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)

A patient with dysphagia and chest pain was shown by manometry to have high-amplitude peristaltic esophageal contractions (nutcracker esophagus). Worsening symptoms over the next two years led to the performance of repeated manometric studies, which showed diffuse esophageal spasm. This demonstration of a transition from nutcracker esophagus to diffuse esophageal spasm lends further support for consideration of the nutcracker esophagus as a manometric disorder associated with chest pain or dysphagia. Furthermore, it suggests a pathophysiologic relationship between the nutcracker esophagus, a disorder with preserved peristalsis, and diffuse esophageal spasm, the classic dysmotility considered to be of neurogenic origin.
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PMID:Transition from peristaltic esophageal contractions to diffuse esophageal spasm. 375 28

Symptomatic assessment and oesophageal investigations were done in 25 consecutive patients with the irritable bowel syndrome attending a gastroenterological clinic. Symptoms of gastro-oesophageal reflux, dysphagia, and a globus sensation were significantly commoner than in a control group of fracture clinic patients. Ambulatory oesophageal pH monitoring showed clearly abnormal reflux in 11 of 22 patients (50%). Nine patients had macroscopic endoscopic changes and a further 11 biopsy changes alone, of oesophagitis which was thus present in 80% overall. Lower oesophageal sphincter pressure was significantly less in irritable bowel patients than in age and sex matched controls, but upper oesophageal sphincter pressure was comparable in the two groups and disordered peristalsis was not found. Oesophageal symptoms in the irritable bowel syndrome are mainly caused by gastro-oesophageal reflux predisposed to by a subnormal lower oesophageal sphincter pressure, rather than by oesophageal spasm.
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PMID:Gastro-oesophageal reflux in the irritable bowel syndrome. 378 23

Chest pain due to esophageal spasm or esophagitis may mimic pain of variant angina. Differential diagnosis of the two diseases is often difficult and requires various tests, the value of which is discussed. These problems are illustrated by three cases. The esophageal investigation should preferably be preceded by coronary arteriography. Chest pain or dysphagia due to iced drinks is not specific for esophageal spasm but may be due to coronary spasm.
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PMID:[Spontaneous precordial pain: coronary spasm or esophageal pathology?]. 395 80

The cause of chest pain associated with mitral valve prolapse remains unclear. A young woman with chest pain ascribed to mitral valve prolapse is described. Response of chest discomfort to atenolol therapy had been poor. The patient's chest discomfort and concomitant esophageal spasm were provoked by intravenous infusion of edrophonium chloride during esophageal manometry. A Bernstein acid infusion test also induced her chest pain. Review of systems revealed intermittent dysphagia and postprandial heartburn. In certain patients with mitral valve prolapse, esophageal motility disorders may be the cause of chest discomfort.
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PMID:Chest pain associated with mitral valve prolapse. Evidence for esophageal origin. 396 63

The effect of nifedipine on esophageal symptoms was evaluated in 20 patients with primary esophageal motor disorders. The patients were randomized to receive nifedipine (10 mg t.i.d.) or placebo for two weeks, and then crossed over to receive the other medication. Ten patients had hypertensive lower esophageal sphincter, four had diffuse esophageal spasm, three had vigorous achalasia, two had "nutcracker esophagus," and one patient had achalasia. The score of chest pain or dysphagia was recorded on a scale of 0 to 10 during each study. The patients who received nifedipine improved significantly compared to those who received placebo. This improvement was most marked in patients with hypertensive lower esophageal sphincter. No significant side effects or changes in blood pressure were encountered in any of the study groups. Our results indicate that patients with primary esophageal motor disorders have a good clinical response to nifedipine therapy.
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PMID:Primary esophageal motor disorders: clinical response to nifedipine. 397 47

The nutcracker esophagus is a newly defined subset of primary esophageal motility disorders that can be responsible for dysphagia and/or chest pain. Any possible relationship between this entity and diffuse esophageal spasm is poorly understood. Herein we report a case of nutcracker esophagus that showed a transition to classical diffuse esophageal spasm during 1 year follow-up. This transition supports the hypothesis that nutcracker esophagus and diffuse esophageal spasm may be related disorders.
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PMID:Transition from nutcracker esophagus to diffuse esophageal spasm. 398 89

A 38-year-old patient, complaining of dysphagia and substernal pain of nine months' duration, was found by manometric studies to have diffuse oesophageal spasm. As has similarly been reported for cholinergic agents in achalasia and in some cases of diffuse oesophageal spasm the oesophageal body responded in a hypersensitive fashion to subcutaneous and intravenous injections of pentagastrin. This effect was inhibited by the intravenous administration of atropine and completely abolished by nitroglycerine. When pentagastrin was subcutaneously injected before a barium examination a distortion of the oesophageal contour, described as curling or corkscrew oesophagus, regularly appeared.
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PMID:Supersensitivity to pentagastrin in diffuse oesophageal spasm. 421 3

Five patients with painful primary esophageal motility disorders underwent pharmacologic testing with isosorbide and hydralazine. While neither agent affected baseline amplitude or duration of distal esophageal contractions, pretreatment with hydralazine significantly blunted the response to bethanechol (mean esophageal contraction duration, 31.4 +/- 4.8 s after bethanechol alone vs. 12.7 +/- 1.8 s after bethanechol and hydralazine p less than 0.005). Premedication with isosorbide was significantly less effective. In addition, while all 5 patients experienced chest pain in response to bethanechol alone, only 1 of 5 experienced chest pain in response to bethanechol after previous hydralazine administration; 3 patients had chest pain after previous administration of isosorbide. Patients who were placed on long-term oral hydralazine therapy experienced improvement in chest pain and dysphagia with concomitant decrease in amplitude and duration of esophageal contractions on repeat motility study (176.5 +/- 23.8 mmHg to 97.3 +/- 27.0 mmHg, p less than 0.05, 7.5 +/- 0.8 s to 5.2 +/- 0.5 s, p less than 0.005). Hydralazine appears to be of value in the treatment of diffuse esophageal spasm and other painful primary esophageal motility disorders.
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PMID:Effect of isosorbide and hydralazine in painful primary esophageal motility disorders. 612 65

Fifty-eight consecutive patients were investigated for spontaneous chest pain without symptoms of effort angina, previous myocardial infarction or other signs of cardiac disease, to determine the incidence of oesophageal spasm. The character of the chest pain, its context and the results of resting ECGs were analysed. An ECG recorded during chest pain was available in 23 cases and exercise stress testing was performed in 43 cases. Coronary angiography was carried out in all patients. The coronary arteries were normal or showed little change in 44 patients. Further investigations were ordered: oesophageal manometry (42 cases), echocardiography 44 cases) and ergometrine provocation tests (44 cases). The patients were then divided into 4 groups: 23 patients (40 p. 100) with coronary artery disease; either atheroma (14 cases) or spasm (9 cases); 8 patients (13,5 p. 100) with non-coronary cardiac pathology (myocardial hypertrophy or mitral valve prolapse); 15 patients (26 p. 100) with oesophageal spasm alone; 12 patients (20,5 p. 100) with no obvious organic disease. Often simulating spontaneous angina, clinically and electrocardiographically, oesophageal spasm may sometimes be distinguished (6 out of 15 cases) by the finding of painful dysphagia on swallowing ice-cold liquid. The condition is confirmed by oesophageal manometry which shows abnormalities of oesophageal contraction. In addition, 13 out of 15 patients in our series had hypotonia of the gastro-oesophageal sphincter. Dyskinetic phenomena and this hypotonia should be taken into consideration in the treatment of this condition.
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PMID:[Esophageal spasm: a common cause of spontaneous precordial pain]. 643 62

Nine patients with severe symptoms of diffuse esophageal spasm and lower esophageal sphincter dysfunction who were unresponsive to medical therapy and bougienage dilatation were treated by forceful pneumatic dilatation. Treatment with pneumatic dilatation in eight of the nine patients produced a marked improvement in dysphagia and regurgitation (average follow-up of 37.4 months). Esophageal motility performed up to three years (average 12.4 months) after clinically successful pneumatic dilatation revealed a decrease in lower esophageal sphincter pressure from 34.0 +/- 4.0 mm Hg (mean +/- standard error) to 19.2 +/- 2.7 mm Hg (P less than 0.01). There were no significant changes in either the percentage of lower esophageal sphincter relaxation or the type of esophageal motor pattern. We conclude from this study that pneumatic dilatation is an effective form of therapy for a select group of patients with severe symptomatic diffuse esophageal spasm with lower esophageal sphincter dysfunction who are unresponsive to conventional medical therapy.
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PMID:Pneumatic dilatation in patients with symptomatic diffuse esophageal spasm and lower esophageal sphincter dysfunction. 661 85


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