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)

In five of seven siblings of healthy parents, dysphagia developed during adolescence or early adult life. A barium swallow was normal in one patient but showed appearances considered to be consistent with achalasia in all others. Oesophageal manometry was successfully performed in four of the five patients, including the patient with symptoms but normal radiological appearance. One patient had achalasia, two had oesophageal body motor dysfunction associated with a hypertensive, but normally relaxing lower oesophageal sphincter, and one had diffuse oesophageal spasm alone. The occurrence of three different oesophageal dysmotility disorders within members of a single sibship suggests that these conditions are intimately related and probably genetically determined as an autosomal recessive trait.
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PMID:Familial coexistence of achalasia and non-achalasic oesophageal dysmotility: evidence for a common pathogenesis. 144 73

Although more extensive research is required to fully characterize the pathophysiology of the gastrointestinal symptoms in PD, much of the presently available data suggest that the primary PD process is the major factor in the etiology of gut dysfunction in this patient population. This may be mediated by both central and peripheral mechanisms. Involvement of the dorsal motor nucleus of the vagus might produce dysfunction of muscles controlling deglutition and esophageal motility, thereby leading to drooling, dysphagia, and gastroesophageal reflux. The presence of Lewy bodies, the primary neuropathologic finding in the CNS in PD, in the myenteric plexus of both the esophagus and colon suggests that the PD process may also affect the enteric nervous system and contribute to the development of esophageal dysmotility and constipation through this peripheral mechanism. Dopamine receptors have been identified in the lower esophageal sphincter and the esophageal body of animals. If similarly present in humans, involvement of this dopaminergic system could contribute to the development of dysphagia and nausea of PD. Constipation may reflect both peripheral involvement, indicated by Lewy bodies in the colonic myenteric plexus, leading to colonic inertia, and central mechanisms, leading to pelvic floor dysfunction.
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PMID:Gastrointestinal dysfunction in Parkinson's disease: frequency and pathophysiology. 845 Oct 18

Fifty-one patients with systemic sclerosis (scleroderma) underwent videofluoroscopy during barium swallow to evaluate the incidence of oropharyngeal deglutition abnormalities and to correlate the radiologic patterns of esophageal motility abnormalities with patients' clinical features. Thirteen patients (26%) showed swallowing dysfunction, (e.g., oral leakage, retention, penetration, mild or moderate aspiration, and upper esophageal sphincter incoordination). These dysfunctions were more severe in patients with prominent esophageal dysmotility. Normal esophageal motility was not associated with swallowing alterations. Patients with an oropharyngeal disorder had a higher incidence of pulmonary disease. The clinical picture of the above-mentioned 13 patients was more severe, based on the duration of Raynaud's phenomenon and duration of skin sclerosis. Patients with primary Raynaud's phenomenon had no oral or esophageal abnormalities. The esophageal phase of swallowing was abnormal in 80% of the patients with scleroderma. Esophageal dysfunction, therefore, seems to be frequent in the early stages of the disease. However, patients with advanced or extensive disease may have normal esophageal function.
Dysphagia 1991
PMID:Oropharyngeal and esophageal function in scleroderma. 177

Forty-six patients with progressive systemic sclerosis (37 women and 9 men) were successively evaluated by endoscopy, manometry, and esophageal pH monitoring. Fourteen patients (30.4 percent) had erosive esophagitis. Twenty-four patients were symptomatic; nineteen patients complained of dysplagia. Erosive esophagitis was significantly more frequent in symptomatic patients than in asymptomatic patients (50.0 percent vs 9 percent, P less than 0.01) and especially in patients complaining of dysphagia (57.9 percent vs 11.1 percent, P less than 0.01). Erosive esophagitis was not correlated with symptoms of gastroesophageal reflux. Abnormal esophageal motility was found in 34 patients (73.9 percent). Occurrence of erosive esophagitis was not linked with esophageal dysmotility. In patients with erosive esophagitis lower esophageal sphincter pressures were significantly lower than those in patients without erosive esophagitis. Twenty-four hr-pH monitoring showed pathological gastroesophageal reflux in 20 patients (43.5 percent). Erosive esophagitis was more frequent in patients with pathological gastroesophageal reflux than in patients with normal gastroesophageal reflux (50.0 percent vs 15.4 percent, P less than 0.02) especially in patients with pathological supine nighttime gastroesophageal reflux (61.5 percent vs 18.2 percent, P less than 0.01). Our data suggest that symptoms, dysphagia, diminished lower esophageal sphincter pressures, and pathologic nighttime gastroesophageal reflux are reliable predictors of the presence of erosive esophagitis in patients with progressive systemic sclerosis.
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PMID:[Esophagitis in progressive systemic scleroderma. Prevalence and risk factors in forty-six patients]. 178 50

Allgrove syndrome (isolated glucocorticoid deficiency, achalasia and alacrima) was found in eight members of an inbred French Canadian/North American Indian pedigree. The high degree of consanguinity supports an autosomal recessive mode of inheritance for this disorder. Six patients presented with hypoglycaemia and other evidence of cortisol deficiency between 2.5 and 8 years of age; however, two others became cortisol deficient after initial testing showed normal cortisol responses to ACTH, evidence that the glucocorticoid insufficiency of this syndrome may not be congenital, but may develop as late as the third decade. No evidence of mineralocorticoid deficiency has been found during 65 patient-years of follow-up. Alacrima was the earliest and most consistent clinical sign of Allgrove syndrome. Other manifestations of peripheral or autonomic neuropathy were found in four patients. The patients showed similar facial features, and three had significant velo-pharyngeal incompetence. All showed oesophageal dysmotility even in the absence of symptomatic dysphagia. In-vitro studies of lymphocyte ACTH binding showed no differences from normal controls. If such lymphocyte binding, as has been suggested, reflects adrenal ACTH receptor activity, these data would suggest that the glucocorticoid deficiency of Allgrove syndrome is not the result of a defect in that receptor. However, the observation that ACTH does not elicit increased adenylate cyclase activity even in normal lymphocytes casts considerable doubt on the physiological significance of ACTH binding to lymphocytes. It seems likely, therefore, that true ACTH receptors are not expressed on peripheral lymphocytes, and any conclusions regarding a possible receptor defect in Allgrove syndrome must await studies of receptor expression on adrenal cell membranes.
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PMID:Allgrove syndrome: an autosomal recessive syndrome of ACTH insensitivity, achalasia and alacrima. 185 Jun 71

Occult (silent) gastroesophageal reflux disease (GER, GERD) is believed to be an important etiologic factor in the development of many inflammatory and neoplastic disorders of the upper aerodigestive tract. In order ot test this hypothesis, a human study and an animal study were performed. The human study consisted primarily of applying a new diagnostic technique (double-probe pH monitoring) to a population of otolaryngology patients with GERD to determine the incidence of overt and occult GERD. The animal study consisted of experiments to evaluate the potential damaging effects of intermittent GER on the larynx. Two hundred twenty-five consecutive patients with otolaryngologic disorders having suspected GERD evaluated from 1985 through 1988 are reported. Ambulatory 24-hour intraesophageal pH monitoring was performed in 197; of those, 81% underwent double-probe pH monitoring, with the second pH probe being placed in the hypopharynx at the laryngeal inlet. Seventy percent of the patients also underwent barium esophagography with videofluoroscopy. The patient population was divided into seven diagnostic subgroups: carcinoma of the larynx (n = 31), laryngeal and tracheal stenosis (n = 33), reflux laryngitis (n = 61), globus pharyngeus (n = 27), dysphagia (n = 25), chronic cough (n = 30), and a group with miscellaneous disorders (n = 18). The most common symptoms were hoarseness (71%), cough (51%), globus (47%), and throat clearing (42%). Only 43% of the patients had gastrointestinal symptoms (heartburn or acid regurgitation). Thus, by traditional symptomatology, GER was occult or silent in the majority of the study population. Twenty-eight patients (12%) refused or could not tolerate pH monitoring. Of the patients undergoing diagnostic pH monitoring, 62% had abnormal esophageal pH studies, and 30% demonstrated reflux into the pharynx. The results of diagnostic pH monitoring for each of the subgroups were as follows (percentage with abnormal studies): carcinoma (71%), stenosis (78%), reflux laryngitis (60%), globus (58%), dysphagia (45%), chronic cough (52%), and miscellaneous (13%). The highest yield of abnormal pharyngeal reflux was in the carcinoma group and the stenosis group (58% and 56%, respectively). By comparison, the diagnostic barium esophagogram with videofluoroscopy was frequently negative. The results were as follows: esophagitis (18%), reflux (9%), esophageal dysmotility (12%), and stricture (3%). All of the study patients were treated with antireflux therapy. Follow-up was available on 68% of the patients and the mean follow-up period was 11.6 +/- 12.7 months.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The otolaryngologic manifestations of gastroesophageal reflux disease (GERD): a clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an experimental investigation of the role of acid and pepsin in the development of laryngeal injury. 189 64

Salivary gland dysfunction is uniformly detrimental to the oral cavity. Its effects on the GI tract have begun to be explored. Dry mouth is a common complaint among older adults, probably due to systemic disease and its therapy rather than the aging process per se. Evaluation of complaints of dry mouth should include medical history, sialometry and physical examination. Numerous medications can elicit drug-induced xerostomia. Patients who have received radiation therapy to the head and neck region often have permanent radiation-induced xerostomia, which has been linked to esophagitis. SS is an autoimmune systemic exocrinopathy resulting in irreversible salivary gland dysfunction. SS has numerous GI manifestations, including dysphagia, temporal defects of deglutition, esophageal dysmotility, gastritis, pancreatitis and liver disease. Management of salivary hypofunction is directed toward preserving the dentition and improving patient comfort. Drug-induced xerostomia is often correctable by altering the therapeutic modality.
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PMID:Interactions of the salivary and gastrointestinal systems. II. Effects of salivary gland dysfunction on the gastrointestinal tract. 191 20

Esophageal intramural pseudodiverticulosis (EIP) is a rare disease, characterized by multiple, small flask-shaped diverticula in the esophageal wall, and best demonstrated on single-contrast barium examination. Though the condition is often associated with reflux esophagitis, Candida esophagitis, and esophageal dysmotility, corrosive-acid injury is not a commonly recognized cause. In a radiological study involving 59 patients with sequelae of corrosive-acid injury of the upper gastrointestinal (GI) tract, evaluated over a 5-year period, 14 cases (23.7%) of EIP were found. Esophageal stricture was a constant association; the diverticula tended to involve either the entire length of the stricture or its upper part. There was, however, no correlation between the length of the stricture and number of diverticula (p greater than 0.05). Endoscopic dilatation resulted in relief of dysphagia, and the diverticula regressed in number of disappeared altogether. Our experience suggests that EIP is a common sequelae of esophageal acid injuries, and that diverticula tend to form at the site of initial contact between acid and susceptible esophageal mucosa. Stricture dilatation leads to reduction or total disappearance of the diverticula.
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PMID:Corrosive acid-induced esophageal intramural pseudodiverticulosis. A study of 14 patients. 150 Jun 73

The history, physical examination, and the results of the upper gastrointestinal series, esophageal manometry, 24-h pH recording, endoscopy, and biopsy are reviewed in 16 children (mean age of 10.6 years, range of 3 years 5 months to 15 years 3 months) who presented to the Alberta Children's Hospital with dysphagia ("food-sticking") without previously identified provocative disorders since January 1985. Of the 16 patients, 11 had had intermittent obstruction, and 7 had had intervention to relieve obstruction (2 Heimlich maneuvers, 1 intravenous glucagon, and 4 endoscopy after failure of intravenous glucagon). Although only five children had a recent history suggestive of gastroesophageal reflux, 12 had histologic evidence of reflux esophagitis (including 1 with a peptic stricture, 1 with "nutcracker" esophagus, and 1 with esophageal dysmotility characteristic of Down's syndrome) and all responded clinically to antireflux therapy. Of the remaining four patients, one had extrinsic esophageal compression from a vascular ring (right aortic arch with left ligamentum arteriosum), one had a single and another had recurrent episodes of food-sticking without any identified abnormality, and one declined investigation. In childhood, dysphagia may be the presenting symptom of reflux esophagitis in the absence of a history suggestive of gastroesophageal reflux and without evidence of a peptic stricture.
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PMID:The role of gastroesophageal reflux in pediatric dysphagia. 205 Dec 65

Two patients were referred because of persistent dysphagia which developed for the first time after Nissen fundoplication. Investigations, including oesophageal manometry, demonstrated the presence of achalasia in one case, confirmed histologically, and aperistaltic oesophagus associated with an underlying connective tissue disorder in the other case. Our observations highlight the importance of assessing oesophageal motility before referring patients for anti-reflux surgery and illustrate the effect of such surgery on patients in whom oesophageal dysmotility was not suspected.
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PMID:Aperistaltic oesophageal disorders unmasked by severe post-fundoplication dysphagia. 208 51


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