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)

Esophageal motility disorders are now known to be a heterogeneous group of conditions that commonly cause dysphagia and chest pain. Motor dysphagia is usually provoked by solids and liquids (in contrast to mechanical dysphagia, which is usually provoked by solids only). Chest pain with these disorders is nonspecific and can mimic angina pectoris. In many patients with diffuse esophageal spasm or nutcracker esophagus, pain appears to be caused by abnormal sensory function rather than contraction abnormalities. Barium esophagography and esophageal manometry are complementary studies in the evaluation of motility disorders.
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PMID:Diagnosis of esophageal motility disorders. 239 4

The three main symptoms of esophageal disease or disorder are dysphagia, chest pain, and heartburn. Dysphagia in achalasia is mainly due to a non-relaxing lower esophageal sphincter (LES). The mechanism of dysphagia in diffuse esophageal spasm and related motor disorders is related to a combination of several factors including incomplete LES relaxation, failed or weak peristalsis (pressure less than 30 mmHg in the distal esophagus, and orad positive pressure gradient). Meal manometry and balloon distention may prove to be useful provocation tests. Chest pain of esophageal origin may be due to gastroesophageal reflux and esophageal motility disorders; it may also be a manifestation of an irritable esophagus, in which the esophagus is hypersensitive to various stimuli (chemical, mechanical, ischemic). Esophageal provocation tests may suggest the esophageal origin of the pain but do not give information on the nature of the esophageal disorder. Twenty-four-hour pH and pressure measurements may, however, yield this information. Heartburn and acid regurgitations are the most typical symptoms of gastroesophageal reflux. Transient relaxations of the LES are considered to be an important contributory mechanism of reflux. Absent basal LES pressure is another mechanism, which accounts for about one-fourth of the reflux episodes in patients with severe reflux esophagitis. During long-lasting inappropriate relaxations, swallows often produce deglutitive contraction waves that die out in the upper esophagus, suggesting that reflux often occurs during periods of inhibition of both LES tone and peristaltic esophageal activity.
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PMID:Recent studies of the pathophysiology and diagnosis of esophageal symptoms. 223 80

Manometric criteria for diffuse esophageal spasm have recently been restated. In this study, a cohort of 358 subjects was evaluated in a gastrointestinal motility laboratory for dysphagia and/or chest pain. Applying the recently proposed criteria of Richter and Castell, 18 subjects (5%) were diagnosed as having DES. Dysphagia was the major complaint (89%), while 44% of patients complained of chest pain and 33% of both symptoms. All patients shared more than 30% simultaneous contractions after wet swallows interspersed with normal peristaltic sequences. Associated manometric findings were repetitive (greater than 3 peaks) contractions (67%), high-amplitude contractions (33%), spontaneous activity (22%), prolonged duration (11%), and lower esophageal sphincter abnormalities (5%). Radiology disclosed significant abnormalities in only 27% of DES patients.
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PMID:Clinical and manometric aspects of diffuse esophageal spasm in a cohort of subjects evaluated for dysphagia and/or chest pain. 224 5

Ambulatory 24-hour esophageal manometry was applied to analyze motility in 12 normal subjects and 9 patients with chest pain and dysphagia caused by diffuse esophageal spasm (DES). Pain episodes characterized by nonperistaltic activity occurred in 7 of 9 patients. A score based on 10 variables of the motility pattern differentiated patients from normal subjects and quantitated the severity of the disorder. Ambulatory motility monitoring was prospectively performed in 8 normal subjects and 37 patients: 8 with DES, 13 with hypertensive contractions, and 16 with a nonspecific disorder on standard manometry. The score was positive in 6 of 8 patients with DES and negative in all normal subjects (accuracy 87 percent). Nine of the 13 patients with hypertensive contractions (70 percent) and 6 of 16 with nonspecific disorders (38 percent) had a pathologic score reflecting a dysmotility as severe as DES. Ambulatory esophageal manometry is a more physiologic way to identify a motor disorder than standard manometry and has the potential to improve selection of patients for a surgical myotomy.
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PMID:A new technique to define and clarify esophageal motor disorders. 229 91

Epiphrenic diverticula occur in association with motor disorders of the distal esophagus, including achalasia and diffuse esophageal spasm. Four patients with huge symptomatic epiphrenic diverticula are presented to emphasize the need for complete radiographic and manometric studies of the esophagus to document this motor dysfunction prior to performing combined diverticulectomy and esophagomyotomy. Each patient had achalasia with symptoms extending from 4 to 25 years. Diverticulectomy and esophagomyotomy were performed in every patient. One patient had previously undergone diverticulectomy alone, with prompt recurrence of the lesion. During a follow-up period extending from 2 to 10 years, three patients were alive and well. One patient developed recurrent dysphagia due to reflux esophagitis and stricture requiring dilatation. It is essential that esophagomyotomy be part of the initial operative procedure. In selected patients, an antireflux procedure may also be indicated.
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PMID:Management of huge epiphrenic esophageal diverticula. 249 4

Simultaneous recordings of myoelectric and manometric activities of the esophagus were made in two groups of patients with scleroderma. Group A consisted of patients who suffered from functional dysphagia that had appeared recently, and who had a normal size esophagus when examined radiographically. Patients in group B had complained of functional dysphagia for several years and showed a dilated hypotonic esophagus on x-ray. A control group of five normal subjects was also examined in the same manner. The study was carried out by means of a peroral probe with two pairs of suction-needle electrodes and two manometric side-hole catheters positioned at the same levels as the electrodes. Standard manometric examination of the esophagus was carried out in all patients. Normal subjects after each deglutition showed a propagated burst of spikes in correspondence with the ascending phase of the peristaltic wave, whereas, in the period between deglutitions, rare spikes and no pressure waves were recorded. Group A patients were characterized by the frequent appearance during the interdeglutitive period of spontaneous rhythmic sequences or bursts of spikes associated with pressure waves. In these patients, repetitive nonpropagated spike bursts with a higher than normal amplitude and duration were observed after deglutitions in association with high-amplitude nonpropagated repetitive pressure waves similar to those observed in diffuse esophageal spasm (DES). Five of the seven group B patients showed spike bursts and pressure waves with both amplitude and duration markedly lower than normal. The remaining two patients from group B presented no spike bursts or pressure waves at all. Standard manometry demonstrated findings equivalent to those obtained via electromyography (EMG) in all patients of group B and in only two patients of group A. In conclusion, the functional dysphagia of patients with scleroderma can be attributed to two different motor disorders. The first one is characterized by disorganized myoelectric hyperactivity and may have a manometric appearance similar to that of diffuse spasm. The second one is characterized by a marked decrease in myoelectric activity and corresponds to the classic manometric finding of scleroderma involvement of the esophagus. Both these myoelectric patterns seem to be related to subsequent stages of esophageal scleroderma involvement.
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PMID:Esophageal electromyography in scleroderma patients with functional dysphagia. 259 50

Five adolescents, 13-18 years of age, underwent esophageal manometric studies because of chronic symptoms suggestive of esophageal dysfunction. Four of five patients had episodic nonexertional midchest pain; two patients experienced intermittent dysphagia. The manometric findings for these adolescents were consistent with a primary motility disorder known as diffuse esophageal spasm, a condition not previously reported in this age group. This represents approximately 1% of all pediatric patients undergoing esophageal manometry at our institution for the past 5 years. They have been followed for at least 2 years and three have experienced gradual resolution of their symptoms with normalization of manometric findings. Our report emphasizes two main points: (a) Diffuse esophageal spasm may cause chest pain and dysphagia in adolescents; and (b) the clinical history and esophageal manometric findings establish the diagnosis of diffuse esophageal spasm.
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PMID:Chest pain and dysphagia in adolescents caused by diffuse esophageal spasm. 262 23

Seven patients with epidermolysis bullosa dystrophica and chronic and recurrent oesophageal lesions such as spasm, strictures, and complete occlusion were studied. Dysphagia could be cured with drugs if it was caused by bullae formation or spasm. If oesophageal strictures were present, endoscopy and bouginage with corticosteroid prophylaxis during the quiescent phase of the disease was a safe and useful procedure. We have also given corticosteroids, which reduced the oedema caused by bullae formation and oral phenytoin, which reduced epithelial detachment by inhibiting collagenase activity. Verapamil counteracted oesophageal spasm and pureed food during periods of dysphagia reduced blistering of the upper oesophagus.
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PMID:Management of oesophageal stenosis in epidermolysis bullosa dystrophica. 275 29

Since the pharynx and the esophagus are a functional unit, functional radiodiagnosis has to be directed at pharyngo-esophageal interaction. Among our collective of 73 patients suffering from achalasia or diffuse esophageal spasm, we were able to recognize a substantially increased incidence of morphological or functional pharyngeal disorders by means of cineradiography. The functional alterations in particular were often not revealed by conventional fluoroscopy. High-speed cineradiography, with its high temporal and spatial resolution, turned out to be a valuable tool in analysis of the origin of pharyngeal dysphagia. Manometry correlated very well with the radiologic findings in tubular esophagus, but proved unreliable in the detection of alterations of the upper esophageal sphincter region, because of problems inherent in the method. Furthermore, membranous stenosis (webs), lateral or dorsal diverticula, and asymmetry of the pharynx were observed strikingly often.
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PMID:[Functional and morphological changes in the pharynx in achalasia and diffuse esophageal spasm]. 279 49

Various oesophageal manometric disorders have been associated with chest pain or dysphagia. The classic motility disorders are achalasia and diffuse oesophageal spasm. In achalasia, a disorder of aperistalsis in the oesophageal body and incomplete relaxation of the lower oesophageal sphincter, either surgical myotomy or pneumatic dilatation is an effective approach, although some investigators have suggested a role for pharmacological therapy. For the treatment of diffuse oesophageal spasm, a disorder of non-peristaltic motor activity in the oesophagus, various pharmacological approaches with nitrates, anticholinergics, and calcium antagonists have been used. In the presence of associated lower oesophageal sphincter dysfunction, bouginage or pneumatic dilatation may be indicated. Long oesophagomyotomy should be considered for those patients who fail to respond to these measures. Recent manometric techniques have led to the identification of patients with chest pain or dysphagia who have abnormalities of increased contractile amplitude ('nutcracker' oesophagus) or duration. An association with gastro-oesophageal reflux or with psychiatric disturbance has been suggested. Treatment directed towards these factors is indicated and may be supplemented by pharmacological intervention, e.g. by calcium antagonists or anticholinergics.
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PMID:Primary oesophageal motility disorders. Current therapeutic concepts. 286 26


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