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Helicobacter pylori–associated gastropathy
Sunday 4 March 2012
Helicobacter pylori–related gastric pathology
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HP gastritis
Following HP infection the mucosa may become inflamed producing acute gastritis and then chronic active gastritis.
Early, the chronic inflammation remains confined to the superficial mucosa.
Superficial lamina propria lymphoplasmacytosis then extends for variable distances into the glandular compartment.
With time, the inflammation becomes confluent until it occupies the full thickness of the mucosa.
T cells increase in number in both the epithelium and the lamina propria.
Neutrophils, eosinophils, basophils, B cells, macrophages, monocytes, plasma cells, and mast cells infiltrate the mucosa resulting in mucosal damage.
When the infection is treated, the mucosa regenerates and returns to normal;ifthe destroyed glands fail to regenerate, the space that they previously occupied inthe lamina propria may be replaced by fibroblasts and extra-cellular matrix leading to an irreversible loss of functional mucosa and a change diagnosable as
atrophy.
As atrophy develops, areas of intestinal metaplasia replace the native gastric mucosa.
This may represent anadaptive response because HP bacteria cannot colonize the metaplastic cells since they lack the necessary bacterial adhesion factors discussed earlier.
However, attachment of HP to areas of what appears to be incomplete intestinal metaplasia has been documented.
These cells in fact represent a hybrid epithelium whose cells share characteristics of bothgastric surface mucous cells and intestinal metaplastic cells.
The intestinal metaplasia decreases the sites hospitable to the growth of the
HP.
However, the inflammation and its associated reparative processes continue in sites of persisting infection.
As a result, the stomach acquires a mixed pattern of architecturally normal but inflamed areas (gastritis) alternating with expanding patches of atrophy and metaplasia producing multifocal atrophic gastritis (MAG).
Synopsis
Atrophic gastritis in the setting of Helicobacter pylori infection
loss of pit
mucous neck and glandular areas of the mucosa associated with a mononuclear and neutrophilic cell infiltrate
lymphocytic aggregate at the base of the mucosa.
area of glandular destruction showing epithelial dropout.
Superficial gastritis.
The superficial portion of the gastric mucosa is populated with a bandlike infiltrate of mononuclear cells.
presence of large numbers of lymphocytes and plasma cells.
References
Duodenal gastrinoma with multiple gastric neuroendocrine tumors secondary to chronic Helicobacter pylori gastritis. Grin A, Kim YI, Mustard R, Streutker CJ, Riddell RH. Am J Surg Pathol. 2012 Jun;36(6):935-40. PMID: 22588069
