Lymphocytic gastritis in patients with celiac sprue or spruelike intestinal disease

Wolber, Robert; Owen, David A.; DelBuono, Lisa; Appelman, Henry D.; Freeman, Hugh James

doi:10.1016/0016-5085(90)90819-m

Cited by 153 publications

(72 citation statements)

References 24 publications

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“…Between 10 and 45% of celiac patients have lymphocytic gastritis (90,92). Most of these patients have an endoscopically normal stomach and do not have lesions of varioliform gastritis or hypertrophic gastritis.…”

Section: Lymphocytic Gastritismentioning

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: Lymphocytic Gastritismentioning

confidence: 99%

Gastritis and Carditis

Owen

2003

Modern Pathology

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“…Endoscopically, three different findings have been described for lymphocytic gastritis: (1) Normal, or only slightly inflamed, mucosa [8]; (2) Varioliform gastritis with multiple raised chronic erosions – also known as ‘gastritis en nappes’ in the fundus and corpus [1, 2, 3, 8, 9, 10, 11, 12, 13]. (3) Hypertrophic gastritis in the fundus and corpus, with and without a gastric protein-losing syndrome [14, 15, 16, 17]. …”

Section: Introductionmentioning

confidence: 99%

Healing of Lymphocytic Gastritis by Eradication of <i>Helicobacter pylori</i>

Müller

Volkholz²,

Stolte³

2001

Digestion

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Background: It is not yet clear whether lymphocytic gastritis might not be a sequela of Helicobacter pylori (Hp) infection. The aim of the present pilot study was, therefore, to investigate whether lymphocytic gastritis can be cured by Hp eradication, which, if affirmed, would provide indirect evidence for an etiopathogenic relationship. Patients and Methods: 98 of 220 patients with lymphocytic gastritis diagnosed between 1988 and 1998 were investigated at least twice, with 61 of them undergoing Hp eradication treatment. In 29 of these patients, the pretreatment histological work-up using the Warthin-Starry silver stain revealed Hp colonisation, while in the remaining 32 patients the biopsies from the antrum and corpus were negative for Hp. The other 37 patients received no treatment, and served as a control group. Results: Both in the group with Hp-positive, and in the group with Hp-negative histology prior to treatment, eradication treatment led to healing of the gastritis, i.e. to regression of the gastritis parameters including normalisation of the intra-epithelial lymphocyte count, in 93.1% and 84.3% of the cases, respectively. In the control group the histological findings did not change. Conclusions: The results of our retrospective study support the notion that most cases of lymphocytic gastritis might be a consequence of Hp infection. This, however, needs to be clarified definitively by a prospective, randomized, double-blind study.

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“…L'ingestion chronique de gluten chez les patients coeliaques produit une inflammation et une infiltration lymphocytaire intraépithéliale de la muqueuse gastrique. La prévalence de la gastrite lymphocytaire ou atrophique demeure néanmoins faible [17,18]. Ces lésions peuvent être aggravées par la présence d'un autre antigène environnemental tel que l'Hp [17,19].…”

Section: Discussionunclassified