Severe peptic oesophagitis

Brunnen, Peter L.; Karmody, Allastair M.; Needham, C. D.

doi:10.1136/gut.10.10.831

Cited by 70 publications

(35 citation statements)

References 11 publications

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“…In the present study, 3% of patients with ZES were found to have Barrett's mucosa which is similar to the 0.5-2.0% prevalence found in the general population [62][63][64][65]. In contrast, despite the fact that 72% of the patients with ZES in the present study had had, during their initial visit, moderate to severe GERD symptoms, the frequency of Barrett's mucosa was lower than the mean frequency of 23% (range 5-44%) noted in patients with moderate to severe idiopathic GERD [20,[64][65][66] and the 56% occur rence reported in patients with chronic reflux symptoms and idiopathic gastric acid hypersecretion [21].…”

Section: Discussionsupporting

confidence: 69%

Esophageal Function and Occurrence of Barrett’s Esophagus in Zollinger-Ellison Syndrome

et al. 1995

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Manifestations of esophageal disease are present in up to 60% of patients with Zollinger-Ellison syndrome (ZES), although esophageal function has been studied in only a few patients and the prevalence of Barrett’s mucosa is unknown in these patients. It is unclear whether the high prevalence of esophageal disease is related to gastric acid hypersecretion alone or to abnormalities of esophageal motility or lower esophageal sphincter (LES) function in addition. To address these issues in the present study esophageal function was evaluated prospectively in 92 consecutive patients with ZES (66 with active disease, 26 disease-free after curative resection) seen during a 1-year period after controlling acid hypersecretion. In the patients with active disease the mean basal acid output (BAO) was 33 ± 3.0 mEq/h, the maximal acid output (MAO) was 56 ± 4.0 mEq/h, fasting serum gastrin was 8,736 ± 4,813 pg/ml and duration of disease prior to study was 12.5 ± 2.0 years. At the time of manometry, gastric acid secretion was controlled in all patients and no patient had evidence of gastroesophageal reflux disease at upper gastrointestinal endoscopy. Esophageal manometry revealed normal motility in 85% of patients. Eleven percent had low LES pressures, and only 1 % of patients had an elevated LES pressure. The frequency of Barrett’s mucosa (3%) was similar to that found in the general population but much less than that reported in patients with idiopathic GERD. No correlation was noted between LES pressures or manometric abnormalities and the fasting serum gastrin, BAO, MAO or the presence or absence of multiple endocrine neoplasia type I or previous vagotomy. Esophageal manometric results and LES pressure were similar in disease-free patients and those with active ZES. In conclusion, these results suggest that hypergastrinemia or other disease-specific abnormalities are not contributing to the high incidence of esophageal disease in patients with ZES because esophageal function in patients with ZES is similar to normals. Specifically, motility disorders in patients with ZES occur in similar frequency to normals, and LES pressure is normal in most patients. Despite the high levels of acid secretion and prominence of symptoms, the occurrence of Barrett’s mucosa was uncommon (3%) raising the possibility of additional protective mechanisms in patients with ZES.

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Section: Discussionsupporting

confidence: 69%

Esophageal Function and Occurrence of Barrett’s Esophagus in Zollinger-Ellison Syndrome

et al. 1995

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“…Epidemiologically flimsy data [24] and a strong clinical impression suggest that severe oesophagitis is more prevalent in elderly patients. This knowledge has probably led many to the view that reflux disease worsens endoscopically over time.…”

Section: Natural History Of Reflux Diseasementioning

confidence: 99%

Gastro-Oesophageal Reflux Disease

Dent¹

1998

Digestion

107

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New approaches to the grading of reflux oesophagitis and the definition of reflux disease have been proposed which should improve the precision of descriptions of this common problem. Endoscopy and 24-hour pH monitoring studies, though of great value, have significant limitations for assessment of reflux disease. Only about one third of reflux disease patients have oesophageal mucosal erosion or ulceration. Analysis of symptoms is probably the most useful method for diagnosis. Further research is needed into the best strategies for maximising the potential of symptom analysis. In the pathogenesis of reflux disease, Helicobacter pylori infection is not a major factor but the interaction of H. pylori gastritis and eradication therapy are important areas of great current interest. Troublesome reflux disease arises primarily from abnormally frequent gastro-oesophageal reflux, though heightened oesophageal mucosal sensitivity and defective oesophageal clearance play a role in some patients. Transient lower oesophageal sphincter relaxation appears to be the most important mechanism of reflux. This distinctive, swallow-independent type of lower oesophageal sphincter relaxation has a complex triggering system, apparently located in the brain stem. Medical and surgical treatments of reflux disease are now well characterised and have improved very substantially over recent years. Drugs that inhibit the occurrence of transient lower oesophageal sphincter relaxation are an intriguing possible future therapy.

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“…In the same geo graphical region, however, a review of barium swallows estimated the annual incidence of GORD. based on radiological evidence of gastro-oesophageal reflux, to be far higher, at 86 per 100,000 [12].…”

Section: Prevalence and Incidencementioning

confidence: 99%

Epidemiology and Natural History of Gastro-Oesophageal Reflux Disease

1992

Digestion

398

211

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Epidemiological studies of gastro-oesophageal reflux disease (GORD) are confounded by the lack of a standardized definition and a diagnostic ‘gold-standard’ for the disorder. In Western countries, 20-40% of the adult population experience heartburn, which is the cardinal symptom of GORD, but only some 2% of adults have objective evidence of reflux oesophagitis. The incidence of GORD increases with age, rising dramatically after 40 years of age. There is also wide geographical variation in prevalence. Complications, including oesophageal ulcer and stricture, and Barrett’s oesophagus, are found in up to 20% of patients with verified reflux oesophagitis. The signs and symptoms of GORD often wax and wane in intensity, and spontaneous remissions have been reported. In most cases, however, GORD is a chronic condition that returns shortly after discontinuing therapy. Although GORD causes substantial morbidity, the annual mortality rate due to GORD is very low (approximately 1 death per 100,000 patients), and even severe GORD has no apparent effect on longevity, although the quality of life can be significantly impaired. There are data to suggest that the use of non-steroidal anti-inflammatory drugs (NSAIDs) contributes to oesophagitis and stricture formation in patients with GORD. Although these data are not conclusive, it seems prudent, if possible, to avoid the use of NSAIDs in patients with GORD, particularly those with oesophageal stricture.

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Severe peptic oesophagitis

Cited by 70 publications

References 11 publications

Esophageal Function and Occurrence of Barrett’s Esophagus in Zollinger-Ellison Syndrome

Esophageal Function and Occurrence of Barrett’s Esophagus in Zollinger-Ellison Syndrome

Gastro-Oesophageal Reflux Disease

Epidemiology and Natural History of Gastro-Oesophageal Reflux Disease

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