Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastro-oesophageal reflux occurs when the pressure barrier of the lower oesophageal sphincter (LOS) fails due to a low basal pressure (less than or equal to 6 mm Hg), sphincteric relaxations or a noncompensated increase in intragastric pressure. This reflux becomes pathological when it leads to symptoms severe enough for the patient to seek medical help or results in reflux oesophagitis or its complications. Damage to the oesophageal mucosa develops when the balance between aggressive and defensive factors is no longer in equilibrium. The main aggressive factor is acid-pepsin or alkaline bile secretion. Defence against this aggression is based on rapid removal of the refluxate from the oesophagus (oesophageal clearance) and on poorly understood mucosal resistance. The length of time acid is in contact with the oesophageal mucosa is shortened by adoption of an upright position, by swallow-induced oesophageal peristalsis and saliva. Treatment of pathological reflux aims (1) to decrease acid aggression by means of H2-receptor antagonists or proton pump inhibitors; (2) to strengthen the anti-reflux barrier and improve oesophageal clearance by prokinetic drugs that increase the LOS pressure and enhance peristaltic contractions; and (3) to boost mucosal resistance by sucralfate or prostaglandin analogues. Initial treatment of gastro-oesophageal reflux disease may be symptomatic provided that there are no alarming symptoms, such as dysphagia, anaemia or weight loss. Usually either H2-receptor blockers or prokinetic drugs are used. Endoscopy is indicated whenever alarming symptoms are present and when there is insufficient symptomatic improvement after a 4-6-week therapeutic trial. Moderate oesophagitis may be treated in the same way.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology and treatment of gastro-oesophageal reflux disease. 257 7

We report a case of a 38-yr-old man presenting with dysphagia due to stricturing of an isolated patch of heterotopic acid-secreting gastric mucosa ("inlet patch") in the proximal esophagus who was successfully treated with endoscopic thermal coagulation while receiving acid suppression with a proton pump inhibitor. Follow-up endoscopy at 15 months after completion of therapy revealed repopulation of the heterotopic gastric mucosa with normal squamous epithelium and continued resolution of the patient's symptoms. The clinical significance of the inlet patch is discussed, and the role of mucosal ablation in treatment of this entity is described.
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PMID:Combined endoscopic thermal electrocoagulation with high dose omeprazole therapy in complicated heterotopic gastric mucosa of the esophagus. 748 16

A combination of the typical symptoms heartburn and regurgitation may be considered virtual proof of gastroesophageal reflux disease. In the case of the atypical symptoms dysphagia, odynophagia, pharingitis, reflux-induced attacks of respiratory distress and intermittent chest pain further diagnostic investigation is indicated. Endoscopy reveals patchy reddening and possibly erosions, ulcers and strictures. Although the decisive pathophysiological factor in reflux disease is motility, the use in particular of acid suppressors represents an important part of treatment; in more severe reflux esophagitis (grades III and IV), proton pump inhibitors are the drugs of first choice. Gastro-esophageal reflux disease is a chronic condition with a recurrence rate of 60-80 percent. For prophylaxis, the minimum dose of antacids required to treat the stage must be administered.
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PMID:[Gastroesophageal reflux. Pathophysiology, diagnosis and rational therapy]. 819 14

Peptic strictures of the esophagus are a common sequelae of long-standing reflux esophagitis. They occur in approximately 10% of patients with gastroesophageal reflux disease seeking medical evaluation. Factors predisposing to stricture formation are poorly understood; however, stricture patients are typically older, have a longer duration of reflux symptoms, and more frequently display abnormal esophageal motility than reflux patients without strictures. Diagnosis can usually be made with a careful history but should be confirmed with a barium esophagram followed by endoscopy with biopsies to exclude malignancy. Relief of dysphagia, which is the initial goal of therapy, can be readily accomplished in most patients using polyethylene or mercury-filled dilators or balloons. An equally important therapeutic objective should be the complete healing of associated esophagitis using proton pump inhibitors. Surgical treatment is reserved for the subset of patients with intractable esophagitis, irreversibly damaged esophagus, or extraesophageal manifestations.
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PMID:Diagnosis and management of peptic esophageal strictures. 895 96

Gastro-oesophageal reflux disease is a very common disorder. Treatment intends to relieve symptoms, prevent complications and recurrence of the disease. The initial approach in a patient with heartburn alone is to begin a therapeutic trial with antacids sucralfate, a prokinetic agent, a histamine-receptor antagonist or a low dose of a proton pump inhibitor. If the therapeutic trial fails, dysphagia or atypical symptoms are present, therapy depends on diagnostic findings. In mild and moderate disease, acute treatment consists of 20 to 40 mg of a proton pump inhibitor (omeprazole, lansoprazole or pantoprazole) and maintenance treatment of low dose omeprazole (10 mg). In severe disease a higher dose is administered, 40 to 80 mg of omeprazole, lansoprazole or pantoprazole for acute treatment and 20 mg of omeprazole for maintenance treatment. Maintenance treatment is adjusted to symptoms and in the case of severe disease also to endoscopic findings.
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PMID:[Internal medicine therapy in reflux disease]. 897 52

Symptomatic stricturing of the esophagus complicates the course of about 10% to 15% of patients with gastroesophageal reflux disease, particularly if they are elderly or if there is an associated Barrett's esophagus. Treatment goals include relief of symptoms of reflux disease and dysphagia, and prevention of their recurrence. The main therapeutic option to date has been endoscopic dilation. Although more than 30% of patients require serial long term dilations, this proportion can be minimized by the concomitant use of long term, high dose proton pump inhibition. Indications for surgery include failure of medical management. It is too early to assess the impact of laparoscopic technology on the treatment of peptic strictures. At this time, well designed prospective comparative trials are needed to quantify better the cost effectiveness of available treatment strategies in the management of patients with esophageal peptic strictures.
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PMID:The treatment of peptic esophageal strictures. 934 87

Laparoscopic Nissen fundoplication has replaced open approaches for refractory gastroesophageal reflux disease (GERD) in many major medical centers. Here we report our preliminary results of the Belsey Mark IV antireflux procedure performed by video-assisted thoracoscopy (VATS-Belsey). Fifteen patients underwent VATS-Belsey. The indications for surgery included GERD refractory to medical therapy (n=10), achalasia (n=2), diffuse esophageal spasms (n=1), epiphrenic esophageal diverticulum (n=1), and paraesophageal hernia (n=1). The median operative time was 235 min. There were three conversions to open minithoracotomy (8-10 cm) necessitated by severe adhesions (n=2) and repair of a gastric perforation (n=1). The median hospital stay was 4 days. Postoperative complications included persistent air leaks, requiring discharge with a Heimlich valve in one patient. There were no perioperative deaths. At a median follow-up of 19 months, ten patients (66%) were asymptomatic and were not taking any antacids. One patient who had taken proton pump inhibitors preoperatively required postoperative H2 blockers for mild heartburn. In three patients, recurrent GERD symptoms (mean follow-up 6 months) led to laparoscopic takedown of the Belsey and Nissen fundoplication. One patient with achalasia, who had recurrent dysphagia after 1 year of relief following VATS myotomy and Belsey, underwent esophagectomy. The Belsey Mark IV antireflux procedure is technically feasible by VATS with minimal morbidity. However, our preliminary results suggest that open thoracotomy for Belsey Mark IV should remain the standard operation for GERD with poor esophageal motility when a thoracic approach is desired. We have modified our approach to laparoscopic partial fundoplications (Toupet or Dor) for severe GERD and poor esophageal motility when an abdominal approach is possible.
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PMID:Preliminary results of thoracoscopic Belsey Mark IV antireflux procedure. 964 40

The principal mechanism leading to gastro-oesophageal reflux is an increased frequency of transient lower oesophageal sphincter relaxations; other factors are oesophageal hypersensitivity to gastric juice, hiatus hernia, and possible duodenal reflux. Patients with classical symptoms such as heartburn and regurgitation may be treated pharmaceutically combined with life style counselling. If the symptoms have not improved after 6 to 12 weeks, endoscopical examination is performed and, if necessary, 24-hour pH monitoring, barium radiographing and manometry. In the case of atypical symptoms such as dysphagia, laryngitis, asthma and chest pain, there is more reason to pursue diagnostic testing. In patients with dysphagia endoscopy is indicated to exclude malignancy. Drug treatment can be subdivided into antacids, H2 receptor antagonists, cytoprotective agents, prokinetics and proton pump inhibitors. In general practice a step-up approach to treatment is preferable, while for specialist treatment a stepdown approach is more (cost-)effective. Drawbacks of medical treatment are considerable frequency of recurrence of oesophagitis, persistence of regurgitation in 'volume refluxers' and controversial data on the possible development of (pre)malignant lesions of oesophagus and stomach. Surgical treatment is a good alternative for patients with persistent severe regurgitation during medical therapy and for young patients who prefer surgery to lifelong medication. Patients with Barrett's oesophagus should undergo regular endoscopic biopsy surveillance.
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PMID:[Gastroesophageal reflux disease: pathophysiology, diagnosis and drug therapy]. 975 35

Peptic esophageal strictures occur in the context of inadequately treated gastroesophageal reflux, especially in elderly patients. Studies show more pronounced abnormalities of esophageal function resulting in an increased number of prolonged reflux episodes. The diagnosis is best made by a combination of barium esophagram and endoscopy. Patients usually require esophageal dilation to relieve dysphagia followed by adequate medical therapy. Proton pump inhibitors are effective for preventing the recurrence of strictures after dilation. In young patients and patients with strictures that are difficult to dilate or need frequent dilations, surgery may be required; however, results can be disappointing.
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PMID:Peptic strictures of the esophagus. 1069 7

AIMS: Few published studies have detailed the long-term results of antireflux surgery. The aim of this study was to assess the long-term success of open Lind fundoplication in controlling the symptoms of gastro-oesophageal reflux disease. METHODS: One hundred and thirty-two patients with reflux symptoms underwent a primary Lind fundoplication between April 1986 and February 1994; all operations were supervised or performed by one surgeon. The median age at operation was 47 (range 17-77) years. All patients attended for follow-up in the early postoperative period. It was possible to conduct a telephone interview to assess long-term symptom control, at a median time of 9.5 (range 5-13) years following operation, in 112 of the 124 patients who were still alive. RESULTS: Ninety-one patients underwent oesophageal pH studies before and soon after operation. The oesophageal pH was less than 4 for a mean 14.9 per cent of the time before operation, falling to 2.4 per cent in the early postoperative period (P < 0.001, Wilcoxon test). At early postoperative assessment, two patients complained of mild reflux symptoms and 44 (33 per cent) complained of postfundoplication symptoms (dysphagia, epigastric bloating and early satiety). At telephone interview, 106 patients (95 per cent) were symptom free with regard to heartburn and regurgitation. Six patients have developed recurrent reflux symptoms, in four of whom symptoms are controlled by a proton pump inhibitor. Two patients have required further antireflux surgery, one within 2 months of the first procedure for severe dysphagia and the other for recurrent reflux. Significant postfundoplication symptoms persist (dysphagia with or without gas bloat) in three patients (3 per cent). CONCLUSIONS: Open Lind fundoplication appears to be effective in the long-term control of gastro-oesophageal reflux in 95 per cent of patients and represents a standard against which the long-term results of laparoscopic surgery will need to be compared.
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PMID:Long-term symptomatic follow-up after lind fundoplication 1071 58


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