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Stomach

Infections

Helicobacter pylori gastritis


Reviewers: Elliot Weisenberg, M.D. (see Reviewers page)
Revised: 6 August 2012, last major update August 2012
Copyright: (c) 2003-2012, PathologyOutlines.com, Inc.

General
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● Chronic infection in approximately 2/3 of population worldwide, prevalence is decreasing due to improved sanitation and antibiotic use
● Prevalence in developing countries up to 90% where infection usually occurs in childhood
● In industrialized countriesm infection typically (not always) occurs in adulthood, prevalance 20-30% by age 50
● Without treatment, infection usually lifelong
● Infection usually asymptomatic
● Infection conveys 15-20% lifetime risk of peptic ulcer disease
● Linked to 70% of gastric cancer, especially intestinal type, and most gastric lymphoma
● Atrophy with concomitant intestinal metaplasia and dysplasia are seedbed for carcinoma
● Acquired mucosal associated lymphoid tissue is seedbed for H. pylori associated gastric lymphoma
● In children in Colombia, with higher risk for gastric cancer, have more several gastric injury and less regenerative capacity - more infiltration of neutrophils and lymphocytes, more mucus depletion, higher H. pylori density; more CD8+ T cells and macrophages, fewer B cells (Hum Pathol 2003;34:206)
● Bacterial toxins (cagA, VacA, urease, ammonia, acetaldehyde, phospholipases) are toxic to epithelial cells
● Mast cells release platelet activating factor, disturb microcirculation, cause ischemia, erosions
● Different strains of H. pylori have different potential for carcinogenesis (Gastroenterology 2003;125:1636)

Patterns of inflammation
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● Non-atrophic antral predominant gastritis: most common in developed world, normal to elevated acid secretion, estimated 20% lifetime risk of duodenal ulcer
● Non-atrophic corpus predominant gastritis: associated with proton pump inhibitor use
● Non-atrophic pangastritis: frequent in areas with poor sanitation
● Antrum restricted atrophic gastritis: usually in West, may be early multifocal atrophic gastritis
● Multifocal atrophic gastritis: most advanced stage, more prevalent, but not exclusive to areas with poor sanitation (Best Pract Res Clin Gastroenterol 2007;21:205)

H. pylori characteristics
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● Non-spore forming, curvilinear gram negative rod, 3.5 x 0.5 microns
● Has adapted to niche provided by gastric mucus by motility (flagella) to swim through viscous mucous, urease to buffer gastric acid, adhesin to bind to gastric epithelial cells (better binding with cells that express type O antigen)
H. pylori sits on surface or in lumen, needs acid to survive, otherwise urease causes pH to be too high
● More inflammation in H. pylori gastritis than NSAID gastritis

Treatment
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● Usually antibiotics
● Post-treatment, chronic inflammation persists, but neutrophils, reactive epithelial changes, erosions, ulcers dissipate quickly
● Takes months/years for elimination of low grade MALT, lymphoid follicles, atrophy, metaplasia
● Incidence of antibiotic resistance is increasing, work is ongoing to develop vaccine (Gastroenterology 2007;133:288)
● Can test for mutations associated with antibiotic resistance (Arch Pathol Lab Med 2001;125:493)

Gross description
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● Red mucosa, coarser texture than normal, may have thickened rugal folds or thin/flat mucosa
● With long term disease, mucosa may be thin/flat
● Usually affects antrum (particularly in children, Hum Pathol 2002;33:1133) and cardia

Micro description
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● Bacteria is curved, spirochete-like, in superficial mucus layer and along microvilli of epithelial cells
● Invasion is unusual, proton pump inhibitor use may increase risk of invasion (Gastroenterology 2007:132;1009, Gastroenterology 2007:132;1177)
● Usually not seen in areas of intestinal metaplasia
● Associated with chronic inflammatory infiltrate with germinal centers (follicular gastritis) and plasma cells in lamina propria
● Active inflammation if neutrophils in glandular or surface epithelial layer, presence of active inflammation after eradication therapy is sign of treatment failure
● Antibiotics may cause H. pylori to assume coccoid appearance
● Presence of follicles is strongly associated with H. pylori, the density of follicles is highest in the angulus, the most common site of gastric lymphoma and lowest in the proximal greater curvature, where incidicence of H. pylori induced gastric lymphoma is lowest (Arch Pathol Lab Med 1994;118:740)
● Chronic proton inhibitor use without antibiotics leads to relatively decreased inflammation in the antrum and increased inflammation in the body with decreased numbers of microorganisms
Regenerative change: enlarged, hyperchromatic nuclei in surface epithelial cells, with diminished mucus vacuoles and frequent mitotic figures
● Acute infection associated with erosions, ulcers, hemorrhage

Micro images
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Various images

Positive stains
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● 70% of cases seen on H&E, Giemsa, Warthin-Starry, Thiazine, Diff-Quik, HP Blue/HP Yellow, immunohistochemistry
● IHC may be especially useful to detect coccoid forms and cases with low numbers of microorganisms

End of Stomach > Infections > Helicobacter pylori gastritis


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