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)

The effect of oesophageal stimulation with acid on the exertional angina threshold was examined in 12 subjects. Each walked until the angina threshold was reached on four successive occasions; during two tests the oesophagus was instilled with 0.1 mol/l hydrochloric acid and during the other two with physiological saline. Oesophageal instillation was carried out for 20 min at rest before each walk. In 10 patients the angina point was reached after walking a significantly shorter distance on the treadmill when acid was instilled than when the saline was instilled. ST-segment changes and rate-pressure product were not significantly different during the acid and saline tests. The mechanism responsible for the reduction of angina threshold is not known. However, the effect was more pronounced in the 6 patients who had experienced regular oesophageal symptoms than in those who had not. Ischaemic heart disease and gastro-oesophageal reflux are both common, and the possibility that acid reflux may aggravate angina should be borne in mind, particularly when oesophageal symptoms are present.
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PMID:Oesophageal stimulation lowers exertional angina threshold. 285 64

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

Oesophageal transit and gastric emptying of liquids and solids was measured in eight normal subjects with a single test meal containing In113 labelled water and an omelette labelled with Tc99m sulphur colloid. Each volunteer was studied, basally, whilst continuously smoking, and while chewing nicotine gum. Neither liquid, nor solid oesophageal transit were affected by smoking, or gum. Liquid gastric emptying occurred exponentially and clearance was not affected by smoking nor gum (mean basal t1/2 17.4 (2.7) (SEM) min, smoking t1/2 16.6 (7.4) min, gum t1/2 12.5 (2.9) min). Gastric emptying of solid had three components. An initial mean lag phase increased from 17.5 (2.7) min, to 27.5 (6.1) min (p less than 0.05) during smoking, but was not prolonged by nicotine gum (17.5 (1.1) min). A subsequent linear emptying phase was also slowed by smoking from a mean of 1.01 (0.15)% min to 0.80 (0.15)% min (p less than 0.05), but was not affected by nicotine gum, 1.06 (0.2)% min. A third complex phase of solid gastric emptying was not analysed. Smoking delays gastric emptying of solids, but not liquids; nicotine is not responsible for this effect. This observation may partly explain the adverse effect of smoking in patients with gastro-oesophageal reflux.
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PMID:Smoking delays gastric emptying of solids. 292 Sep 27

Esophageal function was evaluated in 53 patients with increasing severity of esophageal injury caused by gastroesophageal reflux disease (study 1), and the findings were applied to the treatment of 28 patients with reflux-induced strictures (study 2). Fifty asymptomatic volunteers served as controls for both studies. In study 1 there were 14 patients without reflux complications, 14 with esophagitis grade I to III, 13 with esophageal stricture, and 12 with Barrett's epithelium (6 of whom had a stricture). The prevalence of a mechanically defective sphincter increased with the progression of the esophageal injury; 50% in the patients without complications to 84% and 92% in those with stricture or Barrett's epithelium, respectively. Similarly, a decrease in amplitude of contractions in the distal esophagus was observed in patients with stricture and patients with Barrett's epithelium. In study 2, these findings were applied in the surgical management of 28 consecutive patients with a reflux-induced stricture. Preoperative motility studies were performed after patients were dilated to 60F. Control of reflux by a Nissen fundoplication gave excellent (86%) to good (14%) results in patients who had relief of dysphagia after dilation or adequate motility, or both. Four patients with both persistent dysphagia after dilation and inadequate motility underwent resection. Transmural presented are helpful in the selection of the optimal surgical procedure for the treatment of dilatable reflux-induced strictures.
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PMID:Esophageal function in patients with reflux-induced strictures and its relevance to surgical treatment. 293 Mar 1

Oesophageal motor function was studied by oesophageal manometry in 48 patients with progressive systemic sclerosis: 25 with proximal scleroderma and 23 with diffuse scleroderma. Oesophageal lesions were noted in 70% (74% in diffuse scleroderma; 64% in proximal scleroderma). Classical manometric signs of scleroderma were found in only 31% of patients. Peristaltic modifications might begin at the junction of the two muscular coats, since a four centimeter long aperistaltic suspended area was noted in that region in 20% of patients, especially in the proximal scleroderma group. Oesophageal motility and low lower oesophageal sphincter pressure account for the gastro-oesophageal reflux and may compromise respiratory function, as suggested by the high frequency of concurrent oesophageal and respiratory dysfunction in diffuse scleroderma. Systematic prevention of gastro-oesophageal reflux should perhaps be advocated as soon as abnormalities in oesophageal motility are diagnosed.
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PMID:[Systemic scleroderma. Contribution of esophageal manometry]. 294 50

Oesophageal injury secondary to gastro-oesophageal reflux is unlikely to be due to the effects of hydrochloric acid alone. The present authors have investigated the development of acid and bile salt-induced oesophageal mucosal injury in a rabbit model. Solutions of hydrochloric acid and sodium taurocholate (ST) were perfused through an isolated oesophageal preparation and mucosal injury was determined by measuring the rate of H+ disappearance. Perfusion with acid alone in concentrations up to 10 mmol/l did not affect the H+ disappearance rate. Addition of 1 mmol/l ST to an acid perfusate resulted in loss of H+ from the system. The increase in H+ disappearance rate was associated with loss of ST from the perfusate. Sodium taurocholate was only lost from the system when in an acid medium. Increased rate of H+ disappearance occurred even after the bile salt had been washed out of the perfused oesophagus. The mechanism of bile salt-induced mucosal injury was unlikely to be due to mucosal disruption secondary to micelle formation since the critical micellar concentration of taurocholate was found to be greater than that used in the perfusate. These findings indicate that bile salts may be an important factor in hydrochloric acid-related damage to oesophageal mucosa, by acting through mechanisms unrelated to micelle formation.
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PMID:Bile salt-induced injury of rabbit oesophageal mucosa measured by hydrogen ion disappearance. 303 65

Twenty one children with achalasia of the esophagus were treated from 1970 to 1986. There were 11 girls and ten boys (average age, 10.9 years; range, 6 months to 16 years). Diagnosis was established by barium swallow in 21 cases and confirmed by manometrics and motility studies in 14. Four children had unsuccessful dilatation (range, 1 to 16 dilatations/pt). All 21 children underwent modified anterior Heller esophagomyotomy (transabdominal in 15 and transthoracic in six). Concomitant Nissen fundoplication was performed in three. Follow-up from 1 to 14 years (mean, 6.3 years) showed complete relief of obstruction in 18 patients (86%), while three required additional procedures for persistent dysphagia. One child improved after a single dilatation, but two others eventually required a second esophagomyotomy. Three additional patients subsequently developed gastroesophageal reflux (GER), and two were managed with Nissen fundoplication; the third responded to medical management. The mortality for this series was zero. Postoperative complications occurred in nine children (42%) and was due to atelectasis and postoperative fever. Modified Heller esophagomyotomy is safe and effective in children with achalasia (mortality, 0%; relief of obstruction, 86%). Results were similar after a transabdominal or transthoracic approach. Esophageal dilatation was not an effective method of treatment. Although postsurgical barium swallow showed relief of obstruction, abnormal esophageal motility persisted, suggesting that long-term follow-up is important.
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PMID:Late results following esophagomyotomy in children with achalasia. 304 57

Oesophageal problems are common. There are three areas where drug treatment can be helpful, namely in the control of gastro-oesophageal reflux and its symptoms, the treatment of oesophageal motility disorders and when oesophageal infection occurs. In this review the management of these three disorders is considered.
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PMID:Therapeutic progress--review XXXIII. Are we making progress in the drug treatment of oesophageal disease? 306 49

Esophageal mucosal biopsy specimens frequently show numerous distended squamous cells with pale cytoplasm, which we term "balloon cells." These cells often occur in clusters, have a patchy distribution, and predominate in the prickle-cell layer in biopsies from patients with gastroesophageal reflux. We studied the immunohistochemical characteristics of balloon cells and their associated clinical findings. We demonstrated by immunoperoxidase technique that balloon cells contain intracytoplasmic albumin and immunoglobulin light chains and show reduced staining for keratin, suggesting cellular injury with resultant uptake of plasma proteins and fluid. Balloon cells were absent or sparse in esophageal mucosal biopsy specimens from 12 normal control persons, but were observed in 7 of 10 patients (70%) with gastroesophageal reflux confirmed by pH-probe test (P = 0.001 versus normal controls), in 16 of 25 patients (64%) with clinically suspected reflux (P less than 0.001), and in 4 of 5 patients with infectious or chemotherapy-associated esophagitis. However, no consistent association was found between balloon cells and the presence of the usual histopathologic criteria for epithelial injury, such as increased height of vascular tufts or width of basal zone. We conclude that balloon cells are most commonly observed in biopsy specimens from patients with various causes of esophageal injury. We propose that balloon cells may be a marker for epithelial injury, possibly even when other histopathologic criteria for injury are absent.
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PMID:Intracytoplasmic plasma proteins in distended esophageal squamous cells (balloon cells). 307 May 52

We evaluated five children with severe psychomotor retardation who developed frequent vomiting and poor weight gain after surgical placement of a feeding gastrostomy tube. Prolonged pH probe testing before surgery did not reveal notable gastroesophageal reflux (GER). Treatment with 12-hour gastrostomy tube feeding resulted in a marked reduction in vomiting; after one year of continuous feeding, all patients had achieved significant weight gain (mean, 44.0%). Esophageal manometrics and 24-hour pH probe testing before and at the end of the 12-month continuous-feeding period demonstrated low pressures of the lower esophageal sphincter and significant GER in the five children studied. These results indicate that children may develop symptomatic GER after gastrostomy tube placement. In such patients continuous gastrostomy tube feeding may result in a cessation of vomiting and achievement of significant weight gain. Definitive antireflux surgery can then be performed with the patient in an improved nutritional state.
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PMID:Gastroesophageal reflux secondary to gastrostomy tube placement. 308 57


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