Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-seven patients with symptomatic gastro-oesophageal reflux received cimetidine 1.6 g daily for 6 weeks and matching placebo for 6 weeks in a randomised double-blind crossover trial. They complained of significantly more episodes of pain on placebo than on cimetidine (1186 vs 581) and consumed significantly more antacid tablets on placebo than on cimetidine (1645 vs. 1011). Cimetidine and placebo had similar effects on mucosal sensitivity to acid and on oesophagitis assessed endoscopically and histologically, suggesting that the symptomatic benefit is the result of a simple antacid effect.
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PMID:Effect of cimetidine in symptomatic gastro-oesophageal reflux. 8 86

Although the therapeutic approach to gastroesophageal reflux in children is well established, there are differences of opinion regarding the management of esophageal strictures, viz bougienage with medical therapy, fundoplication without dilatation, preoperative dilatation followed by fundoplication with intraoperative and postoperative dilatation, or resection and interposition. Sixteen consecutive children (mean age, 30.2 months) with reflux strictures were evaluated, constituting 12% of children operated on for gastroesophageal reflux. The strictures became clinically apparent 22.4 months (mean) from the onset of symptoms and were diagnosed by contrast studies and endoscopy. At first endoscopy all the patients had well-established fibrotic strictures. The strictures were mostly situated in the middle or lower esophagus and 7 were longer than 3 cm in length. All 16 were treated with antacids, H2-receptor blockers (Cimetidine), prokinetic agents, and intense nutritional resuscitation, together with preoperative stricture dilatations (average, 3.6 times). This was followed by fundoplication when nutritional parameters had been restored, esophagitis improved, and the strictures dilated to adequate size. Seven children required concomitant gastrostomies for prograde esophageal dilatations. Twelve children needed postoperative esophageal dilatations. The results were satisfactory in 14 (88%). Two required endoesophageal resection for localized unyielding strictures. One child responded only after failed reflux surgery was corrected at a second procedure. During an average follow-up of 8.2 years (range, 3 to 11) there has been no stricture recurrence and growth velocity was restored in all. We conclude that our preferred method is preoperative in-hospital management of gastroesophageal reflux with maximum nutritional support and careful evaluation of the degree and extent of esophagitis and fibrous scarring.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reflux strictures of the esophagus in children. 152 57

Although H2-receptor antagonists have been the mainstay of therapy for gastroesophageal reflux disease (GERD), none of these agents has been approved by the FDA as effective in healing lesions. Since proton pump inhibitors may be associated with long-term disadvantages, a healing regimen with cimetidine would be useful clinically. This multicenter, randomized, double-blind study was conducted to evaluate the efficacy of cimetidine 800 mg b.i.d. in healing lesions and in providing symptomatic relief in patients with ulcerative or erosive esophagitis. Patients with greater than or equal to 8 heartburn episodes during a 1-week screening period, reflux confirmed by esophageal pH monitoring, and esophageal ulcers or erosions confirmed by endoscopy were randomized to treatment with placebo or cimetidine for 12 weeks. Cimetidine provided significantly greater (p less than 0.01) improvement (74% vs. 51%) and complete healing (67% vs. 36%) of esophageal lesions than did placebo. In these patients with erosive or ulcerative esophagitis, the median time to achieve 24 h without heartburn was 13 days with cimetidine and 30 days with placebo (p = 0.01). The mean heartburn severity score in the cimetidine group decreased rapidly during the first week and was consistently lower than in the placebo group. Cimetidine, 800 mg twice daily, is effective in promoting healing of esophageal ulcers and erosions and in providing heartburn relief in patients with symptomatic erosive/ulcerative GERD.
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PMID:Cimetidine 800 mg twice daily for healing erosions and ulcers in gastroesophageal reflux disease. 224 93

To evaluate long-term medical therapy in patients with Barrett's esophagus, six patients were studied before and after long-term therapy with cimetidine for a mean period of 11.7 months. Some patients also received bethanechol. All had severe symptoms of gastroesophageal reflux resistant to intensive antacid therapy, specialized columnar epithelium by biopsy, and endoscopic evidence of severe inflammation. Esophageal manometry documented a hypotensive lower esophageal sphincter in three patients and low peristaltic amplitude in the distal esophagus in four. Treatment was begun with cimetidine, 300 mg orally four times daily. If symptoms did not totally abate, bethanechol, 25 mg orally four times daily, was added. Cimetidine completely relieved or dramatically reduced symptoms in all patients. Adding bethanechol produced further symptomatic improvement in three of four patients. After initial dilatation in the two patients with strictures, there was no recurrence. Endoscopic evidence of inflammation resolved completely in four patients and was markedly improved in two. Treatment with both drugs was well tolerated by all patients. The abnormally placed squamo-columnar junction did not regress during follow-up.
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PMID:Effects of long-term medical treatment with cimetidine and bethanechol in patients with esophagitis and Barrett's esophagus. 288 58

The comparative efficacy of a 12-week acute treatment with 800 and 1600 mg cimetidine daily and the effectiveness of a 400-mg single-dose maintenance treatment versus placebo lasting 6 months were studied in a double-blind fashion in 30 and 24 patients, respectively, with gastroesophageal reflux (GER) disease. Cimetidine in a dose of 800 or 1600 mg daily resulted in a significant symptomatic improvement and a decrease in the extent of endoscopic esophagitis. An improvement in the gastroesophageal sphincter function during treatment was suggested by a significant decrease in the frequency of reflux, as evaluated by isotope scintigraphy. No significant differences were found between the two doses of cimetidine. The overall initial improvement tended to be maintained during maintenance treatment, but no significant differences were found between cimetidine and placebo. The present study thus supports the use of 800 mg of cimetidine daily for short-term treatment of GER disease but provides no support for maintenance treatment with a low dose. The study further suggests that cimetidine treatment, by reducing the tendency to GER, may induce long-lasting remission of the disease.
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PMID:Gastroesophageal reflux disease. Acute and maintenance treatments with cimetidine. 352 Jul 94

This study was carried out on 104 patients of whom 94 were asthmatic and 10 patients presented with a spasmodic intractable cough; all presented with symptoms evocative of an associated gastro-oesophageal reflux (RGO). The clinical symptoms revealed a nocturnal cough (67%), cough preceeding asthma (46%) and heartburn in 60%. The asthma was severe (type III and IV in 89% of cases), or dependent on corticosteroids (37% of cases). pH monitoring of the oesophagus is the most sensitive examination (88% with positive results) slightly ahead of manometry and scintigraphy (both 81%), these examinations were clearly superior to radiographic examination (49%) and oesophageal fibroscopy (36%). The combination of pH monitoring and of scintigraphy enabled 98% of RGO cases to be identified by their clinical data. Medical treatment with Tagamet, Gaviscon and Primperan (alone or in combination) produced an improvement in the respiratory symptoms in 50% of the cases. Of the 14 surgically treated, 7 obtained an improvement in their respiratory symptoms. Seven of the ten patients with spasmodic cough were improved by medical treatment. Our study shows the frequency of oesophageal reflux in patients with severe asthma. In half of them RGO intervened as an aggravating factor and the medical treatment of RGO led to a clear improvement in the respiratory symptoms.
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PMID:[The association of asthma and gastroesophageal reflux: strategy of paraclinical studies]. 383 97

The etiology, pathogenesis, diagnosis, and treatment of reflux esophagitis are reviewed. Reflux esophagitis is the subjective or objective response to gastroesophageal reflux (GER), which is defined as the entrance of gastroduodenal contents into the esophagus not associated with vomiting or belching. The pathogenesis of reflux esophagitis may involve a number of mechanisms, including changes in lower esophageal sphincter pressure, gastric volume, composition of the refluxate, esophageal acid clearance, and esophageal tissue resistance. The most common symptom of reflux esophagitis is heartburn. Regurgitation of fluid into the mouth, usually after bending or during the night, is an unequivocal symptom of GER. Treatment can be divided into three phases. Phase 1 involves the avoidance of certain foods and habits, elevation of the bed head, antacid, and alginic acid-antacid therapy. Phase 2 involves drug therapy with agents not yet approved by the FDA for this indication: bethanechol chloride, cimetidine, and metoclopramide hydrochloride. Bethanechol chloride 25 mg is generally given four times daily. Cimetidine is given in doses of 300-400 mg after meals and at bedtime. Metoclopramide hydrochloride is administered in doses of 10 mg before meals and at bedtime. Phase 3 is antireflux surgery. Clinical experience has shown that phase 1 therapy is successful for about 75% of all patients. Of the 25% that do not respond to phase 1 therapy, about 90% will respond to phase 2 therapy, leaving only 5-10% of all patients with this disorder who will require phase 3 treatment. Current data favor cimetidine and bethanechol over metoclopramide. The least proof of efficacy and the most frequent adverse side effects are seen with metoclopramide. Cimetidine and bethanechol appear to have similar efficacy and relatively infrequent side effects. Evidence confirming the superiority of cimetidine over bethanechol is lacking. Further research is needed to determine the optimal pharmacologic combinations and treatment regimens.
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PMID:Current concepts in the pathogenesis and treatment of reflux esophagitis. 636 Apr 95

Using a method described earlier, an investigation of the gastro-oesophageal region was made on duodenal ulcer patients before and during cimetidine treatment. During cimetidine treatment there was a small increase in the gastro-oesophageal sphincter pressure (p less than 0.05), although the pressure still was lower than in normal individuals (p less than 0.05). The acid perfusion test and the acid-clearing test were unchanged. The intensity of the acid gastro-oesophageal reflux at pH less than or equal to 4 was reduced p less than 0.05) but still greater than in normal individuals (p less than 0.05). A tendency to an increase of the intragastric pH postprandially (0.05 less than p less than 0.01) was found during treatment, whereas the intragastric pH fasting 12 h after the intake of the last tablet was unchanged. There was no change in the number of amplitudes registered at the proximal and distal pressure catheters (p greater than 0.1), whereas the reversed peristaltic activity still was increased compared with normal individuals (p less than 0.00u). Before treatment a reflux episode at pH less than or equal to 3 needed longer time and greater peristaltic activity to be cleared than was the case during treatment. Nineteen of 20 patients improved their symptoms during treatment. Cimetidine increased the gastro-oesophageal sphincter pressure in duodenal ulcer patients, which may be due to either the reduced intragastric acid secretion or to a direct influence on the gastro-oesophageal region. The reduction in the acid gastro-oesophageal reflux is partly due to an increased gastro-oesophageal sphincter pressure and partly due to a reduced output of acid reflux material. Low pH and the volume of the reflux material in the distal part of the oesophagus are important in regulating the peristaltic activity in duodenal ulcer patients.
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PMID:The influence of cimetidine on the acid gastro-oesophageal reflux in duodenal ulcer patients. 699 59

Gastro-oesophageal reflux and its complications are a common clinical management problem. Medical treatment revolves around the use of physical and mechanical methods in prevent reflux, dieting and drug restriction, acid reduction, mechanical foam barriers, and drugs to increase lower oesophageal sphincter (LES) pressure and improve acid clearance. It is recommended that patients elevate the head of their bed at night, eliminate alcohol and smoking, and avoid food known to decrease LES pressure or irritate the oesophageal mucosa. Antacids are effective in the control of reflux symptoms in most patients with mild to moderate reflux oesophagitis. 'Gaviscon' is also effective but no better than antacids. The histamine H2 receptor blocker, cimetidine, alleviates symptoms and may also improve endoscopic and histological oesophagitis. Cimetidine and drugs which augment sphincter pressure (bethanechol, metoclopramide, domperidone and prostaglandins) may be helpful in treating patients with severe reflux oesophagitis.
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PMID:Current approaches in the medical treatment of oesophageal reflux. 701 72

Heartburn was the major gastrointestinal symptom associated with drinking coffee in 31 subjects. These symptomatic subjects had a diminished basal lower-esophageal-sphincter (LES) pressure, 8.3 +/- 1.1 mm Hg, as compared with the pressure in asymptomatic subjects, 19.4 +/- 1.3 mm Hg (P less than 0.01), in response to four separate doses of coffee. LES pressure increased in normal subjects but changed only minimally in the symptomatic group (P less than 0.01). Basal acid output was similar in both groups, but the maximal acid response to coffee was paradoxically greater in normal subjects, 20.9 +/- 3.6 meq per hour, than in the symptomatic group, 9.4 +/- 1.5 meq per hour (P less than 0.01). During coffee instillation into the stomach, 26 of 31 symptomatic subjects (83 per cent) had heartburn at the highest dosage. Cimetidine, but not placebo, reduced acid secretion and heartburn in response to coffee, suggesting that acid was required for the development of symptoms. These studies suggest that LES dysfunction and gastroesophageal reflux, rather than gastric hypersection, are responsible for the heartburn caused by coffee in certain susceptible persons.
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PMID:Pathogenesis of coffee-induced gastrointestinal symptoms. 738 69


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