H.pylori peptic ulcer disease pathophysiology: Difference between revisions
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'''Gastric metaplasia''' | '''Gastric metaplasia''' | ||
*H.pylori causes hypergastrinemia and increased sensitivity to gastrin. | *H.pylori causes hypergastrinemia and increased sensitivity to gastrin. | ||
*Gastric metaplasia (the presence of gastric-type mucus secreting cells in the surface epithelium of the duodenum) occurs as a part of host defence mechanism to protect against the repeated injury caused by arrival of unneutralized acid in the first part of duodenum. | *Gastric metaplasia (the presence of gastric-type mucus secreting cells in the surface epithelium of the duodenum) occurs as a part of host defence mechanism to protect against the repeated injury caused by arrival of unneutralized acid in the first part of duodenum.<ref name="pmid2617162">{{cite journal| author=Kreuning J, vd Wal AM, Kuiper G, Lindeman J| title=Chronic nonspecific duodenitis. A multiple biopsy study of the duodenal bulb in health and disease. | journal=Scand J Gastroenterol Suppl | year= 1989 | volume= 167 | issue= | pages= 16-20 | pmid=2617162 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2617162 }} </ref><ref name="pmid8730266">{{cite journal| author=Walker MM, Dixon MF| title=Gastric metaplasia: its role in duodenal ulceration. | journal=Aliment Pharmacol Ther | year= 1996 | volume= 10 Suppl 1 | issue= | pages= 119-28 | pmid=8730266 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8730266 }} </ref> | ||
*In response to inflammatory process following arrival of unneutralized acid into duodenum, in the goblet cells transforms to gastric phenotype cells.<ref name="pmid2617162">{{cite journal| author=Kreuning J, vd Wal AM, Kuiper G, Lindeman J| title=Chronic nonspecific duodenitis. A multiple biopsy study of the duodenal bulb in health and disease. | journal=Scand J Gastroenterol Suppl | year= 1989 | volume= 167 | issue= | pages= 16-20 | pmid=2617162 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2617162 }} </ref> | *In response to inflammatory process following arrival of unneutralized acid into duodenum, in the goblet cells transforms to gastric phenotype cells.<ref name="pmid2617162">{{cite journal| author=Kreuning J, vd Wal AM, Kuiper G, Lindeman J| title=Chronic nonspecific duodenitis. A multiple biopsy study of the duodenal bulb in health and disease. | journal=Scand J Gastroenterol Suppl | year= 1989 | volume= 167 | issue= | pages= 16-20 | pmid=2617162 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2617162 }} </ref> | ||
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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
- H.pylori is closely associated with both duodenal and gastric ulcers.[1]
- The estimated lifetime risk for the development of peptic ulcer disease is 10-20%, in patients with H.pylori infection.
- H.pylori can be diagnosed in 60-100% of gastric ulcer patients and 90-100% in duodenal ulcer patients.
Duodenal Ulceration
- The patients with higher gastric acid secretion have increased risk of developing duodenal ulcers compared to normal, healthy individuals.
- The most important requirements for the development of duodenal ulceration are:
- Gastric metaplasia in the proximal duodenum
- Active chronic duodenitis
Pathogenesis
Gastric metaplasia
- H.pylori causes hypergastrinemia and increased sensitivity to gastrin.
- Gastric metaplasia (the presence of gastric-type mucus secreting cells in the surface epithelium of the duodenum) occurs as a part of host defence mechanism to protect against the repeated injury caused by arrival of unneutralized acid in the first part of duodenum.[2][3]
- In response to inflammatory process following arrival of unneutralized acid into duodenum, in the goblet cells transforms to gastric phenotype cells.[2]
Active chronic duodenitis
- The gastric metaplasia provides appropriate site for H.pylori to colonize, giving rise to chronic inflammation.
References
- ↑ Kuipers EJ, Thijs JC, Festen HP (1995). "The prevalence of Helicobacter pylori in peptic ulcer disease". Aliment Pharmacol Ther. 9 Suppl 2: 59–69. PMID 8547530.
- ↑ 2.0 2.1 Kreuning J, vd Wal AM, Kuiper G, Lindeman J (1989). "Chronic nonspecific duodenitis. A multiple biopsy study of the duodenal bulb in health and disease". Scand J Gastroenterol Suppl. 167: 16–20. PMID 2617162.
- ↑ Walker MM, Dixon MF (1996). "Gastric metaplasia: its role in duodenal ulceration". Aliment Pharmacol Ther. 10 Suppl 1: 119–28. PMID 8730266.