H.pylori gastritis pathophysiology

Jump to navigation Jump to search

Helicobacter pylori infection Microchapters


Patient Information


Historical Perspective



Peptic ulcer disease
Gastric adenocarcinoma
MALT lymphoma


Differentiating Helicobacter pylori infection from other Diseases

Epidemiology and Demographics

Risk Factors


Natural History, Complications and Prognosis


Guideline Recommendation

ACG guidelines
ESPGHAN and NASPGHAN guidelines

History and Symptoms

Physical Examination

Diagnostic tests

Endoscopic tests
Nonendoscopic tests


X Ray




Other Diagnostic Studies


Medical Therapy


Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

H.pylori gastritis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides


American Roentgen Ray Society Images of H.pylori gastritis pathophysiology

All Images
Echo & Ultrasound
CT Images

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on H.pylori gastritis pathophysiology

CDC on H.pylori gastritis pathophysiology

H.pylori gastritis pathophysiology in the news

Blogs on H.pylori gastritis pathophysiology

Directions to Hospitals Treating Helicobacter pylori infection

Risk calculators and risk factors for H.pylori gastritis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]


The H. pylori induced gastritis includes the following stages. They are acute gastritis, active chronic gastritis, atrophy and intestinal metaplasia.


  • Antral predominant gastritis
  • Corpus predominant gastritis

The acute gastritis

  • In the majority of patients, the initial acute phase of gastritis is subclinical and is of short duration (about 7 to 10 days).
  • The organisms are spontaneously cleared in a small minority of people, especially in childhood.
  • In the majority of cases, the infection is not eliminated and there will be gradual accumulation of chronic inflammatory cells over the next 3 or 4 weeks.[1]


Microscopic pathology

Active chronic gastritis

In the majority of cases, the H. pylori infection persists leading to accumulation of large number chronic inflammatory cells leading to active chronic gastritis.


Also, these polymorphs accumulate around the pit isthmus, which is a proliferative compartment, causing lethal damage to stem cells resulting in glandular atrophy.

Microscopic pathology

Sydney system of grading of chronic gastritis[6]

Feature Definition Grading guidelines
Chronic inflammation Increased lymphocytes and plasma cells in lamina propria
  • Mild, moderate or severe increase in density
Activity Neutrophilic infiltrates of the lamina propria, pits or surface epithelium
  • Mild: less than one-third of pits and surface infiltrated
  • Moderate: one-third to two-thirds
  • Severe: more than two-thirds
Atrophy Loss of specialized glands from either antrum or corpus
  • Mild, moderate, or severe loss
Helicobacter pylori H. pylori density
  • Mild colonization: scattered organisms covering less than one-third of the surface
  • Moderate colonization: intermediate numbers
  • Severe colonization: large clusters or a continuous layer over two-thirds of surface
Intestinal Metaplasia Intestinal metaplasia of the epithelium
  • Mild: less than one-third of mucosa involved
  • Moderate: one-third to two-thirds
  • Severe: more than two-thirds


Atrophy of stomach is defined as loss of glandular tissue due to continuous mucosal injury. This leads to thinning of gastric mucosa.


  • The continuous mucosal injury due to long-standing H. pylori infection, leads to atrophy of stomach.
  • This continuous pathological process results in erosion or ulceration of the mucosa leading to the destruction of the glandular layer and followed by fibrous replacement.
  • The destruction of the glandular basement membrane and the sheath of supporting cells prevents orderly regeneration. This uneven regeneration follows a divergent differentiation pathway producing metaplastic glands (pseudo-pyloric appearance) which are composed of cells of the 'ulcer-associated cell lineage'(UACL).[8]

Microscopic pathology

Intestinal metaplasia

  • The intestinal metaplasia increase in prevalence according to duration of H. pylori infection.[9]
  • The damaged epithelium by H. pylori infection will be further eroded by bile reflux and replaced by intestinal type cells during the regenerative process. This metaplasia is transient but with repetitive injury it aggravates and become more permanent.[10]
  • Hence H. pylori infection and bile reflux are independent risk factors for intestinal metaplasia of stomach.
  • Intestinal metaplasia is a protective mechanism as H. pylori does not attach to intestinal-type cells and also intestinal cells are more resistant to damaging effects of bile than gastric mucosa.

Microscopic pathology

Updated Sydney classification (Sydney criteria for gastritis)

The updated sydney classification of H. pylori induced classification include:[6]

Feature Non-atrophic


Atrophic Helicobacter Autoimmune
Inflammation pattern Antral or diffuse Antrum & corpus, mild inflammation Corpus only
Atrophy & metaplasia Nil Atrophy present, metaplasia at incisura Corpus only
Antral predominant gastritis Corpus predominant gastritis
More predominant in antrum in developed countries Less predominant in developed countries
High acid output Low acid output
Associated with duodenal ulceration


  1. Sobala GM, Crabtree JE, Dixon MF, Schorah CJ, Taylor JD, Rathbone BJ; et al. (1991). "Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations". Gut. 32 (11): 1415–8. PMC 1379180. PMID 1752479.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  2. Slomiany BL, Piotrowski J, Slomiany A (1998). "Induction of caspase-3 and nitric oxide synthase-2 during gastric mucosal inflammatory reaction to Helicobacter pylori lipopolysaccharide". Biochem Mol Biol Int. 46 (5): 1063–70. PMID 9861460.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  3. Crabtree JE (1996). "Gastric mucosal inflammatory responses to Helicobacter pylori". Aliment Pharmacol Ther. 10 Suppl 1: 29–37. PMID 8730257.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  4. 4.0 4.1 Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF; et al. (1993). "Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations". Gut. 34 (8): 1038–41. PMC 1374349. PMID 8174949.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  5. Genta RM, Hamner HW, Graham DY (1993). "Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy". Hum Pathol. 24 (6): 577–83. PMID 8505036.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  6. 6.0 6.1 Dixon MF, Genta RM, Yardley JH, Correa P (1996). "Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994". Am J Surg Pathol. 20 (10): 1161–81. PMID 8827022.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  7. Neithercut WD, Milne A, Chittajallu RS, el Nujumi AM, McColl KE (1991). "Detection of Helicobacter pylori infection of the gastric mucosa by measurement of gastric aspirate ammonium and urea concentrations". Gut. 32 (9): 973–6. PMC 1379031. PMID 1916500.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  8. Pera M, Heppell J, Poulsom R, Teixeira FV, Williams J (2001). "Ulcer associated cell lineage glands expressing trefoil peptide genes are induced by chronic ulceration in ileal pouch mucosa". Gut. 48 (6): 792–6. PMC 1728308. PMID 11358897.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  9. Craanen ME, Blok P, Dekker W, Ferwerda J, Tytgat GN (1992). "Subtypes of intestinal metaplasia and Helicobacter pylori". Gut. 33 (5): 597–600. PMC 1379284. PMID 1612473.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  10. Walker MM (2003). "Is intestinal metaplasia of the stomach reversible?". Gut. 52 (1): 1–4. PMC 1773527. PMID 12477745.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>