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

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

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

An alcoholic man with known reflux esophagitis and Barrett's esophagus developed fever, epigastric pain, subcutaneous crepitus, and leukocytosis from an esophageal perforation at a Barrett's ulcer. Possible risk factors for perforation in this patient included alcoholism, severe gastroesophageal reflux, corticosteroid therapy, noncompliance with antacid and H2 blocker therapy, and the presence of acid-secreting parietal cells in the Barrett's epithelium. Five cases of this complication have previously been reported in a review of the literature, which included 536 cases of Barrett's esophagus or esophageal perforation. This entity may present with a clinical triad of a patient (a) in acute distress with fever and epigastric or noncardiac chest pain and without signs of peritonitis, (b) with symptoms of or known gastroesophageal reflux, and (c) with chest examination revealing subcutaneous crepitus, or chest roentgenogram revealing subcutaneous emphysema, pneumomediastinum, or hydropneumothorax.
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PMID:Esophageal perforation at a Barrett's ulcer. 258 67

Symptomatic involvement of the oesophageal mucosa by pemphigus vulgaris is rare. We describe 1 patient who was treated with oral steroids during a blistering phase, when epigastric pain developed. Endoscopy revealed multiple ulcerations all over the oesophagus, but gastroduodenal mucosa was normal. The symptoms disappeared following cimetidine for gastro-oesophageal reflux and increase of steroid dosage. When painful symptoms appear from the upper digestive tract during corticosteroid treatment of pemphigus, the possibility of acantholytic involvement of oesophageal mucosa must be kept in mind. Its implication for the dosage of steroids is opposite that in steroid-induced peptic ulcers. Carefully performed upper gastrointestinal tract endoscopy is helpful in these patients.
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PMID:Oesophageal pemphigus vulgaris. 338 52

The aim of this study was to describe the clinical features of patients with chronic unexplained dyspepsia and compare the symptoms with peptic ulcer and biliary pain, and determine the prevalence of symptoms that may indicate psychoneurotic traits and measure chronic illness behaviour (days lost from work and doctor visits). Studied were: 113 patients with essential dyspepsia, defined as endoscopically confirmed non-ulcer dyspepsia where gallstones, the irritable bowel syndrome and gastro-esophageal reflux have been excluded and there is no ascertainable cause for the dyspepsia; 55 patients with dyspepsia and peptic ulceration at endoscopy; and 53 patients with diagnosed biliary pain and cholelithiasis, proven at cholecystectomy. All patients completed a detailed structured history questionnaire in the presence of one investigator. More patients with peptic ulcer than with essential dyspepsia experienced night pain, pain relieved by food, and vomiting, while more patients with essential dyspepsia than with cholelithiasis experienced epigastric pain, lack of radiation of pain, continuous pain, mild to moderate pain, pain before meals, pain relieved by food and antacids, pain aggravated by food and alcohol, and an absence of vomiting (all p less than 0.01). Symptoms suggesting psychoneurosis, aerophagy symptoms, and chronic illness behaviour were similar in all groups. We conclude that certain symptoms may be of value in diagnosing the underlying cause of dyspepsia.
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PMID:Comparison of the clinical features and illness behaviour of patients presenting with dyspepsia of unknown cause (essential dyspepsia) and organic disease. 346 12

A gastroesophageal polyp is a rare finding. The case of an adolescent male presenting with epigastric pain and such a polyp is described. These polyps are usually described in the clinical setting of gastroesophageal reflux and esophagitis. Polyps can be identified radiographically as a characteristic filling defect at the gastroesophageal junction. Endoscopy should be used to confirm the diagnosis. Polypectomy is recommended when malignancy is suspected or where there is evidence suggesting that the polyp is causing symptoms.
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PMID:Gastroesophageal polyp diagnosed in an adolescent presenting with epigastric pain. 366 99

The authors reviewed 39 patients in whom bile reflux gastritis and esophagitis were diagnosed and treated. All had epigastric pain not relieved by antacids, 26 had heart burn, 13 dysphagia and 7 hematemesis. On endoscopic examination, all had reflux of bile into the stomach with gastritis, 14 had bile in the esophagus and 21 had esophagitis. Results of biopsy in 15 patients were consistent with gastritis or esophagitis. All but one patient had a history of peptic ulcer disease-gastric or duodenal-and 35 had undergone 48 gastric operationns. Treatment was medical but those refractory to medical management underwent operation. A Roux-en-Y diversion of bile was the most successful operative treatment, benefiting 9 of 12 patients. An adequate length of the efferent limb was found to be important as two patients were not improved until this length was increased to 45 cm. Successful treatment depends on the ability to distinguish this syndrome from recurrent acid peptic disease and esophageal reflux due to sphincteric incompetence.
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PMID:Bile reflux gastritis and esophagitis. 736 84

Gastrointestinal and liver disorders are often observed in high performance athletes, especially those training for the increasingly popular endurance sports including the marathon and the triathlon. The disorders often start with stress before competition or training, followed by dehydration during the event. Insufficient training is an aggravating factor as are certain environmental factors including hot climate, irregular terrain and high altitude. Athletes may also consume non-steroid anti-inflammatory drugs, for example after a minor bone lesion or joint sprain, in an attempt to maintain their highest level of performance. Gastric signs include epigastric pain known to be caused by ischaemic gastritis resulting from decreased splanchnic flow and increased vasoconstriction in the gastric mucosa. Gastrooesophageal reflux results from modifications in sphincter tone and gastric emptying. Drinking hyperosmolar liquids also plays a role. Abdominal pain, diarrhoea, melena and uncommonly ischaemic colitis are the main signs of colic disorders. Mesenteric ischaemia may occur due to lowered splanchnic blood supply (by as much as 80% in some cases). Mechanical trauma is another mechanism; in marathon runners the "caecal slap syndrome" is a repeated microtrauma of the caecum against a hypertrophied muscular wall. Waterborne infectious agents may also lead to colic lesions. Exertion heat stroke is an emergency situation which can cause multiple organ damage and usually occurs after long intense exercise, often, but not always in a hot environment. Uncompensated thermogenesis and excessive loss of water by perspiration leads to central hyperthermia and ischaemic hepatic necrosis. Fatal liver failure has been observed. More or less severe symptoms of gastrointestinal or hepatic disorders are observed in 30% of high performance athletes and the incidence may reach 40% in those who have trained insufficiently. Such disorders lead to reduced performance in 10% of these athletes.
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PMID:[Hepato-digestive disorders in athletic practice]. 802 25

Esophageal diseases frequently cause symptoms such as heartburn, epigastric pain and dysphagia. This article discusses the indications, techniques and limitations of currently available diagnostic procedures. Investigation of symptoms should proceed in a logical stepwise manner, beginning with endoscopy to exclude esophagitis or neoplasia. Symptoms due to acid reflux can be identified by 24h esophageal pH-metry to document a temporal association between symptoms and episodes of esophageal acidification. Stationary or ambulatory manometric recording of esophageal pressures can be used to diagnose esophageal motor disorders such as achalasia, nutcracker esophagus, diffuse esophageal spasm, or dysfunction of the upper or lower esophageal sphincter. Combined 24 h pH-manometry should be used to test the temporal association between pain, reflux, or abnormal motility in patients with non-cardiac chest pain. Video-fluoroscopy is the most appropriate technique to diagnose swallowing disorders. Pulmonary aspiration of gastro-esophageal reflux can be documented with scintigraphy.
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PMID:[Motility disorders and assessment methods of the esophagus]. 821 Oct 52

Nodular duodenum, frequently described as nodular duodenitis, is endoscopically characterized by multiple erythematous nodules in the proximal duodenum and may represent a variant of duodenal inflammation. This study examines the incidence, clinical presentation, histologic correlates, natural history, and response to therapy of nodular duodenum in 83 patients who presented with epigastric pain, heartburn, early satiety, bloating, nausea, vomiting, or gastrointestinal bleeding. There was a previous history of peptic ulcer disease in 58% of patients and gastroesophageal reflux in 33%. None of the patients had associated end-stage renal disease. Endoscopically, in addition to nodular duodenum, esophagitis was found in 17% of patients and gastritis in 32%. Histology of duodenal nodules revealed chronic inflammation in 58% of patients, Brunner's gland hyperplasia in 9%, gastric heterotopia in 7%, and normal mucosa in 26% of patients. In a group of 34 patients studied prospectively, high dosage (300 mg orally bid) therapy with the H2-antagonist ranitidine for 8 wk significantly improved symptoms and endoscopic appearance (p < 0.05). In 26 patients who completely or partially failed H2-antagonist therapy, continuation of therapy with omeprazole (40 mg orally qd) for 8 wk significantly improved symptoms and endoscopic findings (p < 0.05) in 10 patients. These therapeutic approaches led to improvement in the endoscopic findings, but to no statistically significant changes in the underlying histologic appearance of the duodenum. We conclude that nodular duodenum is an endoscopically distinct entity that may respond clinically to antisecretory therapy, but remains difficult to eradicate completely.
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PMID:Clinical and pathologic features of the nodular duodenum. 831 6


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