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

Treatment of patients with an esophageal source of chest pain remains a challenging problem. Although a variety of measures--including nitrates, anticholinergics, sedatives, calcium channel antagonists, esophageal dilation, and psychological reassurance--are available for the management of esophageal chest pain, none has emerged as the treatment of choice. Studies of nitrate preparations for the treatment of painful motility disorders are limited by a small number of patients and the lack of randomized, placebo-controlled investigations. The efficacy of anticholinergic drugs in hypercontractile esophageal motility disorders has not been reported. In the only prospective placebo-controlled trial using an anti-depressant, trazodone was superior to placebo in relieving symptoms in patients with a variety of esophageal motility disorders. Conflicting results have been described in placebo-controlled trials of the calcium channel antagonists nifedipine and diltiazem in patients with "nutcracker esophagus" or diffuse spasm. Information about the efficacy of verapamil and hydralazine is limited. Esophageal dilation has been useful in selected patients. For many patients, esophageal chest pain may be associated with gastroesophageal reflux. Treatment of these patients with nitrates, calcium channel antagonists, or anticholinergics may aggravate their reflux. The mechanisms of esophageal chest pain remain unknown. Recent studies have suggested that abnormal motility may not be the only factor associated with chest pain. An important number of patients have behavioral abnormalities, increased nociception, impaired coronary vasodilatory reserve, or a diffuse abnormality of smooth muscle. Research into rational therapy for chest pain patients should take into account the contribution of these other factors.
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PMID:Current medical therapy for esophageal motility disorders. 159 73

In half of the patients admitted for observation for acute myocardial infarction, this diagnosis is disproved. Gastro-oesophageal reflux and/or disturbances of oesophageal motility are the cause of the thoracic pain resulting in hospitalization in 16-34% of these patients. In 13-59% of the patients with chronic recurrent thoracic pain without demonstrable ischaemic cardiac disease (IHD), oesophageal disease is, similarly, considered to be the cause of the pain. It is not possible to distinguish whether the pain is caused by oesophageal disease or IHD on the basis of the history, but the differential diagnosis is important as patients with pain on account of oesophageal disease have a good prognosis as regards mortality. The physical and mental conditions of the patients may be improved if the correct diagnosis is established and treatment instituted. Methods of examination to demonstrate oesophageal disease are described. On account of the frequency of the condition and the extent of the methods of examination, a programme of investigation is proposed for patients suspected of having thoracic pain due to oesophageal disease.
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PMID:[Acute recurrent chest pain originating in the esophagus. A review]. 159 11

Oesophageal mucosal specimens (n = 250) were taken from 25 normal subjects (14 females, 11 males; median age 52 years; range 19-63 years) and incubated in physiological saline, pepsin and bile acid solutions to determine whether conjugated bile acids modify the epithelial cytotoxic action of pepsin. Short (5 min) and long (22 min) incubations were carried out and the results were assessed by transmission electron microscopy. Six different parameters of epithelial damage were scored (0-4) by a single 'blinded' pathologist for each of four epithelial layers. The scores after incubation in saline (pH 7 and titrated to pH 2 with HCl) were not different from those of the controls (P = 0.35). Both pepsin and bile acids (pH 2) caused more damage than saline at pH 2 (P less than 0.001) which was similar for the two substances (P = 0.136). Conjugated bile acids in combination with pepsin (pH 2) did not alter the overall extent or pattern of damage caused by pepsin alone (pH 2); P = 0.142). Conjugated bile acids, in concentrations commonly encountered during gastro-oesophageal reflux, did not appear to modify the cytopathic effects of pepsin on oesophageal mucosal cells in vitro. Conjugated bile acids may not be important in the pathogenesis of oesophagitis in patients with acid/peptic gastro-oesophageal reflux.
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PMID:Bile acids do not modify the effects of pepsin on the fine structure of human oesophageal epithelium. 161 Mar 26

An aim of the present study is to clarify the changes of esophageal function after surgical treatments of the esophageal varices or the congenital esophageal stenosis in children. Esophageal manometric studies were performed in sixteen children undergoing the esophageal transection with paraesophageal devascularization or the esophago-esophagostomy with partial esophagectomy before, within 1 month and over 7 months after the operation. The pressure of lower esophageal sphincter (LES), the length of LES, the LES relaxation test and the gastroesophageal reflux (GER) inducing test were measured. 1) Esophageal transection; The pressure dropped within 1 month and returned to the preoperative level over 11 months after the operation. Temporal deterioration of LES function was observed during the early postoperative days. However, return to the preoperative state was gained over 1 year. 2) Esophago-esophagostomy; The pressure and the length of LES were not changed after the operation. The LES function was disturbed preoperatively and moreover long postoperatively, in the case when congenital stenosis closely existed to the esophago-gastric junction. Degree of the postoperative disturbance of the LES function may be influenced by the distance to the part of the transection or the partial esophagectomy from the E-C junction.
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PMID:[Studies on changes in low esophageal sphincter function after esophageal transection or esophago-esophagostomy in children]. 163 Apr 33

The relationship between gastro-esophageal reflux (GER) and asthma, and the role of treatment of this disorder in severe asthma cases remain ill-defined. Using esophageal pH monitoring, pathological GER was demonstrated in 57 of 139 children with severe asthma. Among these 57 patients medical treatment of GER lessened the respiratory symptoms in 24 and was without effect in 33. In the latter group, asthma was improved in 29 with surgical treatment of the GER, the results being less satisfactory in those patients without GER digestive symptoms. Our results suggest that there is a place for treatment of GER in selected children with severe asthma. Esophageal pH monitoring appears useful to detect pathological GER and to determine which patients may benefit from surgical treatment.
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PMID:[Role of surgical treatment of gastro-esophageal reflux in children with severe asthma]. 166 40

While an alkaline component to esophageal reflux disease is known to be present, little is known about its etiology and harmful effects. Simultaneous gastric and esophageal 24-hour pH monitoring was performed in 81 patients with foregut symptoms. The presence of a mechanically defective lower esophageal sphincter was determined by manometry and duodenogastric reflux by computer-assisted discriminant analysis of the gastric pH record. Heartburn, dysphagia, and regurgitation occurred more frequently in those with a mechanically defective sphincter (p < 0.05) and epigastric pain in those with duodenogastric reflux (p < 0.05). Esophagitis was more common and severe in those with a mechanically defective sphincter (p < 0.05). In these patients, the percentage of time over 24 hours that the esophageal pH was less than 4 was 40.5% in patients without duodenogastric reflux but only 10.2% in those with duodenogastric reflux (p < 0.005), suggesting acid damage in the former and alkaline damage in the latter. To establish the origin of the esophageal alkaline exposure, episodes of elevated fasting gastric pH greater than 4 lasting longer than 1 minute were searched for and identified in 45 patients. Esophageal pH tracings were compared for 30 minutes before and after these events. The esophageal pH was higher following these episodes in duodenogastric reflux patients (p < 0.05), suggesting a gastroduodenal origin of the esophageal alkalinization. This study shows that esophageal damage may be due to acid or alkaline reflux. The alkaline component of gastroesophageal reflux is important and should be considered in the evaluation of patients with foregut symptoms so that appropriate medical or surgical therapy can be instituted.
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PMID:Etiology and importance of alkaline esophageal reflux. 167 Feb 23

Ambulatory 24 hour oesophageal pH monitoring was performed in order to detect gastro-oesophageal reflux disease (GERD) in 74 patients presenting with poorly explained ear-nose-throat complaints. A significant number of these patients also benefited from other currently used methods for diagnosing GERD. Oesophageal pH-monitoring demonstrated GERD in half of the patients. For atypical GERD, 24 hour oesophageal pH-monitoring seems to be the most sensitive procedure.
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PMID:[Pharyngo-laryngeal consequences of gastroesophageal reflux. Value of esophageal pH measurements in 74 patients]. 175 69

The clinical course of a patient with pyrosis and intractable hiccups is presented. Hiccups persisted six years after an effective fundoplication had cured pyrosis, and the patient was eventually treated with baclofen. Esophageal function during and after hiccups was studied in detail by means of esophageal manometry and 24-hour-pH monitoring. The relationship between hiccups and gastro-esophageal reflux is discussed.
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PMID:Hiccups and related esophageal motor disorders. 176 63

Recent studies suggest that vagal nerve dysfunction may be important in the aetiology of gastro-oesophageal reflux disease. Delayed oesophageal transit and slowed gastric emptying occur frequently and may also be of pathogenic importance. In 48 patients with gastro-oesophageal reflux disease we studied the prevalence of and relations between autonomic nerve dysfunction (as assessed by cardiovascular reflex tests) and oesophageal transit, oesophageal motility, gastric emptying, and endoscopic grade of oesophagitis. Of the 48 patients, 21 (44%) had abnormal autonomic nerve function, which was predominantly parasympathetic. Oesophageal transit was delayed in 28% of the patients and gastric emptying of the solid component of the meal was delayed in 46%. Oesophageal transit was significantly (p less than 0.007) slower in patients with abnormal autonomic nerve function. The percentage of synchronous oesophageal contractions was related to the score for autonomic nerve dysfunction (r = 0.40, p less than 0.05). There was no significant relation of autonomic nerve dysfunction to either delayed gastric emptying or endoscopic grade of oesophagitis. We conclude that in gastro-oesophageal reflux disease there is a high prevalence of parasympathetic nerve dysfunction which relates to delayed oesophageal transit and abnormal peristalsis and may therefore be of pathogenic importance.
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PMID:Relations among autonomic nerve dysfunction, oesophageal motility, and gastric emptying in gastro-oesophageal reflux disease. 177 45

We studied 30 patients. 20 were males and 10 females. Mean age was 48 year old. Esophageal disease was not present neither gastro-esophageal reflux. Biopsy was taken between 24 hours and 25 days after nasogastric tube (NG) was put into place. Endoscopic findings were: hyperemic mucosa, submucosal hemorrhage, clots, erosions and ulcers near Esophago-gastric junction. Intraepithelial edema, vessel congestion, polymorphonuclear infiltration, fibrin thrombosis of submucosal vessels, ischemia, epithelial regeneration and ulcer were common histologic findings. All endoscopic and histologic alterations were related to the length of time of NG tube contact with the esophageal mucosa. We concluded that NG tube damages the esophageal mucosa by two mechanisms: a) Local irritation that favors b) gastric reflux by decreasing lower esophageal sphincter pressure.
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PMID:[Effect of nasogastric tube on esophageal mucosa]. 184 45


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