H.pylori gastritis pathophysiology: Difference between revisions
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*The acute phase is associated with profound hypochlorhydria and a decreased ascorbic acid secretion into the gastric juice.<ref name="pmid8174949">{{cite journal| author=Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF et al.| title=Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. | journal=Gut | year= 1993 | volume= 34 | issue= 8 | pages= 1038-41 | pmid=8174949 | doi= | pmc=1374349 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174949 }} </ref> | *The acute phase is associated with profound hypochlorhydria and a decreased ascorbic acid secretion into the gastric juice.<ref name="pmid8174949">{{cite journal| author=Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF et al.| title=Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. | journal=Gut | year= 1993 | volume= 34 | issue= 8 | pages= 1038-41 | pmid=8174949 | doi= | pmc=1374349 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174949 }} </ref> | ||
*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.<ref name="pmid8174949">{{cite journal| author=Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF et al.| title=Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. | journal=Gut | year= 1993 | volume= 34 | issue= 8 | pages= 1038-41 | pmid=8174949 | doi= | pmc=1374349 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174949 }} </ref> | *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.<ref name="pmid8174949">{{cite journal| author=Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF et al.| title=Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. | journal=Gut | year= 1993 | volume= 34 | issue= 8 | pages= 1038-41 | pmid=8174949 | doi= | pmc=1374349 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174949 }} </ref> | ||
<small>Histology</small> | |||
*Surface epithelial degeneration | |||
*Increased cell exfoliation | |||
*Increased neutrophil polymorphonuclear leucocytes in the superficial lamina propria | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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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 phase
- Active chronic gastritis
- Atrophy
- Intestinal metaplasia
The acute phase
- In majority of patients, the initial acute phase of gastritis is subclinical and is of short duration.
- 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 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 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
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.