Long‐term follow‐up of gastric histology after <i>Helicobacter pylori</i> eradication

Forbes, Geoffrey M; Warren, Janet I.; Gläser, Markus; Cullen, Digby J.; Marshall, Barry J.; Collins, B. J.

doi:10.1111/j.1440-1746.1996.tb00312.x

Cited by 104 publications

(73 citation statements)

References 16 publications

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“…After 4 years, the antral mucosa does revert to nearly normal, although degenerate lymphoid aggregates may persist (38). Some investigators report that intestinal metaplasia remains unchanged (38,42,43), whereas others report a reduction in extent and severity (39,41).…”

Section: The Stomach After H Pylori Eradicationmentioning

confidence: 99%

Gastritis and Carditis

Owen

2003

Modern Pathology

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Dyspepsia is a common clinical problem. Its causes include peptic ulcer disease, gastroesophageal reflux, and functional (nonulcer) dyspepsia. A detailed clinical description of pain does not reliably differentiate the cause. Approximately 80% of gastroscopies are performed for the investigation of dyspepsia. "Gastritis" is diagnosed endoscopically in 59% of all stomachs, although in only 3% are the changes severe. Pathologic examination of unselected gastric biopsy specimens reveals that abnormalities are present in 62-73%, but there is only a weak correlation between endoscopic and histologic findings. For these reasons, it is recommended that endoscopic examination should always be accompanied by biopsy. Ideally, biopsies should be taken in a systematic fashion to include sampling of antrum and corpus. Recent evidence suggests that gastric infection by Helicobacter pylori initially presents as a superficial gastritis. Later it may become atrophic with development of intestinal metaplasia. The onset of atrophic changes may be related to the duration of infection, the strain of the infecting organism, associated dietary factors, or as-yet undefined host factors related to immunity. Persistent superficial gastritis predisposes to duodenal ulcer and gastric mucosa-associated lymphoid tissue lymphoma. Atrophic gastritis predisposes to gastric ulcer and adenocarcinoma. Evidence is accumulating that in some patients, pernicious anemia may be an end result of H. pylori-induced atrophic gastritis. Reactive gastropathy is a relatively common finding in gastric biopsies; in most instances it is associated with either reflux of duodenal contents or therapy with nonsteroidal anti-inflammatory drugs. Lymphocytic gastritis, eosinophilic gastritis, and the gastritis associated with Crohn's disease are distinct morphologic entities. Most gastroscopies are performed for the investigation of dyspepsia (1-7). This is a common clinical problem but is rarely life-threatening. The causes of dyspepsia include peptic ulcer disease (30%), gastroesophageal reflux (29%), and nonulcer (functional) dyspepsia (40%). The cause of functional dyspepsia is unclear at the present time, although in many instances it may be related to abnormalities of gut motility. In Ͻ1% of cases is gastric cancer a cause of dyspepsia. A detailed description of the symptoms of dyspepsia does not reliably differentiate the cause, although the presence of heartburn strongly suggests a component of gastroesophageal reflux. Correlations among patient symptoms, endoscopic appearances, and biopsy findings of gastritis are imperfect (4 -6). Agreement is best in cases where peptic ulcer or another focal lesion is identified. A study by Khakoo et al. (7) from the United Kingdom illustrates the problems encountered. Endoscopic and histologic findings were reviewed in 167 patients who underwent gastroscopy for dyspeptic symptoms. Of these, 98 patients (57%) had endoscopic evidence of gastritis. In 42% of patients, gastritis involved the antrum alone, in 7% it involved the...

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Section: The Stomach After H Pylori Eradicationmentioning

confidence: 99%

Gastritis and Carditis

Owen

2003

Modern Pathology

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“…In the same way, other randomized studies identified that H. pylori eradication in intestinal metaplasia could be important in the regression of this precancerous lesion [76,[109][110][111]119,120]. Oppositely, other trials, both follow-up and randomized control, had not identified regression of intestinal metaplasia when H. pylori eradication was administrated [121][122][123][124][125][126][127][128][129].…”

Section: Discussionmentioning

confidence: 96%

Molecular Epidemiology of Helicobacter pylori in Brazilian Patients with Early Gastric Cancer and a Review to Understand the Prognosis of the Disease

Röesler¹,

Zeitune²

2014

Trends in Helicobacter Pylori Infection

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“…There was no significant difference in gastric atrophy or in intestinal metaplasia between the two patient groups. 50 Annibale et al successfully eradicated H. pylori in 25 of 32 patients. After a year there was no improvement in gastric atrophy or intestinal metaplasia.…”

Section: Bacterial Factorsmentioning

confidence: 99%

Test and treat or test and scope for Helicobacter pylori infection. Any change in gastric cancer prevention?

Loughlin

Sebastian

O'Connor

et al. 2003

Aliment Pharmacol Ther

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SUMMARYA 'test and treat' strategy is advocated for patients with dyspepsia under the age of 45 years, with endoscopy reserved for those with alarm symptoms or aged over 45 years. One of the consequences of this strategy will be a reduction in population infection rates of Helicobacter pylori. It is now clear that H. pylori is one of the prime initiators of gastric cancer with up to 70% of gastric cancers attributable to H. pylori. What remains unclear is if H. pylori reduction will lead to a reduction in gastric cancer.

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Long‐term follow‐up of gastric histology after Helicobacter pylori eradication

Cited by 104 publications

References 16 publications

Gastritis and Carditis

Gastritis and Carditis

Molecular Epidemiology of Helicobacter pylori in Brazilian Patients with Early Gastric Cancer and a Review to Understand the Prognosis of the Disease

Test and treat or test and scope for Helicobacter pylori infection. Any change in gastric cancer prevention?

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