Helicobacter pylori–associated gastritis
Tuesday 6 December 2011
Irrefutable evidence documents that Helicobacter pylori is the major cause of gastritis.
Difficulties arise when biopsy specimens with chronic inflammation do not show Helicobacter, but these organisms were present in a previous biopsy, for example, before eradication therapy, or if the result of some other investigation, such as serology or a breath test, indicates that the infection is or has been present.
To classify such cases as idiopathic would be patently inappropriate; yet a diagnosis of Helicobacter-associated based on the results of additional investigations rather than on the finding of organisms in the biopsy specimens could be misleading.
Under these circumstances, a pragmatic approach would be to dispense with an etiological term and report the case as chronic gastritis without further qualification unless it happened to fall into a distinctive topographical category, in which case that would be appended.
Its association with H. pylori would then be a matter for clinicopathological correlation.
Even when H. pylori is identified, it must not be assumed that it is the sole etiologic factor.
The eventual form of gastritis and its disease associations will reflect the interplay of H. pylori with one or more cofactors, which may be host-related (e.g., secretor status, blood group, and immune responses), or environmental (e.g., excessive salt intake and inadequate consumption of fresh fruit and vegetables).
Diffuse, superficial, chronic, monocytic inflammation.
Neutrophils, if present at neck region, mark active infection.
Usually confined to antrum, but use of PPI without antibiotic therapy leads to cephalad progression.
Large lymphoid follicles may form.
lymphocytic gastritis may be seen.
regenerative foveolar hyperplasia may be present
superficial microerosions may be seen
gastric mucosal xanthoma may be present
After treatment, mild, inactive, or chronic inflammation may be seen
Slender curved rods can be seen on hematoxylin & eosin.
Giemsa, silver, and immunohistochemical stains can highlight bacteria.
Residual coccal form of Helicobacter pylori can be seen after treatment; best seen with immunostain.
- Milder chronic active gastritis
- Infection may be acquired from domestic pets
- Tightly coiled organisms with corkscrew appearance
- Limited risk of gastric cancer and lymphoma
- Corpus-restricted chronic atrophic gastritis
- Anti-parietal cell and anti-intrinsic factor antibodies
- Marked atrophy of oxyntic glands with diffuse lymphoplasmacytic infiltration
- Antrum is devoid of inflammation but displays G-cell hyperplasia
- ECL-cell proliferation and risk of carcinoid tumors
- corpus-restricted chronic atrophic gastritis
- Although it is generally acknowledged that the finding of corpus inflammation and atrophy, with or without metaplasia, in patients with pernicious anemia has an autoimmune basis, a definitive diagnosis of autoimmune gastritis on purely histological grounds is not warranted, especially when dealing with biopsy specimens and their attendant sampling limitations.
- Similar histologic changes are possible, albeit infrequent, in the late stages of H. pylori gastritis and in corpus biopsy specimens from patients with multifocal atrophic gastritis.
- On the other hand, the histologic changes noted in biopsy specimens and their topography at times can strongly suggest autoimmune gastritis.
- For instance, autoimmune gastritis should always be considered when corpus predominant atrophic gastritis is seen, particularly when there is little or no atrophy or metaplasia in accompanying antral biopsy specimens.
- Although H. pylori is rarely seen in this pattern, serological data suggest a role for the organism.
- See also comments above about the possible value of endocrine cell and pepsinogen I and II staining in pseudopyloric metaplasia.
Other etiological agents, such as chemicals and infectious organisms, can be discussed.
- Triple drug therapy
- Proton pump inhibitor (PPI), clarithromycin, and either amoxicillin or metronidazole
- Failure associated with either poor patient compliance or antibiotic resistance
Recommendation for treatment
- Gastric or duodenal ulcer
- atrophic gastritis
- Post gastric cancer resection and 1st degree relative of patients with gastric cancer
Eradication achieved in about 90% of patients.
Chronic infection leads to mucosal atrophy and intestinal metaplasia with heightened risk of cancer.
Sydney system of grading
|Chronic inﬂammation||Increased lymphocytes and plasma cells in the lamina propria||Mild, moderate, or severe increase in density|
|Activity||Neutrophilic inﬁltrates of the lamina propria, pits, or surface epithelium||Less than one third of pits and surface inﬁltrated = mild; one third to two thirds = moderate; more than two thirds = severe|
|Atrophy||Loss of specialized glands from either antrum or corpus||Mild, moderate, or severe loss|
|Intestinal metaplasia||Intestinal metaplasia of the epithelium||Less than one third of mucosa involved = mild; one third to two thirds = moderate; more than two thirds = severe|
|Helicobacter pylori||H. pylori density||Scattered organisms covering less than one third of the surface = mild colonization; large clusters or a continuous layer over two thirds of surface = severe; intermediate numbers = moderate colonization|
- 4x increased risk of developing ulcer
- Lifetime risk of peptic ulcer disease ≥ 5-10%
- 3-6x increased risk of developing gastric cancer
- 70% of distal gastric adenocarcinomas attributable to H. pylori infection
- Stepwise progression from acquisition of mucosal lymphoid tissue to lymphoma
- Lasting remission of lymphoma is achieved in 3/4 of patients by eradication of bacterium alone
Extragastric (systemic) disease
- Association remains debated
- Antigenic mimicry between bacterium and host antigens is possible mechanism
Helicobacter pylori–associated chronic gastritis
active chronic gastritis, non-atrophical
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McNamara D et al: Helicobacter pylori infection and the pathogenesis of gastric cancer: a paradigm for host-bacterial interactions. Dig Liver Dis. 40(7):504-9, 2008
Snaith A et al: Helicobacter pylori: host genetics and disease outcomes. Expert Rev Gastroenterol Hepatol. 2(4):577-85, 2008
Anim JT et al: Assessment of different methods for staining Helicobacter pylori in endoscopic gastric biopsies. Acta Histochem. 102(2):129-37, 2000
Warren JR: Gastric pathology associated with Helicobacter pylori. Gastroenterol Clin North Am. 29(3):705-51, 2000
Steinbach G et al: Antibiotic treatment of gastric lymphoma of mucosa-associated lymphoid tissue. An uncontrolled trial. Ann Intern Med. 131(2):88-95, 1999
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