastritis

Lymphocytic gastritis

Mntrier's disease

Focally-enhanced gastritis

Graphic 73286 Version 6.0



Helicobacter pylori gastritis

Medium power view of a gastric biopsy obtained at endoscopy showsinfiltration of glands with neutrophils (arrow) and increasedmononuclear cell infiltration typical of Helicobacter pylori gastritis.

Courtesy of Robert Odze, MD.


Normal gastric antrum

Left panel: Normal surface (SE) and foveolar epithelium (FE) and glands (G).Right panel: Higher power view of the glands shows mucous cells (M) andgastrin-secreting endocrine cells (arrows).

Courtesy of Robert Odze, MD




Helicobacter pylori adherence on gastric surfacecells

High power view of surface and foveolar epithelium shows numerousHelicobacter pylori organisms lining the surface of the cells (arrows).

Courtesy of Robert Odze, MD.




Helicobacter pylori in gastric crypts

A 600x magnification of a Helicobacter pylori immunostain with theluminal organisms shown in brown.

Courtesy of Pamela J Jensen, MD.




Disclosures: Pamela J Jensen, MD Nothing to disclose. Mark Feldman, MD, MACP, AGAF, FACG Nothing to disclose. J ThomasLamont, MD Nothing to disclose. Shilpa Grover, MD, MPH Employee of UpToDate, Inc.Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vettingthrough a multi-level review process, and through requirements for references to be provided to support the content. Appropriatelyreferenced content is required of all authors and must conform to UpToDate standards of evidence.Conflict of interest policy

Disclosures

Documents

Acute and Chronic Gastritis Due to Helicobacter Pylori