H.pylori peptic ulcer disease pathophysiology
|
Helicobacter pylori infection Microchapters |
|
Differentiating Helicobacter pylori infection from other Diseases |
|---|
|
Diagnosis |
|
Guideline Recommendation |
|
Treatment |
|
Case Studies |
|
H.pylori peptic ulcer disease pathophysiology On the Web |
|
American Roentgen Ray Society Images of H.pylori peptic ulcer disease pathophysiology |
|
Directions to Hospitals Treating Helicobacter pylori infection |
|
Risk calculators and risk factors for H.pylori peptic ulcer disease pathophysiology |
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 causes upto 90% of duodenal ulcers and 60-80% of gastric ulcers.
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
The three stages in the pathogenesis of duodenal ulcer include:[2]
- Gastric metaplasia
- Active chronic duodenitis
- Ulceration
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.[3][4]
- In response to inflammatory process following arrival of unneutralized acid into duodenum, in the goblet cells transforms to gastric phenotype cells.[3]
Active chronic duodenitis
- The gastric metaplasia provide sites for H.pylori to colonize, passing through the duodenum. The organism do not colonize the native duodenal epithelial cells.[4]
- After colonization, H.pylori stimulates an active chronic inflammatory response similar to that seen in the gastric mucosa.
Ulceration
- Due to gastric metaplasia, the pH of the duodenal mucosa alters.[2]
- This along with chronic inflammation and direct bacterial effects on epithelium, the duodenal mucosa is more susceptible to acid attack leading to ulcer formation.
Gastric ulceration
- The bacteria either proliferates maximally at the transitional zone because of the favorable local environment( optimal pH) or generates inflammatory products due to induction of stress proteins.
- Hence it is an optimal site for adhesion, growth and release of inflammatory products and cytokine release.
- The maximal development of atrophy and intestinal metaplasia occurs at this site and is at greatest risk of ulceration.
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 Wyatt JI, Rathbone BJ, Dixon MF, Heatley RV (1987). "Campylobacter pyloridis and acid induced gastric metaplasia in the pathogenesis of duodenitis". J Clin Pathol. 40 (8): 841–8. PMC 1141122. PMID 3654985.
- ↑ 3.0 3.1 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.
- ↑ 4.0 4.1 Walker MM, Dixon MF (1996). "Gastric metaplasia: its role in duodenal ulceration". Aliment Pharmacol Ther. 10 Suppl 1: 119–28. PMID 8730266.