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 existence of specific, age-related changes in gastrointestinal motility with clinical significance is controversial. Beside the more infrequent primary motility disorders, secondary motility disturbances associated with collagen vascular diseases, endocrinopathies, and neuromuscular diseases are prominent in the older and often multimorbid patients. Especially in geriatric patients, motility associated symptoms are undesired side-effects of drug therapy. The pathophysiology, clinical syndromes, and therapeutic principles of motility disorders in the elderly are discussed. The major symptoms of esophageal dysfunction are dysphagia, chest pain, heartburn, and regurgitation. Oropharyngeal dysphagia, mostly caused by cerebrovascular accidents and other neurologic disorders, leads to disturbances in food intake, and is often complicated by broncho-pulmonary infections arising from recurrent aspiration of food or saliva. Gastrointestinal reflux disease and spastic motility disorders of the esophagus are regarded as possible causes of angina-like chest pain after exclusion of cardiac diseases. Motility disturbances of the stomach and small bowel are often related to systemic disease (i.e., diabetes mellitus, chronic intestinal pseudo-obstruction) of drug side-effects. Mental and physical decline, reduced fluid intake, and constipating drugs are the most relevant factors for idiopathic constipation in the elderly. Fecal incontinence means a great psychological strain for older patients and leads to social isolation.
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PMID:[Gastrointestinal motility in the elderly]. 144 9

Nifedipine has been proven to be effective and safe in the treatment of primary oesophageal motility disorders which can cause angina-like chest pain and/or dysphagia. The effects of the calcium channel blockers nifedipine, nitrendipine, nimodipine and nisoldipine on oesophageal smooth muscle function in healthy male volunteers were studied by oesophageal manometry using the rapid pull-through-technique, in two randomized, double-blind crossover studies. Lower oesophageal sphincter pressure, oesophageal contraction amplitude and duration after a wet swallow (measured 5 cm and 10 cm above the lower oesophageal sphincter) were determined 30 min before and at 10 minute intervals up to 90 min after the administration of nimodipine and up to 120 min after nifedipine, nitrendipine and nisoldipine. The plasma drug concentration was measured at baseline (-15 min) and in parallel with the manometric measurements. Compared to placebo, lower oesophageal sphincter pressure was significantly decreased by 24% by nifedipine and 17% by nimodipine, whereas the effects of nitrendipine (decrease of 15%) and nisoldipine (9%) were not significant. Nifedipine significantly decreased by 17% the oral contraction amplitude compared to placebo and nimodipine by 11%. The duration of the contraction amplitudes was not altered. The decrease in sphincter pressure was correlated with the corresponding plasma drug levels of nifedipine r = 0.92, nitrendipine r = 0.80 and nisoldipine r = 0.79. Nimodipine showed no such correlation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of the calcium antagonists nifedipine, nitrendipine, nimodipine and nisoldipine on oesophageal motility in man. 180 45

35 patients with angina-like chest pain underwent esophageal manometry after a coronary artery disease had been ruled out by angiography. Furthermore, patients after gastric or esophageal surgery, with pathologic upper gastrointestinal endoscopy or with pathologic gastroesophageal reflux as seen on 24-hour-pH-metry were excluded from this study. 29 out of 35 patients (83%) had a normal manometric study, six patients (17%) had a motility disorder; five of these showed an unspecific dismotility pattern and were asymptomatic while the study was done; only one patient presented with esophageal spasm. Since only this latter patient was symptomatic while the study was done, a correlation between symptoms and this motility disorder seems likely. --If pathologic gastroesophageal reflux has been ruled out, esophageal manometry can establish a diagnosis in only 3% of patients with angina-like chest pain without esophageal symptoms (dysphagia, odynophagia, heartburn or regurgitation). We conclude that this complicated examination should not be done in these patients.
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PMID:[Esophageal motility disorders with thoracic pain of unknown origin]. 188 9

In this paper the pharmacodynamic effects of calcium channel blockers (verapamil, nifedipine, diltiazem, fendiline, nitrendipine, nimodipine, and nisoldipine) on esophageal motility in man and their clinical effects in patients with various forms of primary esophageal motility disorders are critically analysed and summarized. The evaluation of efficacy and safety is mainly focused on nifedipine (Bay a 1040, Adalat; CAS 21829-25-4), since it has been best documented clinical pharmacologically and therapeutically in this field. Nifedipine and--with varying potency--the other calcium antagonists reduce effectively the increased lower esophageal sphincter pressure (LESP) and abnormally high and prolonged peristaltic and nonperistaltic contractions in the esophageal body in patients with achalasia, diffuse esophageal spasm (DES), and other disorders which may cause angina-like chest pain and/or dysphagia. Pharmacodynamic effects on esophageal motility are closely correlated with the plasma concentration of nifedipine in healthy volunteers and in patients. However, a final judgement on the therapeutic value of these compounds in esophageal motor abnormalities cannot be given due to conflicting results from clinical studies with fairly small numbers of patients and varying study designs. Among the different calcium antagonists investigated nifedipine represents the best investigated and the most suitable compound for the treatment of primary hypertensive esophageal motor disorders.
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PMID:Clinical efficacy of nifedipine and other calcium antagonists in patients with primary esophageal motor dysfunctions. 193 Mar 46

Patients with esophageal motility disorders usually have dysphagia and many also have chest pain similar to angina. The diagnosis is suggested by the clinical presentation, and supporting evidence is often provided by contrast roentgenography. Esophageal manometry is usually necessary to confirm the diagnosis. Conservative therapy using pharmacologic agents is often useful as an initial trial, although many patients who continue to be symptomatic ultimately require surgical intervention.
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PMID:Disorders of esophageal motility. 200 64

The hypothesis that oesophageal peristalsis can be modified voluntarily was explored. Six healthy male volunteers and eight female patients with angina like chest pain underwent oesophageal manometry. Each was asked to take a series of swallows, and to vary their size, in random order, by taking either a big gulp or a little swallow. None of the subjects experienced difficulty in doing so. In both groups the amplitude of oesophageal contractions were significantly greater after big gulps than little swallows (p less than 0.01) and this was true for wet (82.0 v 68.9 mmHg) and dry swallows (52.3 v 43.3 mmHg). For the patients' wet swallows the mean values were 73.0 and 56.0 mmHg. Thus, the amplitude of oesophageal peristalsis can be controlled voluntarily. This effect may account for some of the within subject variation in the amplitude of oesophageal contractions. During oesophageal manometry subjects should be encouraged to standardise the size of their swallows whenever possible. Patients with symptoms related to abnormal oesophageal peristalsis such as dysphagia, heartburn, and chest pain may benefit from biofeedback training.
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PMID:Power of oesophageal peristalsis can be controlled voluntarily. 201 16

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

We reviewed 123 consecutive patients who underwent esophageal function testing to determine the prevalence and clinical characteristics of the syndrome of high-amplitude peristaltic contractions (HAPC). Twenty-eight patients (23%) were found to have HAPC, including 16 males and 12 females with a median age of 54 years. Barium esophograms yielded no evidence of motility disorders, while 35% of those tested had pathologic gastroesophageal acid reflux. Twenty (71%) were initially referred for evaluation of angina-like chest pain, and 8 were referred with other symptoms. Of those with chest pain, 19 initially underwent extensive evaluation for coronary artery disease before the diagnosis of HAPC. Symptoms of heartburn, regurgitation, and dysphagia were absent or minimal in most patients. Lower esophageal sphincter pressure was normal in 27 patients, and lower esophageal sphincter relaxation was normal in all patients. Mean distal esophageal peak peristaltic pressure was 147.8 mm Hg, while the highest peak peristaltic pressure for each patient averaged 193.2 mm Hg. Seven patients had mean peristaltic wave durations of more than 7 seconds. Patients with atypical chest pain or those with typical angina in whom coronary artery disease is eliminated as a possible cause should be evaluated for HAPC with esophageal manometry. Patients with symptoms are usually successfully treated with smooth muscle relaxants, and surgical intervention is rarely necessary.
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PMID:Angina-like chest pain associated with high-amplitude peristaltic contractions of the esophagus. 317 68

Acute epiglottitis in adults is a potentially fatal but self-limiting disease of increasing incidence world-wide. Forty-two patients, seen consecutively over a four year period at the ENT Department, Singapore General Hospital were reviewed retrospectively. A strong male predominance with a peak age incidence in the sixth decade was noted. A severe sore throat and dysphagia with disproportionate signs of oropharyngeal inflammation was the main presenting picture. Only three patients had stridor on presentation. Vigilant monitoring of the airway with empirical high-dose intravenous ampicillin, cloxacillin and steroids resulted in a dramatic clinical improvement in most patients and none developed stridor after admission. The yield from throat swabs and blood cultures were low. Two patients developed complications, a Ludwigs angina and an epiglottic abscess. Recurrent epiglottitis was a problem in one patient. There was low morbidity and no mortality on the management regime outlined.
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PMID:Acute epiglottitis in adults (the Singapore experience). 320 35

We prospectively evaluated 22 patients with manometrically proven "nutcracker esophagus" (high amplitude peristaltic contractions). All patients were symptomatic with angina-like chest pain, dysphagia, or both. Patients underwent barium esophagram with video-recording of the images. Video tapes were reviewed independently by a gastrointestinal radiologist who was unaware of the patients' manometric diagnoses. The video-esophagram was normal in 12 of 22 (55%) patients. Eight of 22 (36%) had dysmotility: either diffuse spasm (9%) or tertiary contractions (27%) (Fig. 2). A hiatal hernia was the only abnormality in two patients. Although the presence of diffuse spasm or tertiary contractions may suggest the presence of the underlying motor disorder in patients with nutcracker esophagus, we conclude that the "barium swallow" lacks sufficient sensitivity to screen adequately for this disorder in patients with atypical angina or dysphagia.
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PMID:Radiology of the nutcracker esophagus. 373 53


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