Evidence-Based Medicine

Chronic Gastritis

Chronic Gastritis

Overview

  • Chronic gastritis is a chronic inflammatory condition of gastric mucosa
    • "chronic gastritis" is often used interchangeably with "chronic gastropathy" in referring to pathologic changes in the gastric mucosa on a noninflammatory basis, as in portal hypertension or the late effects of radiation
    • chronic gastritis is very common, occurring in up to 60% of reported populations
    • most common cause is Helicobacter pylori gastric mucosal infection
    • chronic gastritis may be asymptomatic or may be associated with gastrointestinal symptoms, benign peptic ulcer disease, and gastric malignancy
    • chronic gastritis is often diagnosed during evaluation of upper gastrointestinal symptoms or by screening of populations at high risk for gastric cancer.
  • Ask about risk factors for chronic gastritis, including
    • East Asian heritage
    • prior history of H. pylori infection
    • history of drug use associated with gastritis
      • alcohol
      • nonsteroidal anti-inflammatory agents
      • proton pump inhibitors
      • chemotherapy agents
      • steroids
    • history of gluten sensitivity
    • history of autoimmune disease or vasculitis
    • history of Crohn disease
    • history of chronic liver disease or portal hypertension
    • food allergy
    • radiation exposure
    • caustic exposure
    • prior gastric surgery.
  • Diagnosis made by evaluation of endoscopic biopsies of gastric mucosa.
  • Updated Sydney System for classification and grading of gastritis describes standards for biopsies:
    • diagnosis is made on basis of upper endoscopic appearance and results of surgical pathology
    • diagnosis based on at least 5 endoscopic biopsies from corpus, antrum, and incisura
    • classification of gastritis based on morphology, topography, and etiology.
  • Operative Link on Gastritis Assessment (OLGA) staging system is proposed for staging gastritis:
    • OLGA staging integrates atrophy score (from biopsy) with atrophy topography (from directed biopsy mapping) and reports antral and corpus atrophy scores (inflammatory infiltrate grades 1-4), stage for gastric cancer risk (0-IV) and H. pylori status
    • OLGA staging distinguished benign lesions (stages 0-II) from neoplastic lesions (stages III-IV).
  • Management is dependent on the type of gastritis:
    • treat H. pylori when identified
    • consider treatment with proton pump inhibitor, histamine-2 blocker, sucralfate, or misoprostol
    • ursodeoxycholic acid may be useful for bile salt reflux associated gastritis.
  • Screening for dysplasia and early gastric cancer may be useful in high risk populations, as in Korea and Japan:
    • endoscopic screening with classification guided by Sydney criteria and OLGA staging
    • screening with pepsinogen 1 and 2 levels may correlate with gastric atrophy, a precursor for dysplasia.

General Information

Description

  • inflammatory condition of gastric mucosa that covers a broad histopathologic and topographic spectrum
  • chronic gastritis includes 3 major forms
    • atrophic
    • nonatrophic
    • special forms that are identified by historical and clinical features

Also called

  • Chronic gastropathy
    • Nonatrophic gastritis also called:
      • superficial gastritis
      • diffuse antral gastritis
      • chronic antral gastritis
      • interstitial-follicular gastritis
      • hypersecretory gastritis
      • type B gastritis.
    • Atrophic gastritis also called:
      • diffuse corporal gastritis
      • pernicious anemia-associated gastritis
      • metaplastic gastritis
      • environmental gastritis
      • type A gastritis, type B gastritis, or type AB gastritis.

Types

  • nonatrophic gastritis may be caused by Helicobacter pylori or other factors
  • atrophic gastritis may be caused by autoimmunity, H. pylori, dietary factors, or possibly environmental factors
  • special types of chronic gastritis, classified based on historical features and histology that allows them to be distinguished from nonspecific chronic gastritis or H. pylori-associated gastritis

Epidemiology of atrophic and nonatrophic gastritis

Incidence/Prevalence

Likely risk factors

Associated conditions

Etiology and Pathogenesis of Atrophic and Nonatrophic Gastritis

Causes

Pathogenesis of atrophic and nonatrophic gastritis

  • Natural progression of Helicobacter pylori gastritis.
  • H. pylori lives between epithelium and mucus:
    • inflammation in antrum into adjacent corpus
    • front of advancing injury leads to reduced acid secretion
    • may progress to
      • loss of parietal cells and development of atrophy (atrophic gastritis)
      • dysplasia as premalignant lesions
    • rate of progression depends on acid environment, which may be influenced by
      • use of proton pump inhibitors
      • dietary factors
      • childhood infections
  • Progression of gastric atrophy:
    • atrophy begins at border of antrum-corpus
    • atrophy replaces fundic gland mucosa with both pseudopyloric metaplasia and/or intestinal metaplasia
    • locations high on greater curvature among last to atrophy
    • higher density of mucosa mononuclear cells that infiltrate deep into lamina propria predict presence of gastric atrophy.
  • Autoimmune diseases may be associated with antibody against intrinsic factor and parietal cells.

Etiology and Pathogenesis of Special Types of Gastritis

Causes

  • special types of chronic gastritis, classified based on clinical features and histology that allow them to be distinguished from nonspecific chronic gastritis or Helicobacter pylori-associated gastritis

Caustic associated gastritis

  • Relatively rare, but over 5,000 cases of caustic ingestion per year in United States (Gastroenterol Clin North Am 1991 Dec;20(4):847).
  • May follow accidental ingestion or suicide attempt (BMJ Case Rep 2009;2009.pii:bcr02.2009.1612).
    • patients may present early after ingestion or months after ingestion of caustic substance
    • may be associated with oropharyngeal and/or esophageal lesions, as esophageal strictures
  • Symptoms include
  • Endoscopic findings may include:
    • microgastria
    • gastric stricture.
  • Hydrogen peroxide ingestion may be associated with gastritis:
    • may also be associated with
      • oropharyngeal lesions
      • foaming at the mouth
      • pulmonary aspiration
      • cerebrovascular accident and cardiovascular collapse due to oxygen embolization
    • Reference - Toxicol Rev 2004;23(1):51

Chemical or reactive gastritis

  • May be caused by chemical irritation from agents, such as bile or nonsteroidal anti-inflammatory drugs (NSAIDs).
  • Foveolar hyperplasia, edema, and smooth-muscle proliferation in the lamina propria, together with only normal numbers or a minor increase in chronic inflammatory cells; neutrophilic polymorphonuclear cells are not seen unless erosion is present.
  • Term "type C gastritis" no longer recommended.

Collagenous gastritis

  • Thick band of collagen is present immediately below surface epithelium of gastric mucosa
  • very rare
  • no well-established therapy available
  • two forms described
    • pediatric - usually presenting with abdominal pain or other upper gastrointestinal symptoms and with anemia
    • adult
      • often seen in combination with collagenous colitis
      • presentation varies with severity of inflammation and areas of gastrointestinal tract affected
    • Reference - World J Gastrointest Endosc 2015 Mar 16;7(3):265

Eosinophilic gastritis

  • For diagnosis, eosinophils must be the dominant cell type with little or no increase in other inflammatory cell types; mere presence of eosinophils insufficient to make diagnosis:
    • may be caused by food sensitivity or other allergies
    • also called allergic gastritis.
  • Eosinophilic gastritis is a manifestation of eosinophilic gastroenteritis:
  • May be associated with eosinophilic infiltration of esophagus, small bowel, colon, biliary tree, ascites, or pleural effusions:
  • Symptoms are nonspecific:
    • abdominal pain
    • weight loss
    • nausea and vomiting
    • poor appetite
    • diarrhea, especially with concomitant colonic involvement.
  • Diagnosis requires absence of these other known causes of tissue eosinophilia:
    • bacterial infection (H. pylori)
    • celiac disease
    • Churg-Strauss syndrome
    • connective tissue disease (as polyarteritis nodosa)
    • drug allergy
    • hypereosinophilic syndrome (peripheral eosinophilia > 1500 cell/microliter persisting for greater than 6 months)
    • inflammatory bowel disease
    • myeloproliferative disorders
    • parasitic infection:
  • Diagnosis requires demonstration of increased eosinophils on biopsy of involved tissue, but pathologic criteria are not well established:
    • endoscopic evaluation may reveal macroscopically normal mucosa, or erythema, friability, granularity, ulceration, thickened mucosal folds or nodules, white specks
      • eosinophils not normally seen in esophagus
      • > 20 eosinophils per high power field consistent with eosinophilic gastritis and distal colon colitis
      • some authorities require > 30 eosinophils per high power field in gastric mucosal biopsies for diagnosis
      • ≥ 50 eosinophils per high power field in duodenum consistent with eosinophilic gastroenteritis
      • > 30 eosinophils per high power field consistent with eosinophilic colitis in right colon and pericecal area
      • if eosinophilic gastritis or gastroenteritis under consideration, consider multiple biopsies, including biopsies of normal appearing mucosa.
    • radiologic evaluation is of limited value, as findings are nonspecific.
  • History of allergy in 50% of patients but symptoms exacerbated by foods in only 8% of patients (Scott Med J 1990 Dec;35(6):163).
  • In immediate phase, food allergens activate mast cells via high affinity immunoglobulin E (IgE) receptors.
  • In late phase, food allergens:
    • activate Th2 lymphocyte helper cells and produce lymphokines IL-3, IL-5, GM-CSF
    • activate monocytes and generate IL-8, monocyte chemotactic protein
      • leads to accumulation of eosinophils and basophils
      • eosinophils release inflammatory mediators that cause tissue destruction and organ dysfunction
        • eosinophil cationic protein
        • eosinophil derived neurotoxin
        • eosinophil peroxidase
        • eotaxins
        • GM-CSF
        • IL-1, IL-3, IL-4, IL-5, IL-6, IL-8
        • leukotrienes
        • major basic protein
        • transforming growth factor alpha and beta
        • tumor necrosis factor
  • rare, estimated 1-20 cases per 100,000
    • seen in all age groups, peak incidence 30-50
    • male to female ratio 3:2
    • seen in all ethnic groups, most common in White population
    • 70% of patients have history of atopy
      • asthma
      • eczema
      • hay fever.

Gastritis post gastric surgery

Granulomatous gastritis

Infectious gastritides

  • May be caused by bacteria other than H. pylori, as well as viruses, fungi, parasites:
  • Also called phlegmonous gastritis
    • rare disease
      • primary form develops consequent to a break in mucosa of stomach, as by malignancy, ulcer, foreign bodies as nasogastric tubes, or endoscopic interventions
      • secondary form consequent to hematogenous spread from another site of infection
      • idiopathic form has no obvious source for infection.
    • often presents as acute or subacute infection of gastric wall, and may develop into a chronic form, with scarring and fibrosis
    • Reference - SAGE Open Med Case Rep 2015 Dec 15;3:2050313X15596651

Lymphocytic gastritis

  • May be caused by idiopathic immune mechanisms, gluten, drugs (such as ticlopidine), possibly H. pylori.
  • Characterized by the presence of large numbers of mature lymphocytes infiltrating the surface and foveolar epithelium.
  • Increase in intraepithelial lymphocytes can be associated with significant chronic inflammatory cell infiltration of the lamina propria, activity, and focal erosions, or possibly only a minor increase in chronic inflammatory cells with no activity.
  • Also called varioliform (endoscopic) gastritis, celiac disease associated gastritis.
  • Diagnostic threshold for lymphocytic gastritis generally > 25 intraepithelial lymphocytes (IELs) per 100 cells.
  • Lymphocytic gastritis (defined as ≥ 30 lymphocytes per 100 epithelial cells on gastric biopsy) reported in only 4 of 400 patients (1%) in case series from Brazil (Arq Gastroenterol 1998 Jan-Mar;35(1):26).

Portal hypertensive gastritis

Radiation gastritis

  • Radiation may cause early or late effects on the gastric mucosa (Case Rep Oncol 2015 Jan-Apr;8(1):9)
    • acute damage causes inflammation
    • late damage causes vasculopathy, mucosal ischemia, ulceration, telangiectasia
    • radiation damage may be exacerbated by H. pylori.
  • Intrahepatic cholangiocarcinoma patients have risk of developing bleeding from gastritis after radiation therapy; volume of stomach exposed to radiation therapy should be minimized (Pract Radiat Oncol 2013 Oct-Dec;3(4):344).
  • Gastric adenocarcinoma may be complication of gastric irradiation for B-cell lymphoma (BMC Cancer 2013 Oct 26;13:499).

History and Physical

History

Chief concern (CC)

  • patients may be asymptomatic or may have complaints, including
    • abdominal pain or upset
    • belching
    • bloating
    • dyspepsia
    • feeling of burning in upper abdomen
    • feeling of fullness
    • nausea
    • reflux
    • vomiting

Medication history

  • ask about
    • chemotherapeutic agents
    • nonsteroidal anti-inflammatory drugs (NSAIDs)
    • proton pump inhibitors
    • steroids

Past medical history (PMH)

  • ask about history of Helicobacter pylori infection or peptic ulcer disease
  • ask about history of gastric surgery (may increase risk of bile reflux)

Family history (FH)

Social history (SH)

  • ask about alcohol use

Physical

General physical

  • no physical signs are sensitive or specific for chronic gastritis

Diagnosis

Making the diagnosis

  • Diagnosis is typically made by upper gastrointestinal endoscopic biopsies:
    • Sydney system for grading of biopsies
    • Operative Link on Gastritis Assessment (OLGA) system used for staging and prognosis of gastritis.
  • Serologic testing may provide additional diagnostic information:
    • pepsinogen I, II
    • gastrin
    • Helicobacter pylori.

Differential diagnosis

Testing overview

  • Tests for suspected Helicobacter pylori infection:
    • noninvasive tests
      • H. pylori antibody serology
      • urea breath test
      • stool antigen
    • invasive tests on biopsy specimen
      • rapid urease test
      • histology
      • culture
    • see Helicobacter pylori Infection for details.
  • Tests for suspected pernicious anemia caused by atrophic gastritis:
    • complete blood count
    • vitamin B12 level
    • folate level (B12 may be falsely low if severe folate deficiency)
    • anti-intrinsic factor antibody
    • antiparietal cell antibody
    • serum gastrin level
    • Schilling test
    • see Pernicious anemia for details
  • Upper gastrointestinal endoscopy and endoscopic biopsy.

Blood tests

  • Helicobacter pylori positive antibody testing is consistent with either current active infection or infection in past, and cannot distinguish between these 2 possibilities (Am J Gastroenterol 2007 Aug;102(8):1808)
  • Pepsinogen levels
  • Consider allergy radioallergosorbent test (RAST) in diagnosis of eosinophilic gastritis, although positive skin tests may not correlate with reactions after ingestion of food (Scand J Gastroenterol 2015;50(11):1309)

Upper gastrointestinal endoscopy and biopsy

  • Updated Sydney System for classification and grading of gastritis:
    • diagnosis based on at least 5 endoscopic biopsies from corpus, antrum, and incisura
    • classification of gastritis based on morphology, topography, and etiology
    • morphology
      • visual analog scale developed to aid in grading histologic features
      • drawings on visual analog scale are schematic representations of magnitude of each feature
      • variables graded as mild, moderate, or significant (previously called severe)
      • if variations within same biopsy sample, average different areas and score specimen accordingly
      • grading variables for morphology
        • presence or absence of H. pylori
        • polymorphonuclear neutrophil activity
        • chronic inflammation indicated by presence of mononuclear cells in lamina propria
        • glandular atrophy
          • antral atrophy indicated by decrease to ≤ 2 gland cross-sections or replacement of antral epithelium with intestinal metaplasia
          • corpus atrophy
        • intestinal metaplasia indicated by presence of goblet cells, absorptive cells, and cells resembling colonocytes, or by enzyme or mucin content
      • other nongraded variables to note include
        • surface epithelial damage, mucous depletion, and erosions
          • differentiate between true erosions and detached parts of surface epithelium from specimen handling and processing
          • true erosions will show fibrin deposition, neutrophilic infiltration and regenerative changes in adjacent epithelium
        • lymphoid follicles
          • lymphoid aggregates with germinal centers characteristic of chronic H. pylori gastritis
          • consider mucosa-associated lymphoid tissue (MALT) lymphoma if irregularly shaped or large lymphoid follicles present or large portions of mucosa densely populated with lymphocytes
          • foveolar hyperplasia
            • may be seen in all forms of gastritis to some degree
            • most pronounced in chemical gastritis
          • pseudopyloric metaplasia
            • pancreatic (acinar) metaplasia
            • endocrine cell hyperplasia - most pronounced in autoimmune atrophic gastritis
          • topography
            • assess and categorize pattern of chronic gastritis as "antral predominant" or "corpus predominant" if possible
            • categorize pattern of atrophy or intestinal metaplasia as "multifocal" or "diffuse"
            • use pattern of inflammation and atrophy to classify gastritis
          • etiology
            • use pattern of inflammation and atrophy to indicate etiology, if possible
            • H. pylori is major cause of gastritis, but may not be sole etiology
          • interobserver variability persists among gastrointestinal pathologists, despite updated Sydney System guidelines
            • based on review of 40 biopsy specimens of H. pylori gastritis reviewed by 3 pathologists
              • chronic inflammation, inflammatory activity, atrophy, intestinal metaplasia and H. pylori surface epithelial damage were evaluated
              • best interobserver agreement for intestinal metaplasia (kappa 0.62)
              • poorest agreement for atrophy (kappa 0.31)
              • Reference - World J Gastroenterol 2003 Oct;9(10):2232
            • based on review of biopsies of antrum and corpus from 30 patients with H. pylori gastritis
            • OLGA staging system proposed for gastritis staging
              • international group (Operative Link on Gastritis Assessment [OLGA]) proposed gastritis staging system based on hepatitis staging system, which has been accepted as clinically useful
              • OLGA staging integrates atrophy score (from biopsy) with atrophy topography (from directed biopsy mapping) and reports antral and corpus atrophy scores (inflammatory infiltrate grades 1-4), stage for gastric cancer risk (0-IV) and H. pylori status
              • Reference - Dig Liver Dis 2011 Mar;43 Suppl 4:S373
                • OLGA staging distinguished benign lesions (stages 0-II) from neoplastic lesions (stages III-IV) in prospective cohort of 439 patients with dyspepsia, OLGA stage had good correlation with dysplasia and cancer (Gastroenterol Hepatol Bed Bench 2016 Winter;9(1):25)
                • in a Korean population undergoing screening for gastric cancer, higher OLGA stages were independently correlated with age over 40, smoking and H. pylori status; high OLGA stages rare in patients without history of H. pylori infection (Helicobacter 2014 Apr;19(2):81)
                • higher OLGA grades of gastritis correlated with the presence of serum immunoglobulin G (IgG) antibodies against H. pylori secretory peptidyl propyl isomerase, rHP0175, a suspected proinflammatory and procarcinogenic protein (higher grades of gastric inflammation [odds ratio (OR) 4.4, 95% CI 1.9-9.9] [P = 0.001] and stages of gastric atrophy [OR 18.3, 95% CI 1.4-246.6] [P = 0.028]) (J Gastrointest Cancer 2016 Dec;47(4):375)
                • incident neoplastic lesions developed exclusively in patients with OLGA stages III-IV in prospective cohort of 1,755 patients with dyspepsia in Italy (Gut 2018 Jan 6 early online)
    • Upper gastrointestinal endoscopy
      • magnifying endoscopy may be accurate for predicting histologic gastritis
    • Gastric mucosal biopsy
      • inform pathologist of biopsy locations and of clinical and endoscopic findings
      • stain for biopsy specimens
        • hematoxylin and eosin (H&E) stain can identify many positive cases of H. pylori
        • special stain for H. pylori may be needed if H&E stain negative despite chronic active inflammation

Management

Management overview

  • Discontinue causative or exacerbating factors, such as nonsteroidal anti-inflammatory drugs or alcohol
  • Eradicate Helicobacter pylori Infection if identified
  • Medications for treatment of chronic gastritis
    • sucralfate has limited and inconsistent evidence
    • misoprostol may decrease symptoms of gastritis
    • pirenzepine (Gastrozepin) has limited, inconclusive evidence
    • ursodeoxycholic acid (Actigall) 1,000 mg/day may decrease symptoms of bile reflux gastritis.

Treatment of Helicobacter pylori infection

Treatment of nonspecific gastritis

  • Some medications appear to be have some effectiveness in nonspecific gastritis:
    • Sucralfate has limited and inconsistent evidence:
      • sucralfate and rabeprazole both reported to reduce dyspeptic symptoms compared to observation in postcholecystectomy patients with gastric bile reflux and chronic gastritis in randomized trial of 60 patients (Eur J Gastroenterol Hepatol 2003 Sep;15(9):975)
      • sucralfate no more effective than placebo or colloidal bismuth subcitrate for improving symptoms and less effective than colloidal bismuth subcitrate for endoscopic and histologic healing in randomized trial in 63 patients with H. pylori infection and nonulcer dyspepsia (Indian J Gastroenterol 1996 Jul;15(3):90)
      • sucralfate associated with improvement in symptoms at 1 month in randomized placebo-controlled trial of 151 patients with nonulcer dyspepsia, but symptomatic response primarily occurred in patients without gastritis (Am J Med 1987 Sep 28;83(3B):51)
    • Pirenzepine (Gastrozepin) has limited, inconclusive evidence for reduction of symptoms related to nonspecific gastritis:
      • neither pirenzepine 50 mg twice daily nor aluminum-magnesium antacid 120 mmol/day improved symptoms or histologic gastritis compared to placebo in randomized trial of 89 patients with nonulcer dyspepsia and erosive prepyloric changes (Gastroenterology 1988 Sep;95(3):619)
    • Surgery is generally not indicated in management of atrophic and nonatrophic gastritis uncomplicated by cancer or gastrointestinal hemorrhage.

Treatment of caustic gastritis

  • Patients with caustic gastritis who do not have oral intake are less likely to develop esophageal strictures than when given early feeding (Med Arh 2010;64(6):320)
  • treatment of chronic caustic gastritis usually surgical
    • management options include
      • jejunostomy may be provided to allow for nutritional support prior to surgery
      • total gastrectomy and Roux en Y esophagojejunostomy
      • partial gastrectomy and Roux en Y gastrojejunostomy
      • gastrojejunostomy
    • Reference - J Visc Surg 2011 Feb;148(1):59

Treatment of eosinophilic gastritis

  • Treatments
    • no large scale studies available
    • therapies proposed
      • elimination diets, analogous to management of eosinophilic esophagitis
      • elemental diets
      • systemic or topical steroids often effective in severe disease or in patients not responsive to dietary therapy
      • cromolyn, mast cell stabilizer
      • ketotifen, mast cell stabilizer and antihistamine (not available in United States)
      • suplatast, inhibits expression of Th-2 cytokines (not available in United States)
      • montelukast, leukotriene receptor antagonist
      • omalizumab, humanized anti immunoglobulin E (IgE) Ab
      • reslizumab and mepolizumab, humanized anti IL-5 antibodies
      • infliximab, anti-tumor necrosis factor (TNF) antibody
      • OC000459 is selective chemoattractant receptor homologous molecule Th-2 antagonist
    • Reference - Scand J Gastroenterol 2015;50(11):1309
    • see Eosinophilic esophagitis in adults for additional information

Treatment of granulomatous gastritis

  • In cases where granulomatous gastritis is secondary to an underlying problem, treatment of the underlying etiology has been recommended.
  • In case reports of idiopathic granulomatous gastritis, corticosteroids have been used in treatment, but dosing and length of treatment have not been established (Singapore Med J 2008 Sep;49(9):e222)

Treatment of portal hypertensive gastritis

  • Treatment of bleeding from PHG is analogous to management of portal hypertensive bleeding:
    • octreotide has been used off-label in management of bleeding from PHG (Clin Res Hepatol Gastroenterol 2016 Sep;40(4):373)
    • transjugular intrahepatic portosystemic shunt (TIPS) may be used for uncontrolled bleeding or bleeding associated with varices
    • see Acute variceal hemorrhage - treatment for additional information
    • nonselective beta blockade may prevent bleeding or rebleeding
    • TIPS and liver transplantation may prevent rebleeding
    • see Esophageal variceal hemorrhage - primary prophylaxis and Esophageal variceal hemorrhage - prevention of rebleeding for additional information

Treatment of radiation gastritis

Published: 25-06-2023 Updeted: 25-06-2023

References

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  5. Kim GH, Liang PS, Bang SJ, Hwang JH. Screening and surveillance for gastric cancer in the United States: Is it needed? Gastrointest Endosc. 2016 Jul;84(1):18-28
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  7. Gjeorgjievski M, Cappell MS. Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy. World J Hepatol. 2016 Feb 8;8(4):231-62
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  9. Rugge M, Genta RM; OLGA Group. Staging gastritis: an international proposal. Gastroenterology. 2005 Nov;129(5):1807-8, Gut 2007 May;56(5):631

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