Abstract:SUMMARY Ambulatory oesophageal pH, oesophageal manometry and fasting serum gastrin concentrations were carried out on 28 patients with reflux oesophagitis, before and during treatment with ranitidine 300 mg bd. Fourteen patients healed endoscopically at six weeks (group A) and 14 had residual oesophagitis (group B). Group A were characterised by a lower serum gastrin concentration before treatment (4.52 pmol/l; 2-4-10: mean and range) than group B (11
“…"6 Serum gastrin values are also higher in resistant cases. 67 Collen et al have recently published a study of patients resistant to conventional doses of ranitidine.68 The non-responders had significantly higher basal acid outputs than those who experienced complete symptomatic relief, and 9 of 12 were true hypersecretors (basal acid output > 10 mEq/hour). Symptomatic relief was achieved in 10 of 12 using increased doses of ranitidine (up to 1800 mg/day).…”
Gastro-oesophageal reflux disease is a common condition with a complex pathophysiology. Despite the spectrum of abnormalities, gastric acid has a central role in mucosal damage, and the mainstay of medical treatment is suppression of gastric acid secretion. The results of antisecretory treatment as assessed by endoscopic healing are reviewed. H2 receptor antagonists give more rapid symptom relief than placebo and can produce endoscopic improvement in 31-88% of cases depending on the severity of oesophagitis. Complete healing, however, is seen only in 27-45% of patients and these have mainly grades I-II disease. Improved healing rates can be obtained by increasing the degree of acid suppression or the length of treatment. The addition of a prokinetic agent may be beneficial. Omeprazole heals 67-92% of patients overall and although most successful in the lower grades of oesophagitis, can also heal 48-62% of patients with grade IV disease. The degree and rate ofhealing seem to be related to the reduction in oesophageal acid exposure and thus may correlate with the degree and duration of acid suppression over 24 hours obtained by the various treatments. The underlying pathophysiology is unchanged, however, and long term treatment may be needed to maintain remission.
“…"6 Serum gastrin values are also higher in resistant cases. 67 Collen et al have recently published a study of patients resistant to conventional doses of ranitidine.68 The non-responders had significantly higher basal acid outputs than those who experienced complete symptomatic relief, and 9 of 12 were true hypersecretors (basal acid output > 10 mEq/hour). Symptomatic relief was achieved in 10 of 12 using increased doses of ranitidine (up to 1800 mg/day).…”
Gastro-oesophageal reflux disease is a common condition with a complex pathophysiology. Despite the spectrum of abnormalities, gastric acid has a central role in mucosal damage, and the mainstay of medical treatment is suppression of gastric acid secretion. The results of antisecretory treatment as assessed by endoscopic healing are reviewed. H2 receptor antagonists give more rapid symptom relief than placebo and can produce endoscopic improvement in 31-88% of cases depending on the severity of oesophagitis. Complete healing, however, is seen only in 27-45% of patients and these have mainly grades I-II disease. Improved healing rates can be obtained by increasing the degree of acid suppression or the length of treatment. The addition of a prokinetic agent may be beneficial. Omeprazole heals 67-92% of patients overall and although most successful in the lower grades of oesophagitis, can also heal 48-62% of patients with grade IV disease. The degree and rate ofhealing seem to be related to the reduction in oesophageal acid exposure and thus may correlate with the degree and duration of acid suppression over 24 hours obtained by the various treatments. The underlying pathophysiology is unchanged, however, and long term treatment may be needed to maintain remission.
“…Following food, the antisecretory effects of H2-receptor antagonists at standard dosage are insufficient to keep the pH of gastric juice above 4. This is evident from oesophageal p H monitoring studies performed in patients with peptic oesophagitis during treatment with H2-receptor antagonists, which showed remarkably little reduction of the time that oesophageal pH was less than 4 (3,4).…”
Dent J, Hetzel DJ, MacKinnon MA, Reed WD, Narielvala FM. Evaluation of omeprazole in reflux oesophagitis. Scand J Gastroenterol 1989, 24(suppl 166), 76-82 In patients with reflux disease, pH monitoring has shown that omeprazole virtually eliminates oesophageal exposure to a pH of less than 4. Motility studies concurrent with pH monitoring have indicated that reflux continues on omeprazole. its effect on acid exposure being entirely dependent on elevation of gastric pH. Omeprazole and placebo have been compared in 64 patients with erosive or ulcerative oesophagitis; the 4-week healing rates were 81% with omeprazole, 20 mg or 40 mg daily, and 6% with placebo. The efficacies of omeprazole at doses of 20 mg and 40 mg daily, were then compared in 164 patients. At 4 weeks, oesophagitis was healed in 70% and 82% of patients for the 20 mg and 40 mg doses respectively (p = 0.05). Eight-week healing rates (79% for 20 mg and 85% for 40 mg) did not differ significantly. Symptom response was excellent for both doses. Relapse of oesophagitis was determined over 6 months for patients healed with omeprazole. Relapse was shown to occur in 88 of 107 patients by 6 months. Omeprazole is a highly effective treatment for erosivehlcerative peptic oesophagitis, 40 mg daily being marginally superior to 20 mg. Relapse is almost inevitable within 6 months of cessation of therapy Scand J Gastroenterol Downloaded from informahealthcare.com by Nyu Medical Center on 07/01/15 For personal use only. 1988,2,221-227 349-351 J 1988,296,89-92 Scand J Gastroenterol Downloaded from informahealthcare.com by Nyu Medical Center on 07/01/15 For personal use only.
“…H 2 ‐receptor antagonists are widely used…but as many as 50% of patients fail to respond to conventional high dose regimens….The reason for this high failure rate is unknown 81 …”
Section: Development and Evolution Of Therapies For Reflux Diseasementioning
Summary
Background
Our understanding of gastro‐oesophageal reflux disease has undergone significant changes over the last century.
Aim
To trace the rise in understanding of gastro‐oesophageal reflux disease and highlight remaining areas of uncertainty.
Methods
Literature review.
Results
In 1906, Tileston published his observations on ‘peptic ulcer of the oesophagus’. Winkelstein, in 1934, first correlated symptoms of heartburn with acid regurgitation and reflux oesophagitis. In 1946, Allison described hiatus hernia as a causal factor in the development of gastro‐oesophageal reflux disease. In 1958, Bernstein and Baker showed a direct relationship between oesophageal acidification and heartburn in patients with gastro‐oesophageal reflux disease, irrespective of endoscopic findings, leading to the recognition of non‐erosive gastro‐oesophageal reflux disease. In the 1980s, continuous recordings of the lower oesophageal sphincter showed that episodes of reflux were related to transient relaxations of lower oesophageal sphincter tone. There is now increasing recognition that gastro‐oesophageal reflux disease arises from the interaction of several anatomical and physiological factors. A turning point in the medical treatment of gastro‐oesophageal reflux disease came with the introduction of the first proton pump inhibitor, omeprazole, in 1989.
Conclusions
Future efforts need to identify the multifactorial interactions of gastro‐oesophageal junction anatomy and physiology in patients with gastro‐oesophageal reflux disease. Increased understanding of the disease will guide development of new therapies.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
