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Helicobacter pylori–associated gastritis

Tuesday 6 December 2011

Digital cases

- HPC:311 : Follicular gastritis and active chronic gastritis, non-atrophical, Helicobacter pylori-associated.

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.

The finding of focal H. pylori-negative chronic active gastritis (e.g., only in a single specimen from the corpus) should also alert the pathologist to the possibility of Crohn disease.

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).

Microscopy

- 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.

Differential diagnosis

- Helicobacter heilmanii

  • Milder chronic active gastritis
  • Infection may be acquired from domestic pets
  • Tightly coiled organisms with corkscrew appearance
  • Limited risk of gastric cancer and lymphoma

- autoimmune gastritis

  • 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.

Treatment

- Drugs

  • 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
  • MALToma
  • atrophic gastritis
  • Post gastric cancer resection and 1st degree relative of patients with gastric cancer

Prognosis

- 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

Feature Definition Grading Guidelines
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

Natural History

- Peptic ulceration

  • 4x increased risk of developing ulcer
  • Lifetime risk of peptic ulcer disease ≥ 5-10%

- Gastric cancer

  • 3-6x increased risk of developing gastric cancer
  • 70% of distal gastric adenocarcinomas attributable to H. pylori infection

- Gastric MALToma

  • 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

Types

- Helicobacter pylori–associated chronic gastritis

See also

- follicular gastritis
- active chronic gastritis, non-atrophical
- Helicobacter pylori

References

- Amieva MR et al: Host-bacterial interactions in Helicobacter pylori infection. Gastroenterology. 134(1):306-23, 2008
- 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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El-Omar EM et al: Helicobacter pylori infection and chronic gastric acid hyposecretion. Gastroenterology. 113(1):15-24, 1997