The incidence of esophagitis in peptic ulcer disease

Goldman, Maurice S.; Rasch, James R.; Wiltsie, David S.; Finkel, Martin

doi:10.1007/bf02233258

Cited by 27 publications

(6 citation statements)

References 4 publications

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“…Goldman et al . reported a prevalence of mild reflux disease in 58% of patients with gastric or duodenal ulcer 17 . In a study of 27 patients with duodenal ulcer, Boyd found that 33% had endoscopic evidence of oesophagitis and a further 26% had histological changes consistent with oesophagitis 18 .…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have shown that at least 50% of patients with symptoms of GERD have no mucosal lesions at endoscopy 21 , . 22 Patients with symptoms of reflux disease and negative endoscopy frequently progress to develop erosive oesophagitis when followed long term 17 . We evaluated both the symptoms of reflux disease and endoscopic findings in our study because neither is perfect for the diagnosis of GERD.…”

Section: Discussionmentioning

confidence: 99%

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Recurrent symptoms and gastro‐oesophageal reflux disease in patients with duodenal ulcer treated for Helicobacter pylori infection

Vakil¹,

Hahn

McSorley

2000

Aliment Pharmacol Ther

100

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Background: Eradication of Helicobacter pylori has been shown to prevent relapse of endoscopically detected duodenal ulcers. There is controversy regarding symptom improvement after therapy. Some studies have suggested that a substantial number of patients remain symptomatic after eradication therapy. Other studies suggest that gastro‐oesophageal reflux disease (GERD) may develop as a result of H. pylori eradication. Aim: To determine the relationship between symptoms and H. pylori eradication and to determine whether H. pylori eradication results in symptoms or endoscopic findings of GERD. Methods: Two hundred and forty‐two patients with endoscopically documented duodenal ulcer disease and evidence of H. pylori infection by rapid urease testing and histology were studied in four randomized, placebo‐controlled, double‐blind trials of H. pylori eradication therapy. All patients underwent symptom assessment and endoscopy with biopsy before therapy and 1 and 6 months after completing therapy. The rapid urease test and histology were used to determine H. pylori status. Interviewers were blinded to H. pylori status after eradication and were unaware of the endoscopic findings (interviews were performed prior to repeat endoscopy). Results: The presence of epigastric pain was significantly associated with persistent H. pylori infection 1 month after therapy (odds ratio 2.3, 95% CI: 1.02–5.2; P=0.041), as was nausea (OR 7.1, 95% CI: 0.93–55.6; P=0.029). The presence of epigastric pain was significantly associated with ulcer relapse at 6 months (OR 7.5, 95% CI: 3.6–15.7; P < 0.001) as was nausea (OR 5.1, 95% CI: 1.7–16.0; P=0.002). Heartburn was not associated with eradication of H. pylori or ulcer relapse. New onset reflux symptoms were reported by 17% (17 of 101 patients) at 6 months and were not significantly different in patients with (15%) and without (22%) persistent H. pylori infection (P=0.47). Erosive oesophagitis was present at endoscopy in one of the 17 cases that developed new heartburn. Conclusions: One month after completion of therapy, the presence of epigastric pain or nausea is associated with persistent infection and these symptoms at 6 months are suggestive of duodenal ulcer relapse. The incidence of GERD is not increased in patients who have eradication of H. pylori.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Recurrent symptoms and gastro‐oesophageal reflux disease in patients with duodenal ulcer treated for Helicobacter pylori infection

Vakil¹,

Hahn

McSorley

2000

Aliment Pharmacol Ther

100

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“…However, H. pylori can also play a role in producing GERD. For example, H. pylori ‐associated duodenal ulcer (which is associated with the presence of CagA‐positive strains) has also long been known to be strongly associated with GERD [14–31]. Thus, both the presence and absence of H. pylori may play roles in GERD.…”

Section: New Problems Caused By Absence Of H Pylorimentioning

confidence: 99%

Contemplating the Future without Helicobacter pylori and the Dire Consequences Hypothesis

2007

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Helicobacter pylori is a serious chronic transmissible pathogen that causes gastric structural and functional damage and is a major cause of morbidity and mortality worldwide. H. pylori is one of the digestive tract pathogens that has traveled with mankind since before humans moved out of Africa. Some have suggested that the long association of H. pylori with humans means there must be a benefit and suggest dire consequences will follow its eradication. Fortunately, there are now sufficient experiences with the outcome of treatment and with populations where the infection disappeared long ago to support the conclusion that H. pylori is a serious chronic transmissible pathogen that no one needs, deserves, or desires. The dire consequence hypotheses have proven to be erroneous attempts to blame some of the problems facing the modern world on a pathogen that was and is responsible for much suffering, morbidity, and mortality. It is time to join together to eradicate it and to let H. pylori join smallpox and polio on the hit list of undesirables.

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“…More recently, G oldman el al. [3] studied the histological aspect of the mucosa and found a concomitance between peptic ulcer and esophagitis in 58% of their patients. The incidence of reflux esophagitis in gastric and DU patients was quite evident in their figures.…”

Section: Discussionmentioning

confidence: 99%

Esophagitis and Duodenal Ulcer

Moraes-Filho¹,

Zaterka²,

Hw³

et al. 1974

Digestion

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36 male patients (average age, 36 years) with duodenal ulcer (DU) were studied with the purpose of investigating the incidence of reflux esophagitis. Ten of them had duodenal stenosis due to scarring. All patients were submitted to X-ray and endoscopy of the esophagus, histology of the esophagus, gastric secretion of HCl, and manometry of the lower esophageal sphincter. The results were compared with those of ten controls. The following conclusions were reached: (1) esophagitis according to histological and endoscopic study was found in 61.1% of the patients; (2) the incidence of esophagitis is not significantly related to the duration of the disease, as estimated by its symptoms; (3) duodenal stenosis is not significant in the pathogenesis of the esophagitis; (4) no significant statistical relation was observed between the presence of reflux esophagitis in patients with DU and the gastric secretion of HCl as evaluated in basal conditions and after Histalog stimulation; (5) the length of sphincter and the resting gastroesophageal sphincter pressure were not significantly different in patients with or without esophagitis, and do not depend on the presence or the absence of stenosis or gastric hypersecretion of HCl.

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The incidence of esophagitis in peptic ulcer disease

Cited by 27 publications

References 4 publications

Recurrent symptoms and gastro‐oesophageal reflux disease in patients with duodenal ulcer treated for Helicobacter pylori infection

Recurrent symptoms and gastro‐oesophageal reflux disease in patients with duodenal ulcer treated for Helicobacter pylori infection

Contemplating the Future without Helicobacter pylori and the Dire Consequences Hypothesis

Esophagitis and Duodenal Ulcer

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