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Gastritis
Miles C. Layton, DO
Matthew W. Short, MD, FAAFP
image BASICS
DESCRIPTION
  • Inflammation of the gastric mucosa with a spectrum of clinical findings
  • Patchy erythema of gastric mucosa
    • Common on endoscopy; usually insignificant
  • Erosive gastritis or reactive gastropathy
    • A reaction to mucosal injury by a noxious agent (especially NSAIDs or alcohol)
  • Reflux gastritis
    • A reaction to protracted reflux exposure to biliary and pancreatic fluid, usually associated with a pyloric defect
    • Typically limited to the prepyloric antrum
  • Hemorrhagic gastritis (stress ulceration)
    • A reaction to hemodynamic disorder (e.g., hypovolemia or hypoxia [as in shock])
    • Common in ICU patients, particularly after severe burns and trauma
    • Seen rarely with dabigatran (oral thrombin inhibitor)
  • Infectious gastritis
    • Commonly associated with Helicobacter pylori, colonizing organism in much of world's population
    • Viral infection, usually as a component of systemic infection, is common.
    • Significant infection by other microbes is rare.
  • Atrophic gastritis
    • Frequent in the elderly
    • Primarily from long-standing H. pylori infections
    • May be caused by prolonged PPI use
    • Major risk factor for gastric cancer
    • Associated with primary (pernicious) anemia
    • Autoimmune disease
  • Synonym(s): erosive gastritis; reflux gastritis; hemorrhagic gastritis; acute gastritis
Geriatric Considerations
Persons age >60 years often harbor H. pylori infection.
Pediatric Considerations
Gastritis rarely occurs in infants or children.
EPIDEMIOLOGY
  • Predominant age: all ages
  • Predominant sex: male = female
ETIOLOGY AND PATHOPHYSIOLOGY
  • Noxious agents cause a breakdown in the gastric mucosal barrier, leaving the epithelial cells unprotected.
  • Infection: H. pylori (most common cause), Staphylococcus aureus exotoxins, and viral infection
  • Alcohol
  • Aspirin and other NSAIDs
  • Bile reflux
  • Pancreatic enzyme reflux
  • Portal hypertensive (HTN) gastropathy
  • Emotional stress
Genetics
Unknown, but observational studies show that 10% of a given population is never colonized with H. pylori, regardless of exposure. Genetic variations in TLR1 may help explain some of this observed variation in individual risk for H. pylori infection.
RISK FACTORS
  • Age >60 years
  • Exposure to potentially noxious drugs or chemicals (e.g., alcohol or NSAIDs)
  • Hypovolemia, hypoxia (shock), burns, head injury, complicated postoperative course
  • Autoimmune diseases (thyroid disease and diabetes)
  • Family history of H. pylori and/or gastric cancer
  • Stress (hypovolemia or hypoxia)
  • Tobacco use
  • Radiation
  • Ischemia
  • Pernicious anemia
  • Gastric mucosal atrophy
GENERAL PREVENTION
  • Avoid injurious drugs or chemical agents.
  • Patients with hypovolemia or hypoxia (especially patients confined to an intensive care ward) should receive prophylactic antacid therapy.
  • In ICU patients (particularly burn and trauma), H2 receptor antagonists, prostaglandins, or sucralfate commonly used for gastric mucosal protection
  • Consider testing for H. pylori (and eradicating if present) in patients on long-term NSAID therapy.
COMMONLY ASSOCIATED CONDITIONS
  • Gastric or duodenal peptic ulcer
  • Primary (pernicious) anemia—atrophic gastritis
  • Portal HTN, hepatic failure
  • Gastric lymphoma linked to lymphoid follicles
image DIAGNOSIS
PHYSICAL EXAM
  • Assess vital signs. Abdominal exam often normal
  • Mild epigastric tenderness
  • May have heme-positive stool
  • Stool may be black in color.
  • Examine for stigmata of chronic alcohol abuse.
DIFFERENTIAL DIAGNOSIS
  • Functional abdominal pain (dyspepsia)
  • Peptic ulcer disease
  • Viral gastroenteritis
  • Pancreatic disease
  • Gastric cancer (elderly)
  • Cholecystitis
  • Pancreatic disease (inflammation vs. tumor)
DIAGNOSTIC TESTS & INTERPRETATION
Initial Tests (lab, imaging)
  • Usually normal
  • CBC to evaluate for blood loss/anemia
  • 13C-urea breath test for H. pylori
    • 95% specifity and sensitivity
  • H. pylori, serology serum IgG
    • Inexpensive
    • 85% sensitivity, 79% specifity
    • Positive in history of colonization or prior infections, therefore, cannot be used to assess eradication
  • Stool analysis for fecal H. pylori antigen
    • 95% specifity and sensitivity
  • Gastric acid analysis may be abnormal but is not a reliable indicator of gastritis.
  • Low serum pepsinogen I (PG I) relative to PG II is associated with fundal intestinal metaplasia.
  • Drugs that may alter lab results: Antibiotics or PPIs may affect urea breath test for H. pylori.
    • Hold PPIs for 2 weeks, H2 receptor antagonists for 24 hours, and antibiotics for 4 weeks prior to stool or breath tests (1,2)[C].
Follow-Up Tests & Special Considerations
Endoscopy for H. pylori
  • Culture; polymerase chain reaction (PCR); histology; rapid urease testing
Diagnostic Procedures/Other
  • Gastroscopy with biopsy allows for a precise diagnosis and is a first-line diagnostic tool in:
    • Age >55 years with new-onset signs and symptoms
    • Weight loss, persistent vomiting, or GI bleed (1)[C]
  • Biopsies (multiple) in both body and antrum recommended if there is a poor response to the initial treatment (3)[C],(4)[B]. Patient must discontinue PPIs for 2 weeks prior to endoscopy to improve accuracy of result.
Test Interpretation
Acute or chronic inflammatory infiltrate in gastric mucosa, often with distortion or erosion of adjacent epithelium. Presence of H. pylori often confirmed
image TREATMENT
GENERAL MEASURES
  • Treatment of H. pylori is required to relieve symptoms.
  • Parenteral fluid and electrolyte supplements if oral intake is compromised.
  • Consider discontinuing NSAIDs.
  • Encourage alcohol and smoking cessation.
  • Endoscopy indicated for patients not responsive to treatment
MEDICATION
First Line
  • Antacids: best given in liquid form, 30 mL 1 hour after meals and at bedtime; useful mainly as an emollient
  • H2 receptor antagonists (e.g., cimetidine [Tagamet]): oral cimetidine 300 mg q6h (or ranitidine [Zantac] 150 mg BID or famotidine [Pepcid] 20 mg BID or nizatidine [Axid])150 mg BID not shown to be clearly superior to antacids
  • Sucralfate (Carafate): 1 g q4-6h on an empty stomach; rationale uncertain but empirically helpful
  • Prostaglandins (misoprostol [Cytotec]): can help allay gastric mucosal injury; suggested dosage 100 to 200 &mgr;g QID
  • P.399

  • PPIs can be used if there is no response to antacids or H2 receptor blockers (e.g. omeprazole 20 mg daily or BID or esomeprazole 20 mg daily or BID)
  • H. pylori eradication
    • Clarithromycin triple therapy (CTT)
      • A short-course therapy (10 to 14 days) of amoxicillin 1 g BID, standard dose PPI BID (omeprazole 20 mg BID, etc.), and clarithromycin 500 mg BID (1,2,5)[A]
      • 70-85% eradication
      • Optimal treatment still undefined.
      • IF PCN ALLERGIC: Substitute amoxicillin with metronidazole 500 mg BID.
    • Bismuth quadruple therapy (BQT)
      • PPI (omeprazole 20 mg) BID plus bismuth (Pepto-Bismol) 30 mL liquid or 2 tablets QID plus metronidazole 250 mg QID plus tetracycline 500 mg QID for 10 to 14 days (1,2,5,6)[A]
      • 75-90% eradication
      • Use as initial therapy in areas of high clarithromycin resistance (>15%).
      • Consider in penicillin-allergic patients.
  • H. pylori alternative treatment: Consider sequential antibiotic therapy with standard dose PPI (i.e., omeprazole 20 mg) and amoxicillin 1 g BID for 5 days followed by clarithromycin 500 mg and tinidazole 500 mg BID with standard dose PPI (omeprazole 20 mg) BID for 5 days. Some studies show it works just as well or better than triple therapy (1,2)[B],(5)[A].
  • H. pylori treatment failure: use a different regimen, avoiding clarithromycin (unless resistance testing confirms susceptibility):
    • BQT for 7 to 14 days (1,2,5)[A]
    • Consider levofloxacin 250 mg BID, amoxicillin 1 g BID, and standard dose PPI BID for 14 days in those who fail two attempts (1,2,5)[A].
  • Consider probiotics in known symptomatic H. pylori, to decrease the density of H. pylori in the gastric antrum and body, decrease severity of gastritis, peptic ulcers, and possibly slow the progression toward atrophic gastritis and gastric adenocarcinoma (7)[A],(8)[C],(9)[A].
    • Probiotics alone likely do not eradicate H. pylori.
  • Contraindications: hypersensitivity
  • Precautions:
    • If bismuth is prescribed, warn the patient about the side effect of stool becoming black.
    • Refer to the manufacturer's profile of each drug.
  • Significant possible interactions: Refer to the manufacturer's profile of each drug.
INPATIENT CONSIDERATIONS
Gastritis may occur in ICU patients.
Admission Criteria/Initial Stabilization
Outpatient, except for severe hemorrhagic gastritis
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Usually no restrictions
  • Confirm H. pylori eradication in patients with:
    • Gastric ulcer
    • Persistent dyspepsia despite treatment
    • H. pylori associated mucosa-associated lymphoid tissue (MALT) lymphoma
    • History of resection of gastric cancer
Patient Monitoring
  • Repeat gastroscopy after 6 weeks if gastritis was severe or if patient has a poor treatment response.
  • Surveillance gastroscopy every 3 to 5 years in patients with atrophic gastritis in both the antrum and body; within 1 year for patients with low-grade dysplasia, (with extensive biopsy sampling); 6 and 12 months in patients with high-grade dysplasia (4)[B]
DIET
Restrictions, if any, depend on symptom severity (e.g., bland, light, soft foods); avoid caffeine and spicy foods and alcohol.
PATIENT EDUCATION
  • Smoking cessation; limit alcohol
  • Dietary changes
  • Relaxation therapy
  • Avoid NSAIDs as possible
PROGNOSIS
  • Most cases clear spontaneously when the cause has been identified and treated.
  • Recurrence of H. pylori infection requires a repeated course of treatment.
REFERENCES
1. McColl KE. Clinical practice. Helicobacter pylori infection. N Engl J Med. 2010;362(17):1597-1604.
2. Chey WD, Wong BC; Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102(8):1808-1825.
3. Hirota WK, Zuckerman MJ, Adler DG, et al. ASGE guideline: the role of endoscopy in the surveillance of premalignant conditions of the upper GI tract. Gastrointest Endosc. 2006;63(4):570-580.
4. Dinis-Ribeiro M, Areia M, de Vries AC, et al. Management of precancerous conditions and lesions in the stomach (MAPS): guideline from the European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter Study Group (EHSG), European Society of Pathology (ESP), and the Sociedade Portuguesa de Endoscopia Digestiva (SPED). Endoscopy. 2012;44(1):74-94.
5. Malfertheiner P, Megraud F, O'Morain CA, et al. Management of Helicobacter pylori infection—the Maastricht IV/Florence Consensus report. Gut. 2012;61(5):646-664.
6. Venerito M, Krieger T, Ecker T, et al. Meta-analysis of bismuth quadruple therapy versus clarithromycin triple therapy for empiric primary treatment of Helicobacter pylori infection. Digestion. 2013;88(1):33-45.
7. Patel A, Shah N, Prajapati JB. Clinical application of probiotics in the treatment of Helicobacter pylori infection—a brief review. J Microbiol Immunol Infect. 2014;47(5):429-437.
8. Emara MH, Elhawari SA, Yousef S, et al. Emerging role of probiotics in the management of Helicobacter pylori infection: histopathologic perspectives [published online ahead of print May 22, 2015]. Helicobacter. 2015:1-8.
9. Ruggiero P. Use of probiotics in the fight against Helicobacter pylori. World J Gastrointest Pathophysiol. 2014;5(4):384-391.
Additional Reading
&NA;
  • El-Zimaity H, Serra S, Szentgyorgyi E, et al. Gastric biopsies: the gap between evidence-based medicine and daily practice in the management of gastric Helicobacter pylori infection. Can J Gastroenterol. 2013;27(10):e25-e30.
  • Eslami L, Nasseri-Moghaddam S. Meta-analyses: does long-term PPI use increase the risk of gastric premalignant lesions? Arch Iran Med. 2013;16(8):449-458.
  • Graham DY, Rimbara E. Understanding and appreciating sequential therapy for Helicobacter pylori eradication. J Clin Gastroenterol. 2011;45(4):309-313.
  • Lanza FL, Chan FK, Quigley EM, et al. Guidelines for prevention of NSAID-related ulcer complications. Am J Gastroenterol. 2009;104(3):728-738.
Codes
&NA;
ICD10
  • K29.70 Gastritis, unspecified, without bleeding
  • K29.71 Gastritis, unspecified, with bleeding
  • K29.00 Acute gastritis without bleeding
Clinical Pearls
&NA;
  • H. pylori is the most common cause of gastritis.
  • >50% of adult patients are colonized with H. pylori.
  • H. pylori antibodies decline in the year after treatment and should not be used to determine eradication. H. pylori antibody titers rise significantly with reinfection.
  • H. pylori stool antigen tests can be used before and after therapy to assess for eradication and reinfection.
  • Several courses of rescue therapy may be necessary to eradicate H. pylori.
  • Discontinue PPIs 2 weeks prior to endoscopy to improve diagnostic accuracy in cases of suspected gastritis.
  • Consider probiotics as adjunct treatment in symptomatic H. pylori gastritis.