The gastric cardia in gastro-esophageal reflux disease

El‐Zimaity, Hala; Verghese, Vino J; Ramchatesingh, Jacqueline; Graham, David Y.

doi:10.1016/s0016-5085(00)84037-8

Cited by 2 publications

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“…However, intestinal metaplasia is more likely to be found in columnar mucosa located at the squamocolumnar junction than it is in gastric mucosa 1-2 cm distal to this site (124). The last powerful piece of evidence linking H. pylori with carditis is the reduction or elimination of inflammation after antibiotic treatment (125,126).…”

Section: Causation Of Carditismentioning

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: Causation Of Carditismentioning

confidence: 99%

Gastritis and Carditis

Owen

2003

Modern Pathology

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“…We clearly have to wait for further and better evidence. Another study compared cardia biopsies from 65 GERD patients and 71 control individuals; no difference was found in the presence of SIM (15 % and 16 %) and only 3 % of SIM-GERD patients were H. pylori-negative [48].…”

Section: "Natural" Course and Scope Of The Problemmentioning

confidence: 99%

Gastroesophageal Reflux Disease and Barrett's Esophagus

Rösch

2000

Endoscopy

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There was enormous interest in the diagnosis and treatment of gastroesophageal reflux disease (GERD) and Barrett's esophagus (BE) at this year's Digestive Diseases Week (DDW). Since this topic predominated over other areas of clinical research in gastrointestinal endoscopy, it will be given broader scope in this series of DDW reports. As usual in recent years, data have been taken from the published abstracts, to avoid confusion; exceptions are only made for some of the new endoscopic antireflux treatments. Gastroesophageal Reflux Disease Diagnostic AspectsThree abstracts dealt with the appearance of GERD after Helicobacter pylori eradication therapy. In a large study in 168 peptic ulcer patients in Korea, with careful followup at one, six, 12, and 24 months, no difference was found in the development of reflux esophagitis between patients with successful eradication (n = 12) and those in whom eradication failed (n = 43) -3.2 % versus 4.7 % [1]. In a much smaller study in Greece, 24 % of 50 patients developed reflux esophagitis, 75 % of those during the first year; a control group was not included in this study [2]. In another study examining 52 patients with known GERD after H. pylori eradication, both the subjective and objective reflux parameters worsened, but the percentages were not quite clear from the entire group [3]. No conclusive evidence was therefore presented to solve this question in this year's DDW abstracts; regional differences may possibly play a role.Intraobserver and interobserver variability in the grading of reflux esophagitis using two different scales was good (with kappa values between 0.39 and 0.56) when both experts and trainees examined 325 photographs [4]. Histolo-gy did not contribute significantly to the clinical management of uncomplicated chronic heartburn [5]. Another study claimed a good accuracy rate for cytological abnormalities (close to 80 % compared with histological changes) in esophagitis-negative patients [6], but the impact on further management is unclear.Other abstracts dealt with the decreasing incidence of peptic esophageal strictures [7], gastric hypersecretion in endoscopy-negative GERD [8], esophageal dysfunction in GERD associated with scleroderma [9], and dental erosions and GERD in children [10]. Laparoscopic and Surgical TreatmentTwo randomized trials comparing laparoscopic Nissen fundoplication (LNF) with medical therapy using proton-pump inhibitors (PPI) were presented this year. One study included 134 patients randomized from 219 GERD patients; the short-term results at three months showed a better De Meester score and quality of life in the LNF group [11]. The long-term outcome at five years in a Scandinavian study, apparently supported by AstraZeneca, showed a better outcome for LNF with regard to time to treatment failure. However, after dose adjustment in case of relapse in the medical group, the differences in the long-term outcome with regard to symptomatic and/or endoscopic relapse were no longer significant [12]. This means that both treatments a...

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The gastric cardia in gastro-esophageal reflux disease

Cited by 2 publications

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Gastritis and Carditis

Gastritis and Carditis

Gastroesophageal Reflux Disease and Barrett's Esophagus

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