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Classification and diagnosis of gastritis and gastropathy

Official reprint from UpToDate

www.uptodate.com 2014 UpToDate
Classification and diagnosis of gastritis and gastropathy
Authors
Section Editor
Beverly A Dickson, MD
J Thomas Lamont, MD
Mark Feldman, MD, MACP, AGAF,
FACG

Deputy Editor
Shilpa Grover, MD, MPH

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: Apr 23, 2014.
INTRODUCTION Gastritis is predominantly an inflammatory process, while gastropathy demonstrates
minimal to no inflammation. The term gastritis is used to denote inflammation associated mucosal injury.
However, epithelial cell injury and regeneration are not always accompanied by mucosal inflammation. This
distinction has caused considerable confusion since the term "gastritis" is often used to describe endoscopic or
radiologic characteristics of the gastric mucosa rather than specific histologic findings. Epithelial cell damage
and regeneration with minimal or no associated inflammation is properly referred to as "gastropathy."
The causes, natural history, and therapeutic implications of gastropathy differ from gastritis:
Gastritis is commonly secondary to infectious or autoimmune etiologies, although it can also result from
drugs or hypersensitivity reactions.
Gastropathy is commonly secondary to endogenous or exogenous irritants, such as bile reflux, alcohol, or
aspirin and nonsteroidal antiinflammatory drugs. However, gastropathy can also be secondary to
ischemia, physical stress, or chronic congestion.
"Gastritis" is a term often used by endoscopists to describe the gastric mucosa rather than representing a
particular endoscopic entity. A gastric mucosal biopsy is necessary to establish a definitive diagnosis of
gastritis versus gastropathy.
This topic review will discuss the classification and diagnosis of gastritis and gastropathy. The causes of acute
and chronic gastritis are presented separately.
HISTORY The existence of gastric inflammation was debated during the 19th and early part of the 20th
century. It was recognized that postmortem digestion markedly altered the gastric mucosa; as a result the
significance of gastric mucosal inflammation was uncertain. This was clarified by the histologic demonstration
of inflammation on gastric specimens prepared shortly after death [1] and by the use of gastroscopy beginning
in the 1920s and gastric biopsy in the 1940s [2].
CLASSIFICATION OF GASTRITIS AND GASTROPATHY There is no universally accepted classification
of gastritis/gastropathy, although several classifications of gastritis and gastropathy (such as the Sydney
system and the Operative Link for Gastritis Assessment [OLGA] staging system) have been proposed (table 1)
[3-8]. The updated Sydney system is the most widely used classification; however, it does not yield actionable
prognostic information concerning cancer risk in cases of chronic atrophic gastritis. The OLGA staging system
may provide information about secondary gastric cancers in autoimmune gastritis [9,10]. The OLGA staging
system, which was proposed by an international group of pathologists for use in standardizing classification of
atrophic gastritis, incorporates histologic phenotypes with extent of disease to aid in prediction of cancer risks
[11]. The high stage disease (OLGA III/IV) is associated with a high risk of gastric cancer. Operative Link on
Gastric Intestinal Metaplasia Assessment (OLGIM), another proposed system, shows less interobserver
variability and is still prognostically useful [9,10,12]. Gastritis has been classified by histologic features, time
course (acute versus chronic), etiology, and proposed pathophysiology. (See "Gastric intestinal metaplasia",
section on 'Definitions'.)
However, classification remains controversial because of gaps in knowledge of etiology and pathogenesis,
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variation in nomenclature, and the coexistence of more than one type of gastritis or gastropathy in individual
patients. Furthermore, the entities overlap morphologically, and so some conditions are classified by etiology
and others by morphologic pattern. Thus, comparisons across studies using different nomenclature can be
difficult.
Most classification systems distinguish acute, short-term disease from chronic, long-term disease. The terms
acute and chronic are also used to describe the type of inflammatory cell infiltrate. Acute inflammation is
represented by neutrophilic infiltration, while chronic inflammation is characterized by a mixture of mononuclear
cells, chiefly lymphocytes, plasma cells, and macrophages.
A clinicopathologic framework for the classification of gastritis and gastropathy based upon these factors has
been proposed (table 2) [13]. However, there are a number of cases with a diagnosis of chronic gastritis (often
mild) for which a specific etiology cannot be determined by histopathologic examination [14].
DIAGNOSIS A mucosal biopsy is required to distinguish between acute, chronic active, or chronic gastritis
from gastropathy, since the endoscopic and radiologic features may be similar and clinical features are often
inaccurate for predicting histologic findings [15-22]. Histologic findings can vary over a wide spectrum ranging
from epithelial hyperplasia to extensive epithelial cell damage with infiltration by inflammatory cells.
An illustrative study included 488 adults who were randomly selected from the general population and were
screened by gastroscopy and biopsy [21]. The authors determined the sensitivity and specificity of
macroscopic features (including erythema, erosions, the absence or rugal folds and the presence of visible
vessels) compared to histologic findings. None of these findings had sensitivity greater than 57 percent for
determining the presence of gastritis or H. pylori infection. Similar conclusions have been reached in other
reports [15,21]. Another problem with relying on endoscopy alone is the interobserver variability for some
features of gastritis such as erythema [20].
Laboratory evaluation Two types of laboratory tests have proven to be useful for predicting gastric
mucosal findings: noninvasive testing for H. pylori infection and serologic biomarker measurements, both
biochemical and immunologic.
Helicobacter pylori testing Noninvasive testing for Helicobacter pylori has high sensitivity and
specificity for gastritis. (See "Acute and chronic gastritis due to Helicobacter pylori" and "Indications and
diagnostic tests for Helicobacter pylori infection".)
Stomach-specific biochemical markers Pepsinogens are secreted by chief cells in the fundus and
body, and by mucous cells in the cardia, fundus, body, antrum, and pylorus. Pepsinogen I is mostly secreted
by chief cells in the gastric fundus, whereas pepsinogen II is also secreted in the antrum. Thus, in conditions
associated with gastritis of the fundus (as in pernicious anemia), serum pepsinogen (PG) I concentrations are
decreased relative to PG II.
Low serum PG I levels are strongly associated with extensive intestinal metaplasia [23]. Intestinal metaplasia
was found in 58 (88 percent) of 66 patients with a serum PG I value of less than 25 ng per milliliter [24]. The
ratio of PG isozymes I and II in serum has good correlation with presence of metaplastic atrophic gastritis
(principally autoimmune metaplastic atrophic gastritis and pernicious anemia) [25]. Measurement of amidated
gastrin-17 evaluated in tandem with PG I:II ratio has been advocated to reflect the degree of inflammation and
grade of atrophic gastritis [26]. The early diagnosis of atrophic gastritis is important as this condition is a
significant independent risk factor for the development of distal gastric tumors, both adenocarcinoma and
carcinoid [10,26]. (See "Metaplastic (chronic) atrophic gastritis", section on 'Hyperplastic and neoplastic
lesions'.)
The ratio of serum PG I:II in the serum of people with normal gastric mucosa is approximately 6.2 [27]. In one
series, the presence of fundic atrophic gastritis was accurately predicted by the concentration of pepsinogen I
and the ratio of pepsinogen isoenzymes in approximately 70 percent of patients [27]. The ratio may also be
useful for screening family members of patients with pernicious anemia and for identifying patients at high risk
for gastric cancer in endemic countries or other populations at increased risk for gastric atrophy [27-30]. On the
other hand, measurement of serum PGs and their ratio do not accurately discriminate nonatrophic versus
antrum-restricted/predominant atrophic gastritis in an asymptomatic population or first-degree relatives of
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patients with gastric cancer [31,32]. (See "Screening and prevention of gastric cancer".)
Serologic immunologic markers Immunological markers of stomach health may be useful in clinically
asymptomatic patients with early autoimmune gastritis (AIG) [33]. Testing for antibodies to intrinsic factor,
parietal cells, and Helicobacter pylori in tandem with serum gastrin may provide noninvasive early evidence of
AIG and facilitate selection of patients for endoscopic examination [33].
Biopsy Accurate histologic assessment of gastritis and gastropathy depends upon optimizing the site and
number of biopsy specimens. Magnification endoscopy may help in the identification of areas to biopsy. (See
"Magnification endoscopy".)
Biopsy site preferences and number vary in clinical practice. However, there is general consensus among
experts on the following biopsy approach [13]:
All gross abnormalities should be biopsied and submitted in separate containers.
Normal appearing mucosa adjacent to the lesional tissue should also be biopsied.
Multiple biopsies (two to five) of both the corpus and the antrum should be obtained when attempting to
establish the diagnosis of Helicobacter pylori or autoimmune gastritis.
Biopsy of the incisura is also useful since it approximates the transition zone between the antrum and body,
where intestinal metaplasia and atrophy are most frequently found in environmental metaplastic atrophic
gastritis. However, biopsy of incisura only does not provide information on the extent of metaplastic atrophic
gastritis, which is a major parameter in determination of cancer risk [10,12].
In first degree relatives of early onset gastric carcinoma patients, endoscopic evaluation with at least four
biopsies in the gastric antrum and corpus are suggested. Multiple biopsies with adequate sampling are
necessary for scoring and staging of premalignant lesions in this subgroup of patients [10].
Biopsies of the duodenum may also be helpful for diagnosing some forms of chronic gastritis. As examples,
duodenal biopsies may show evidence of Crohn disease in patients with granulomatous gastritis or of celiac
disease in patients with lymphocytic gastritis.
Communication with the pathologist Good communication between the endoscopist and pathologist
cannot be overemphasized, and will optimize the interpretation of the biopsy specimens. This has become
greatly facilitated by the availability of digital endoscopic pictures and readily available endoscopic procedural
dictation in the electronic medical record.
The pathologist should include a morphologic classification of the gastritis or gastropathy in the biopsy report
(table 3) [34].
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The Basics"
and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients 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 10th to 12th 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 education articles on a variety of subjects by searching on
"patient info" and the keyword(s) of interest.)
Basics topics (see "Patient information: Gastritis (The Basics)" and "Patient information: Upper
endoscopy (The Basics)")
Beyond the Basics topics (see "Patient information: Upper endoscopy (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
Gastric inflammatory disease can be broadly categorized into gastritides and gastropathies. Gastritis is
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predominantly an inflammatory process while gastropathy demonstrates minimal to no inflammation. (See

'Introduction' above.)
There is no universally accepted classification of gastritis/gastropathy, although several classifications of
gastritis and gastropathy (such as the Sydney system) have been proposed. (See 'Classification of
gastritis and gastropathy' above.)
A mucosal biopsy is required to distinguish between acute, chronic active, and chronic gastritis and
gastropathy. (See 'Diagnosis' above.)
There is general consensus among experts on a biopsy approach. (See 'Biopsy' above.)
Good communication between the endoscopist and pathologist cannot be overemphasized, and will
optimize the interpretation of the biopsy specimens. (See 'Communication with the pathologist' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
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2. Wood IJ, Taft LI. Diffuse lesions of the stomach: An account with special reference to the value of
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3. Price AB. The Sydney System: histological division. J Gastroenterol Hepatol 1991; 6:209.
4. Correa P. Chronic gastritis: a clinico-pathological classification. Am J Gastroenterol 1988; 83:504.
5. Wyatt JI, Dixon MF. Chronic gastritis--a pathogenetic approach. J Pathol 1988; 154:113.
6. 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; 20:1161.
7. Carpenter HA, Talley NJ. Gastroscopy is incomplete without biopsy: clinical relevance of distinguishing
gastropathy from gastritis. Gastroenterology 1995; 108:917.
8. Rugge M, Meggio A, Pennelli G, et al. Gastritis staging in clinical practice: the OLGA staging system.
Gut 2007; 56:631.
9. Rugge M, Fassan M, Pizzi M, et al. Autoimmune gastritis: histology phenotype and OLGA staging.
Aliment Pharmacol Ther 2012; 35:1460.
10. Marcos-Pinto R, Carneiro F, Dinis-Ribeiro M, et al. First-degree relatives of patients with early-onset
gastric carcinoma show even at young ages a high prevalence of advanced OLGA/OLGIM stages and
dysplasia. Aliment Pharmacol Ther 2012; 35:1451.
11. Rugge M, Correa P, Di Mario F, et al. OLGA staging for gastritis: a tutorial. Dig Liver Dis 2008; 40:650.
12. Park JY, Lam-Himlin D, Vemulapalli R. Review of autoimmune metaplastic atrophic gastritis.
Gastrointest Endosc 2013; 77:284.
13. Dixon MF, Genta RM, Yardley JH, Correa P. Histological classification of gastritis and Helicobacter
pylori infection: an agreement at last? The International Workshop on the Histopathology of Gastritis.
Helicobacter 1997; 2 Suppl 1:S17.
14. Sepulveda AR, Patil M. Practical approach to the pathologic diagnosis of gastritis. Arch Pathol Lab Med
2008; 132:1586.
15. Khakoo SI, Lobo AJ, Shepherd NA, Wilkinson SP. Histological assessment of the Sydney classification
of endoscopic gastritis. Gut 1994; 35:1172.
16. Cronstedt JL, Simson IW. Correlation between gastroscopic and direct vision biopsy findings.
Gastrointest Endosc 1973; 19:174.
17. Elta GH, Appelman HD, Behler EM, et al. A study of the correlation between endoscopic and histological
diagnoses in gastroduodenitis. Am J Gastroenterol 1987; 82:749.
18. Jnsson KA, Gotthard R, Bodemar G, Brodin U. The clinical relevance of endoscopic and histologic
inflammation of gastroduodenal mucosa in dyspepsia of unknown origin. Scand J Gastroenterol 1989;
24:385.
19. Tytgat GN. The Sydney System: endoscopic division. Endoscopic appearances in gastritis/duodenitis. J
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Gastroenterol Hepatol 1991; 6:223.

20. Laine L, Cohen H, Sloane R, et al. Interobserver agreement and predictive value of endoscopic findings
for H. pylori and gastritis in normal volunteers. Gastrointest Endosc 1995; 42:420.
21. Reden S, Petersson F, Jnsson KA, Borch K. Relationship of gastroscopic features to histological
findings in gastritis and Helicobacter pylori infection in a general population sample. Endoscopy 2003;
35:946.
22. Kaur G, Raj S. A study of the concordance between endoscopic gastritis and histological gastritis in an
area with a low background prevalence of Helicobacter pylori infection. Singapore Med J 2002; 43:90.
23. Miki K, Urita Y. Using serum pepsinogens wisely in a clinical practice. J Dig Dis 2007; 8:8.
24. Urita Y, Hike K, Torii N, et al. Serum pepsinogens as a predicator of the topography of intestinal
metaplasia in patients with atrophic gastritis. Dig Dis Sci 2004; 49:795.
25. Samloff IM. Peptic ulcer: the many proteinases of aggression. Gastroenterology 1989; 96:586.
26. Agrus L, Kuipers EJ, Kupcinskas L, et al. Rationale in diagnosis and screening of atrophic gastritis with
stomach-specific plasma biomarkers. Scand J Gastroenterol 2012; 47:136.
27. Samloff IM, Varis K, Ihamaki T, et al. Relationships among serum pepsinogen I, serum pepsinogen II,
and gastric mucosal histology. A study in relatives of patients with pernicious anemia. Gastroenterology
1982; 83:204.
28. Yoshihara M, Sumii K, Haruma K, et al. Correlation of ratio of serum pepsinogen I and II with prevalence
of gastric cancer and adenoma in Japanese subjects. Am J Gastroenterol 1998; 93:1090.
29. Graham DY, Nurgalieva ZZ, El-Zimaity HM, et al. Noninvasive versus histologic detection of gastric
atrophy in a Hispanic population in North America. Clin Gastroenterol Hepatol 2006; 4:306.
30. Oishi Y, Kiyohara Y, Kubo M, et al. The serum pepsinogen test as a predictor of gastric cancer: the
Hisayama study. Am J Epidemiol 2006; 163:629.
31. Ricci C, Vakil N, Rugge M, et al. Serological markers for gastric atrophy in asymptomatic patients
infected with Helicobacter pylori. Am J Gastroenterol 2004; 99:1910.
32. Haj-Sheykholeslami A, Rakhshani N, Amirzargar A, et al. Serum pepsinogen I, pepsinogen II, and
gastrin 17 in relatives of gastric cancer patients: comparative study with type and severity of gastritis.
Clin Gastroenterol Hepatol 2008; 6:174.
33. Antico A, Tampoia M, Villalta D, et al. Clinical usefulness of the serological gastric biopsy for the
diagnosis of chronic autoimmune gastritis. Clin Dev Immunol 2012; 2012:520970.
34. Owen DA. Gastritis and carditis. Mod Pathol 2003; 16:325.
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GRAPHICS
Updated Sydney system for the classification and grading of
gastritis
Type of gastritis
Nonatrophic

Etiologic factors

Gastritis
synonyms

Helicobacter pylori

Superficial

? Other factors

Diffuse antral gastritis

(DAG)
Chronic antral gastritis
(CAG)
Interstitial - follicular
Hypersecretory
Type B*

Atrophic
Autoimmune

Autoimmunity

Type A*
Diffuse corporal
Pernicious anemiaassociated

Multifocal atrophic

Helicobacter pylori

Type B*, type AB*

Dietary

Environmental

? Environmental factors

Metaplastic

Chemical irritation

Reactive

Special forms
Chemical

Bile

Reflux

NSAIDs

NSAID

? Other agents

Type C*

Radiation

Radiation injury

Lymphocytic

Idiopathic? Immune mechanisms

Varioliform
(endoscopic)

Gluten

Celiac diseaseassociated

Drug (ticlopidine)
? H. pylori
Noninfectious
granulomatous

Crohn's disease
Sarcoidosis
Granulomatosis with polyangiitis and other
vasculitides
Foreign substances
Idiopathic

Isolated
granulomatous

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Eosinophilic

Food sensitivity

Allergic

? Other allergies
Other infectious
gastritides

Bacteria (other than H. pylori)

Phlegmonous

Viruses
Fungi
Parasites

NSAIDs: nonsteroidal antiinflammatory drugs.

* Alphabetic designations of gastritis were abandoned in the original presentation of the Sydney
System. That approach is also recommended here. Use of "Type B" to denote either atrophic or nonatrophic gastritis is considered to be especially misleading.
Many participants favor substitution of gastropathy for gastritis to describe conditions that result
from chemical injury.
Reproduced with permission from: Dixon M, Genta R, Yardley J, Correa P; the Participants in the
International Workshop on the Histopathology of Gastritis, Houston. Classification and grading of
gastritis: The updated Sydney system. Am J Surg Pathol 1996; 20:1161. Copyright 1996
Lippincott Williams & Wilkins.
Graphic 58995 Version 11.0

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Classification of gastritides and gastropathies

Acute forms
Acute hemorrhagic and erosive
gastropathy
Acute Helicobacter pylori gastritis
Uncommon acute infectious gastritides

Common forms

Uncommon forms
Postantrectomy atrophic gastritis
Eosinophilic gastritis
Infectious gastritis
Bacterial, other than Helicobacter pylori
Helicobacter heilmannii

Helicobacter pylori gastritis

Phlegmonous

Chemical gastropathy

Mycobacterial
Syphilitic

Aspirin and other nonsteroidal

antiinflammatory drugs

Viral

Bile reflux

Parasitic

Alcohol

Fungal

Others (?)

Metaplastic atrophic gastritis

Crohn disease
Sarcoidosis

Autoimmune

Isolated granulomatous gastritis

Environmental

Lymphocytic gastritis

Chronic gastritis/gastropathy of
indeterminate type

Mntrier's disease
Focally-enhanced gastritis

Graphic 73286 Version 6.0

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Morphologic classification of gastritis or gastropathy

Location of process:

Antral predominant, corpus predominant, or pangastritis

Type of inflammation:

Acute, chronic, mixed, eosinophilic, or granulomatous

Topography of inflammation:

Diffuse or focal
Gastric site

Atrophy:

Present or absent, graded*

Intestinal metaplasia:

Present or absent, graded*

Infectious agent:

Helicobacter pylori, Helicobacter heilmannii, virus, other

* Mild, moderate, or marked.

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Disclosures
Disclosures: Beverly A Dickson, MD Nothing to disclose. Mark Feldman, MD, MACP, AGAF, FACG Nothing to disclose. J
Thomas Lamont, 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 vetting
through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately
referenced content is required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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