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)

The predictive value of esophagus-related symptoms for the diagnosis of esophageal dysmotility induced by systemic sclerosis (SSc) was prospectively evaluated in 50 consecutive patients with SSc. Patients were classified as symptomatic when either dysphagia or repeated episodes of heartburn were present. All patients underwent esophageal manometry; SSc-induced esophageal dysfunction was diagnosed when there was aperistalsis or marked hypocontractility of the distal two-thirds of the esophageal body. Twenty-nine patients (58%) had a history of esophagus-related symptoms, while 21 patients (42%) were asymptomatic. Compared to esophageal manometry, esophagus-related symptoms had a sensitivity of 64%, a specificity of 52%, a negative predictive value of 50% and a positive predictive value of 62% for the diagnosis of SSc-induced esophageal dysfunction. In conclusion, the association of esophagus-related symptoms and esophageal motility pattern is poor. As clinical management strategies depend on proof of esophageal dysfunction, screening examinations are mandatory in all patients with SSc.
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PMID:Esophageal manometry in systemic sclerosis: screening procedure or confined to symptomatic patients? 926 22

Dysphagia is related to the impairment of food passage from the mouth to the stomach. Globus pharyngis implies the frequent and often painful sensation of a lump in the throat that usually does not interfere with swallowing and may even be relieved by food intake. The diagnosis is based upon a careful history, clinical examination, endoscopy, dynamic imaging (videofluoroscopy, cinematography, videosonography) and electrophysiologic procedures (including pharyngoesophageal manometry, electromyography and pH determinations). Structural lesions of the cervical spine such as diffuse idiopathic skeletal hyperostosis are rare causes of dysphagia. Dysphagia following anterior cervical fusion as well as globus and dysphonia due to dysfunction of the vertebral joints are more likely. Symptoms with swallowing fluids indicate a neurogenic origin. Dyscoordinated swallowing, nasal reflux, dysphonia or general weakness may also occur. Chronic aspiration with respiratory compromize is the main consequence in a variety of neurological disorders as well as in cases of postsurgical dysphagia. Relaxation of the upper esophageal sphincter indicates coordinated muscle movement between the pharynx and esophagus. Dysfunction of the pharyngoesophageal segment may lead to cricopharyngeal achalasia. A dyskinetic sphincter commonly represents an extrapharyngeal cause: i.e., disease associated with gastroesophageal reflux. Disorders of the esophageal phase of deglutition can produce retrosternal pain, heartburn, regurgitation and vomiting, as well as laryngeal and respiratory signs. Esophageal motility disorders include lower achalasia, tumors, peptic strictures, inflammatory diseases, drug-induced ulcers, rings and webs. Motility disorders present with aperistaltic, spontaneous contractions, diffuse esophagospasm, or a hypermotile esophagus. Gastroesophageal reflux with esophagitis must always be excluded, especially in patients with a globus sensation. The multiple features of the appearance of the symptoms of dysphagia and globus makes multidisciplinary approach necessary in order to establish a diagnosis and begin effective treatment.
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PMID:[Deglutition disorders]. 977 28

Fundoplication performed for gastroesophageal reflux disease may be complicated by postoperative dysphagia despite successful reduction in reflux symptoms. This is more likely in those patients with reflux who have concurrent esophageal dysmotility. The aim of this study was to establish whether esophageal transit studies using a technetium-99m jello bolus (jello esophageal transit) could detect the presence of motility disorders preoperatively and hence predict surgical outcome. Transit studies in 33 healthy volunteers yielded a normal range of 2 to 24 seconds using ninety-fifth percentile distribution. In the second phase of the study, 26 patients accepted for laparoscopic fundoplication were enrolled: jello esophageal transit, manometry, and endoscopy were attempted preoperatively in all subjects. A clinical dysphagia score was assigned from a questionnaire. Six months after surgery, five patients had dysphagia and of these four were found to have abnormal preoperative jello esophageal transit, for a sensitivity of 80%. Of the 21 patients who had no dysphagia after surgery, 20 patients had normal preoperative jello esophageal transit, showing a specificity of 95%. This esophageal transit study is noninvasive, reliable, and sensitive. When performed prior to fundoplication, it appears to be of significant value in detecting a subtle functional motility disorder that predisposes to postoperative dysphagia. Jello esophageal transit may assist the surgeon in planning treatment of gastroesophageal reflux disease.
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PMID:Preoperative esophageal transit studies are a useful predictor of dysphagia after fundoplication. 1048 5

Esophageal dysmotility occurs in association with GERD; however, the cause of these motility abnormalities is not known. It is also not clear whether injury results from the presence of acid itself, inflammatory change or fibrosisin the esophageal wall. It is also unclear if reversal of these abnormalities takes place, and if so, to what degree. There are, however, a subset of patients who seem to have improvement with effective medical or surgical therapy, parodoxically, the same patients in whom a fundoplication, particularly a complete wrap, would lead to severe postoperative dysphagia secondary to preoperative dysmotility. What does all this mean for the individual patient? It is likely that most will not have any important change in esophageal motility abnormalities with standard medical or surgical therapy. Fundoplication might be safely performed in patients with minimal motility abnormalities, but those with severe abnormalities should be approached with caution. The conservative approach is to perform a partial fundoplication (Toupet) in those with ineffective motility (> 30% low-amplitude or nontransmitted contractions). It is hoped that future investigations will aid in understanding the pathogenesis of these abnormalities and how they can be used more precisely to guide antireflux therapy.
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PMID:Motility abnormalities in gastroesophageal reflux disease. 1069 9

Toupet (270 degrees) fundoplication is commonly recommended for patients with gastroesophageal reflux (GER) and esophageal dysmotility. However, Toupet fundoplication may be less effective at protecting against reflux than Nissen (360 degrees) fundoplication. We therefore compared the effectiveness and durability of both types of fundoplication as a function of preoperative esophageal motility. From January 1992 through January 1998, 669 patients with GER underwent laparoscopic fundoplication (78 Toupet, 591 Nissen). Patients scored heartburn, regurgitation, and dysphagia preoperatively, and at 6 weeks and 1 year postoperatively, using a 0 ("none") to 3 ("severe") scale. We compared symptom scores (Wilcoxon rank sum test) and redo fundoplication rates (Fisher exact test) in Toupet and Nissen patients. We also performed subgroup analyses on 81 patients with impaired esophageal motility (mean peristaltic amplitude, <30 mm Hg or peristalsis <70% of wet swallows) and 588 patients with normal esophageal motility. Toupet and Nissen patients reported similar preoperative heartburn, regurgitation, and dysphagia. At 6 weeks after operation, heartburn and regurgitation were similarly improved in both groups, but dysphagia was more prevalent among Nissen patients. After 1 year, heartburn and regurgitation were re-emerging in Toupet patients, and dysphagia was again similar between groups. Patients with impaired motility who have Nissen fundoplication are no more likely to suffer persistent dysphagia than their counterparts who have Toupet fundoplication. In addition, patients with normal motility are more likely to develop symptom recurrence after Toupet fundoplication than Nissen fundoplication, with no distinction in dysphagia rates. We conclude that since Toupet patients suffer more heartburn recurrence than Nissen patients, with similar dysphagia, selective use of Toupet fundoplication requires further study.
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PMID:Heartburn is more likely to recur after Toupet fundoplication than Nissen fundoplication. 1124 51

Transdermal nicotine delivery systems are widely used in smoking cessation. The purpose of this study was to determine whether common symptoms of pyrosis and dyspepsia associated with these patches are related to gastroesophageal reflux or esophageal dysmotility. Twenty-seven paid volunteer cigarette smokers (> 15 cigarettes/day) without symptomatic gastroesophageal reflux disease participated in this single-blinded, placebo-controlled study. Twenty subjects completed the study. Subjects underwent three sequential 24-h intraesophageal pH/motor studies (Synectics model T32342084, Shore View, MN). The pH/motility probe was positioned 5 cm above the manometrically determined LES. A placebo patch was applied for the first 24-h study and a 15-mg nicotine patch (Nicotrol) was applied for the initial 16 h (removed for remaining 8 h) of the second 24-h period. A 21-mg nicotine patch (Nicoderm) was applied for another 24-h study period. All subjects consumed an identical, defined diet documented by meal receipts, and refrained from smoking and tobacco use throughout the study periods (CO breath test confirmation). The Wilcoxon, paired t-test, exact McNemar statistical methods were used. The results showed that there were no significant differences in reflux symptoms (pyrosis, chest pain, nausea, dysphagia), supine gastroesophageal reflux (number of episodes, duration, or cumulative acid exposure), or the total number of reflux episodes between placebo and nicotine patch treatment periods. The number of post-prandial upright acid reflux episodes (p = 004) and number of upright acid reflux episodes lasting more than 5 min (p = 0.007) were statistically higher with the placebo patch compared to the active nicotine patches. No differences in intraesophageal pH or motility indices were noted between the two transdermal nicotine patches (Nicotrol, Nicoderm). It was concluded that dyspeptic symptoms in subjects utilizing transdermal nicotine patches are not related to gastroesophageal reflux or to esophageal motor abnormalities.
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PMID:Transdermal nicotine patches do not cause clinically significant gastroesophageal reflux or esophageal motor disorders. 1107 35

Our aim was to review the use of esophageal investigations in patients with suspected connective tissue disease (CTD). Forty-seven patients (39 women and 8 men) with suspected CTD were referred for esophageal manometry at the gastrointestinal physiology unit in the Royal Victoria Hospital, Belfast, U.K., over a 10-year period (1987-1997). The mean age was 51.7 years (range = 21-79 years). Chart review was conducted 1 to 10 years after manometry to confirm the final diagnoses: scleroderma was found in 11; CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia), 8; mixed connective tissue disease, 14; Raynaud's alone, 5; and other CTDs, 9. All 47 successfully underwent esophageal manometry. In addition to manometry, 24 underwent gastroscopy; 27, barium meal; and 3, esophageal pH studies. Clinically significant esophageal abnormalities were noted in 8 (33%) on gastroscopy, in 15 (56%) on barium meal, and in 31 (66%) on manometry. Gastroscopy had a significantly lower positivity rate than the others (p < 0.05). Only three patients had pH testing, yet all three pH tests were abnormal. During manometry, abnormal findings were significantly more common in scleroderma-CREST when compared with other diagnoses (89% vs. 50%; p < 0.02). Thirty-three patients reported dysphagia. Abnormal manometry was more likely in these cases (82% vs. 33%; p < 0.02). A high percentage of patients with CTD have significant esophageal motility disorders. Investigations were more likely to be positive with scleroderma-CREST than other CTDs, even if dysphagia was present. Barium meal and manometry are more useful than OGD. pH studies were under-used. There is need for a standardized approach to esophageal investigations in patients with CTDs.
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PMID:Esophageal investigations in connective tissue disease: which tests are most appropriate? 1115 66

Esophageal motility disorders often manifest with chest pain and dysphagia. Achalasia is a disorder of the lower esophageal sphincter and the smooth musculature of the esophageal body. In achalasia the lower esophageal sphincter typically fails to relax with swallowing, and the esophageal body fails to undergo peristalsis. In contrast to spastic disorders of the esophagus, achalasia can be progressive and cause pronounced morbidity. Pseudoachalasia mimics achalasia in terms of symptoms but can be caused by infectious disorders or malignancy. Treatment for achalasia is nonstandardized and includes medical, endoscopic, and surgical options. Spastic disorders of the esophagus, such as diffuse esophageal spasm and nutcracker esophagus, and nonspecific esophageal motility disorder are benign and nonprogressive, with similar findings on esophageal manometry. Although the exact cause remains unknown, these disorders may represent a manifestation of gastroesophageal reflux disease. Treatment of spastic disorders includes medical and surgical approaches and is aimed at symptomatic relief.
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PMID:Primary esophageal motility disorders. 1149 31

Dysphagia is a common symptom with which patients present. This review focuses primarily on the esophageal motor disorders that result in dysphagia. Following a brief description of the normal swallowing mechanisms and the messengers involved, more specific motor abnormalities are discussed. The importance of achalasia, as the only pathophysiologically defined esophageal motor disorder, is discussed in some detail, including recent developments in pathogenesis and treatment options. Other esophageal spastic disorders are described, with relevant manometric tracings included. In recent years, the importance of gastroesophageal reflux as a primary cause of esophageal dysmotility has been recognized, and this is also discussed. In addition, the motility disturbances that develop after surgical fundoplication are reviewed.
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PMID:Practical approaches to dysphagia caused by esophageal motor disorders. 1135 54

The optimal "treatment" of postfundoplication complications is preoperative prevention of them. Nonreflux causes of the symptom prompting surgery should be carefully eliminated preoperatively. Failure to respond to optimal powerful antireflux pharmacotherapy suggests that GERD was not the cause of symptoms. Neurologic or respiratory disease, delayed gastric emptying or retching, short esophagus, and esophageal dysmotility may predispose patients to complications, and may require careful tailoring of the fundoplication. The optimal antireflux surgery, with a wrap neither too loose nor too tight, may require a nadir lower esophageal sphincter pressure of more than 5 mm Hg to prevent reflux, but less than some value to prevent dysphagia. This latter value may be approximately 10 mm Hg, but depends on swallowing parameters such as peristaltic pressure, lower esophageal sphincter opening diameter, swallowed bolus diameter, and other considerations. Infants may require a gastrostomy tube for venting because of their lower gastric compliance to deal with swallowed air. Children with delayed gastric emptying may benefit from pyloroplasty, but this is debated. When complications occur, re-evaluate the diagnosis and the competence of the fundoplication with barium fluoroscopy, endoscopy with histology, pH probe, and other modalities as indicated. Initially try conservative management of the patient's complications, including dietary and feeding modifications. Give a trial of antireflux pharmacotherapy for recurrent reflux or pharmacotherapy directed at the specific side-effect of the fundoplication if one is present. Consider endoscopically dilating a persistently tight wrap or surgically revising the fundoplication if it is suggested by the evaluation.
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PMID:Postfundoplication Complications in Children. 1156 Jul 91


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