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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Scleroderma (systemic sclerosis) is a connective tissue disorder characterized by thickening and fibrosis of the skin and visceral involvement that may include the heart, lungs, kidneys, and gastrointestinal tract. At least 40-50% of patients with scleroderma experience esophageal symptoms such as heartburn and dysphagia, while up to 90% of patients have esophageal dysfunction on objective testing at some point in their disease. The disease results in smooth muscle dysfunction that causes esophageal aperistalsis and reduced lower esophageal sphincter pressures. Gastroesophageal reflux with poor acid clearance results with an increased incidence of complications such as peptic stricture and Barrett's esophagus. Aggressive medical therapy is necessary to prevent these and other complications of gastroesophageal reflux.
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PMID:Scleroderma esophagus. 227 19

Gastroesophageal reflux (GER) is a dysfunction of the distal esophagus causing movement of stomach contents into the esophagus. Patients may develop heartburn, regurgitation, dysphagia, odynophagia, and hemorrhage. Respiratory symptoms occur in 10-60 percent of patients with GER or hiatal hernia. Although there is evidence associating pulmonary symptoms and GER, causality has not been proven. The appropriate use of antireflux therapy or surgery to treat GER may consequently alleviate respiratory symptoms.
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PMID:Gastroesophageal reflux and respiratory symptoms: is there an association? Proposed mechanisms and treatment. 227 31

In a 6.5 year period starting January 1982, 121 patients (74 male, 47 female; 1.6:1) with complicated gastroesophageal reflux referred to Alberta Children's Hospital, University of Calgary, required a Nissen fundoplication at a mean age of 35.5 months (range 3 weeks to 18 years). The median age of onset of symptoms was less than 1 month. Symptoms and indications for surgery included regurgitation (88%), failure to thrive (52%), reflux-associated pulmonary symptoms and aspiration (48%), biopsy evidence of esophagitis (35%) with heartburn (17%), dysphagia (18%), hematemesis (17%), anemia (13%), and hypoproteinemia (22%). Sixty-four percent of the patients had a syndrome or chromosomal abnormality, respiratory disease, or neuromuscular disorder. The barium contrast upper-gastrointestinal radiographic series, performed in all patients, identified structural [gastric outlet obstruction (2%), esophageal stricture (11%), erosive esophagitis (9%)], and functional abnormalities [gastroesophageal reflux (90%), barium aspiration (8%), esophageal hypoperistalsis (30%), delayed gastric emptying (4%)]. Barium contrast upper gastrointestinal radiographic series identified gastroesophageal reflux with a sensitivity of 90% (compared to history), was 50% sensitive and 92% specific for erosive esophagitis (compared to biopsy), was 59% sensitive and 74% specific for esophageal dysmotility (compared to esophageal manometry), and there was a significant (p less than 0.01) association between barium aspiration and prior evidence of aspiration pneumonitis. Esophageal manometry demonstrated a significantly (p less than 0.001) lower esophageal sphincter pressure in patients compared with controls, but no significant correlation with failure to thrive, aspiration pneumonia, biopsy evidence of esophagitis, or parameters of the 24-hour esophageal pH study. Twenty-four hour pH monitoring showed significantly (p less than 0.05) more reflux episodes than in asymptomatic controls and there was significant (p less than 0.05) correlation between the percentage of time pH was less than 4 and the presence of hypoalbuminemia, and biopsy-proven erosive esophagitis or Barrett's esophagus. Endoscopic appearance was 91% sensitive and 60% specific for esophagitis when compared to biopsy. Nissen fundoplication was completely effective at resolving gastroesophageal reflux in 83%, and associated with marked improvement in 15%. No patient died as a result of fundoplication. Major complications included: recurrence of symptoms requiring reoperation (2%), subsequent mechanical bowel obstruction (8%), wound infection or pneumonia (12%).
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PMID:Investigation and outcome of 121 infants and children requiring Nissen fundoplication for the management of gastroesophageal reflux. 227 17

We characterized the acute manifestations of gastroesophageal reflux in 46 patients attending an emergency ward. 43 were females and the mean age was 41 +/- 14. The diagnosis of G-E reflux was confirmed in all by the acid reflux test; esophagitis was present in 55% of patients submitted to endoscopy; the Bernstein test was positive in 43%. The population represents 3% of all emergency consults and 8% of gastroenterological consults. Severe epigastric pain, usually burning or constrictive and radiating to the dorsum, left hypochondrium and sternal region was the presenting form in 55% of patients. Pain was refractory to antispasmodic agents but was relieved by antacids. Dyspnea or bronchial obstruction was the main symptom in 16% of cases, heartburn in 13%, hematemesis in 6%. Among these patients a prolonged history of chronic G-E reflux was common. Surgical correction was undertaken in 6%, with some symptoms persisting in 17%.
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PMID:[Prevalence of acute manifestations of pathologic gastroesophageal reflux]. 229 74

We prospectively evaluated gastric acid output (mEq/h), gastric volume output (ml/h), ambulatory 24-h esophageal pH monitoring, and the endoscopic appearance of the esophagus in 23 patients undergoing treatment of chronic long-standing pyrosis. Twelve of these 23 individuals (52%) remained symptomatic after 3 mo of standard antisecretory treatment with ranitidine, 150 mg twice daily. When compared with initial responders, those patients who did not experience complete symptomatic relief on therapy had significantly higher basal acid output (p less than 0.001), basal volume output (p less than 0.02), and basal upright (but not supine) reflux time (p less than 0.05). Nine of the 12 patients who did not respond to initial treatment had gastric acid hypersecretion (basal acid output greater than 10 mEq/h), and 10 of the 12 had Barrett's epithelium compared with only 1 patient in the initial-responder group (p less than 0.001). All 12 nonresponders were treated for an additional 3 mo with increased doses of ranitidine (mean, 1280 mg/day; range, 600-1800 mg/day), and complete disappearance of pyrosis occurred in 10 of the 12, although no significant endoscopic regression was observed in the extent of the underlying columnar mucosa in those with Barrett's esophagus over the 6-mo duration of the study. A significant correlation was shown between the daily ranitidine dose required to eliminate symptoms and the pretreatment basal acid output (r = 0.81, p less than 0.001); gastric acid output had to be almost totally suppressed (i.e., less than 1 mEq/h) for pyrosis to disappear completely. No side effects occurred with any of these high doses of ranitidine. We conclude that a subgroup of patients with long-standing symptomatic gastroesophageal reflux disease who do not respond to standard ulcer-healing doses of histamine2-receptor antagonists are hypersecretors of basal gastric acid and require increased acid-suppressive therapy. Many of these individuals also have underlying Barrett's epithelium.
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PMID:Gastric acid hypersecretion in refractory gastroesophageal reflux disease. 221 Feb 69

Patients with gastroesophageal reflux often describe heartburn after "spicy meals." One ingredient common to most such meals is onion. We investigated the effects of onion on acid reflux and reflux symptoms in 16 normal subjects and 16 heartburn subjects. Subjects were studied with an esophageal pH probe for 2 h after the ingestion of a plain hamburger and a glass of ice water. The identical meal, with the addition of a slice of onion, was ingested on a counterbalanced day. Variables measured were number of reflux episodes, percentage of the time pH was less than four, heartburn episodes, and belches. Ingestion of onions did not increase any of the reflux variables measured in normals. However, onions significantly increased all measures in heartburn subjects, compared with the no-onion condition, and compared with normals under the onion condition. Onions can be a potent and long-lasting refluxogenic agent in heartburn patients.
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PMID:The effect of raw onions on acid reflux and reflux symptoms. 222 Jul 46

In a double-blind, randomized, comparative trial of the prokinetic drug cisapride and the H2-blocker cimetidine, mucosal healing and changes in symptoms of gastroesophageal reflux were evaluated in patients with erosive reflux esophagitis. The patients were treated with either cisapride, 10 mg four times a day (N = 36) or cimetidine, 400 mg four times a day (N = 37) for six weeks, or for 12 weeks if mucosal healing was not obtained by week 6. Upon entry, two thirds of the patients in each group had grade I (Savary-Miller) esophagitis, and the remainder grade II or III. At the end of treatment, endoscopy showed mucosal healing in 56% (38-72%; 95% confidence interval) of cisapride and 57% (39-73%; 95% confidence interval) of cimetidine patients. After six weeks, both drugs significantly (P less than 0.01) decreased the intensity and frequency of heartburn, regurgitation, and the postural syndrome. No significant intergroup differences were found regarding endoscopic parameters or the improvement of heartburn and regurgitation. Concomitant antacid use was also comparable. Adverse effects were reported by four cisapride and nine cimetidine patients. These results indicate that the effects of cisapride compare well with those of cimetidine in terms of both esophageal mucosal healing and symptom relief.
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PMID:Double-blind comparison of cisapride and cimetidine in treatment of reflux esophagitis. 233 57

In 27 patients with uncontrollable gastroesophageal reflux, a modified Nissen fundoplication was performed. To investigate the long term effects of this procedure, 24-hour ambulatory esophageal pH monitoring was performed on three occasions: preoperatively, four weeks and two years postoperatively. Preoperative and postoperative symptoms were assessed. In 13 patients, fundoplication reduced reflux to zero (percentage of time pH less than 4, zero per cent), and in another 11 patients, reflux was reduced to a very low level (percentage of time pH less than 4, 0.75 +/- 0.21 per cent). The procedure failed in three patients, in whom both reflux symptoms and a pathologic pH profile persisted. No significant differences could be demonstrated between reflux variables in the early and late postoperative pH studies. Postoperatively, ten patients complained of heartburn or regurgitation, but pathologic reflux could only be demonstrated in three of these, and in two, there was macroscopic evidence of esophagitis. It is concluded that Nissen fundoplication abolishes or nearly abolishes gastroesophageal reflux in the majority of patients. Also, as in patients not operated upon, symptoms are unreliable indicators of the severity of gastroesophageal reflux after an antireflux procedure.
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PMID:Prospective evaluation of the effects of Nissen fundoplication on gastroesophageal reflux. 238 87

Gastroesophageal reflux (GER) has been reported to be a cause of hiccups. Conversely, some reports state that hiccups cause or adversely affect GER disease. There have been few descriptions in the literature of what hiccups do to esophageal motility. We present a patient with long-standing symptomatic GER and intractable hiccups. Esophageal manometry during hiccups showed absence of LES pressure and absence of peristaltic activity in the esophageal body in response to swallowing, factors which could aggravate GER. Esophageal motility in the absence of hiccups was normal. Antireflux surgery in our patient relieved heartburn but not hiccups. Based on our case and a review of the literature, we believe that clinicians should be cautious in recommending antireflux surgery to treat hiccups in patients with both hiccups and heartburn.
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PMID:Hiccups: esophageal manometric features and relationship to gastroesophageal reflux. 238 28


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