H.pylori gastritis pathophysiology: Difference between revisions
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*The major diagnostic feature of chronic gastritis is an influx of lymphocytes and plasma cells (normally the antral mucosa is devoid of plasma cells and lymphocytes). Hence the presence of these cells is indicative of gastritis. | *The major diagnostic feature of chronic gastritis is an influx of lymphocytes and plasma cells (normally the antral mucosa is devoid of plasma cells and lymphocytes). Hence the presence of these cells is indicative of gastritis. | ||
*H.pylori colonizes more in the antrum than the corpus. Hence there is increased inflammatory cell infiltration in the antrum. | *H.pylori colonizes more in the antrum than the corpus. Hence there is increased inflammatory cell infiltration in the antrum. | ||
*The | *The direct acting antigens of H pylori like lipopolysaccharides, urease etc along with interleukins 1 and 6, activate T-helper cells which produce variety of cytokines including IL4, IL5 and IL6. | ||
*However, this immune response | *These interluekins differentiate into plasma cells releasing cytokines and anti-H.pylori infection like IgM-opsonizing and complement-fixing antibodies. | ||
*The main role of the mucosa immune response is taht the IgA prevents bacterial adhesion and IgG causes opsonisation and complement activation. | |||
*Due to acidic environment, the antibodies produced quickly lose their adhesive properties and catalase produced by H.pylori protects against polymorphs. | |||
*However, this immune response is insufficient to eradicate the organism leading to development of immune response directed towards preventing the damaging effects of the H.pylori. | |||
*Hence the persistent antigenic stimulation leads to formation of follicles, which is the consistent feature of chronic H.pylori infection. | |||
=='''Updated Sydney classification (Sydney criteria for gastritis)'''== | =='''Updated Sydney classification (Sydney criteria for gastritis)'''== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
Pathophysiology
The H.pylori induced gastritis includes the following stages: They are
- The acute gastritis
- Active chronic gastritis
- Atrophy
- Intestinal metaplasia
The acute gastritis
- In majority of patients, the initial acute phase of gastritis is subclinical (does not often give rise to clinical symptoms) 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]
pathogenesis
- Following transmission, H.pylori penetrates the mucous layer of stomach and multiplies close to the surface epithelial cells.
- Following adhesion to epithelial cells, the bacteria releases lipopolysaccharides (endotoxin) and chemotactic mediators which penetrate the surface epithelial cells.[2]Crabtree, J. E. "Gastric mucosal inflammatory responses to Helicobacter pylori." Alimentary pharmacology & therapeutics 10.Sup1 (1996): 29-37.
- These bacterial factors attract the polymorphonuclear leukocytes to the site of infection and also caused mast cell degranulation, which releases acute inflammatory mediators. Mast cell degranulation leads to:
- Increased vascular permeability
- Increased polymorph emigration
- Increased expression of leukocyte adhesion molecules
- The platelet activating factors (PAF) released from mast cells causes microthrombosis in mucosal capillaries resulting in hypoxic injury to the epithelium
- The macrophages release IL-1 and tumor necrosis factor alpha (TNF-α) which stimulates gastric epithelium to produce IL-8.
- The acute phase is associated with profound hypochlorhydria and a decreased ascorbic acid secretion into the gastric juice.[3]
- The acid output reaches pre-infection levels after several weeks but the ascorbic acid remains lower than normal for the duration of chronic gastritis, indicating that it is due to persisting inflammation rather than hypochlorhydria.[3]
Histology
- Surface epithelial degeneration
- Increased cell exfoliation
- Increased neutrophil polymorphonuclear leucocytes in the superficial lamina propria
The active chronic gastritis
In majority of cases, the h.pylori infection persists leading to accumulation of large number chronic inflammatory cells leading to active chronic gastritis.
pathogenesis
- The major diagnostic feature of chronic gastritis is an influx of lymphocytes and plasma cells (normally the antral mucosa is devoid of plasma cells and lymphocytes). Hence the presence of these cells is indicative of gastritis.
- H.pylori colonizes more in the antrum than the corpus. Hence there is increased inflammatory cell infiltration in the antrum.
- The direct acting antigens of H pylori like lipopolysaccharides, urease etc along with interleukins 1 and 6, activate T-helper cells which produce variety of cytokines including IL4, IL5 and IL6.
- These interluekins differentiate into plasma cells releasing cytokines and anti-H.pylori infection like IgM-opsonizing and complement-fixing antibodies.
- The main role of the mucosa immune response is taht the IgA prevents bacterial adhesion and IgG causes opsonisation and complement activation.
- Due to acidic environment, the antibodies produced quickly lose their adhesive properties and catalase produced by H.pylori protects against polymorphs.
- However, this immune response is insufficient to eradicate the organism leading to development of immune response directed towards preventing the damaging effects of the H.pylori.
- Hence the persistent antigenic stimulation leads to formation of follicles, which is the consistent feature of chronic H.pylori infection.
Updated Sydney classification (Sydney criteria for gastritis)
The updated sydney classification of H.pylori induced classification include:[4]
| Feature | Non-atrophic
Helicobacter |
Atrophic Helicobacter | Autoimmune |
|---|---|---|---|
| Inflammation pattern | Antral or diffuse | Antrum & corpus, mild inflammation | Corpus only |
| Atrophy & metaplasia | Nil | Atrophy present, metaplasia at incisura | Corpus only |
References
- ↑ 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.
- ↑ 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.
- ↑ 3.0 3.1 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.
- ↑ 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.