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

Progressive systemic sclerosis (PSS) commonly involves the esophagus. Dysphagia and heartburn are the most common esophageal symptoms. In this study we evaluated the relationship between esophageal symptoms and esophago-gastric motility. On esophageal manometry, loss of peristalsis, peristaltic contraction amplitude of distal esophagus less than 30 mmHg and decreased LES pressure were critical for esophageal symptoms. The degree of symptoms correlated to esophageal dysmotility. The gastric emptying in PSS patients was delayed, but there was no significant difference in gastric emptying between the patients with and without reflux esophagitis. Esophageal dysmotility is considered to be much responsible for the reflux esophagitis in PSS patients than gastric emptying.
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PMID:[Esophageal motility and gastric emptying in PSS patients, correlation with symptoms]. 223 96

In a 6.5 year period starting January 1982, 121 patients (74 male, 47 female; 1.6:1) with complicated gastroesophageal reflux referred to Alberta Children's Hospital, University of Calgary, required a Nissen fundoplication at a mean age of 35.5 months (range 3 weeks to 18 years). The median age of onset of symptoms was less than 1 month. Symptoms and indications for surgery included regurgitation (88%), failure to thrive (52%), reflux-associated pulmonary symptoms and aspiration (48%), biopsy evidence of esophagitis (35%) with heartburn (17%), dysphagia (18%), hematemesis (17%), anemia (13%), and hypoproteinemia (22%). Sixty-four percent of the patients had a syndrome or chromosomal abnormality, respiratory disease, or neuromuscular disorder. The barium contrast upper-gastrointestinal radiographic series, performed in all patients, identified structural [gastric outlet obstruction (2%), esophageal stricture (11%), erosive esophagitis (9%)], and functional abnormalities [gastroesophageal reflux (90%), barium aspiration (8%), esophageal hypoperistalsis (30%), delayed gastric emptying (4%)]. Barium contrast upper gastrointestinal radiographic series identified gastroesophageal reflux with a sensitivity of 90% (compared to history), was 50% sensitive and 92% specific for erosive esophagitis (compared to biopsy), was 59% sensitive and 74% specific for esophageal dysmotility (compared to esophageal manometry), and there was a significant (p less than 0.01) association between barium aspiration and prior evidence of aspiration pneumonitis. Esophageal manometry demonstrated a significantly (p less than 0.001) lower esophageal sphincter pressure in patients compared with controls, but no significant correlation with failure to thrive, aspiration pneumonia, biopsy evidence of esophagitis, or parameters of the 24-hour esophageal pH study. Twenty-four hour pH monitoring showed significantly (p less than 0.05) more reflux episodes than in asymptomatic controls and there was significant (p less than 0.05) correlation between the percentage of time pH was less than 4 and the presence of hypoalbuminemia, and biopsy-proven erosive esophagitis or Barrett's esophagus. Endoscopic appearance was 91% sensitive and 60% specific for esophagitis when compared to biopsy. Nissen fundoplication was completely effective at resolving gastroesophageal reflux in 83%, and associated with marked improvement in 15%. No patient died as a result of fundoplication. Major complications included: recurrence of symptoms requiring reoperation (2%), subsequent mechanical bowel obstruction (8%), wound infection or pneumonia (12%).
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PMID:Investigation and outcome of 121 infants and children requiring Nissen fundoplication for the management of gastroesophageal reflux. 227 17

Dysphagia in the absence of organic esophageal stricture may occur in patients with reflux esophagitis. Although the exact mechanism of this "nonobstructive dysphagia" (NOD) is not known, it is believed to be related to transient segmental esophageal motor disorder. The goals of this study were to determine the frequency of NOD in patients with reflux esophagitis and correlate it with esophageal pH and motility changes. Sixty-three consecutive patients with symptoms of esophageal dysfunction were studied with endoscopy, infusion esophageal manometry, and 24-h ambulatory esophageal pH monitoring. Forty-seven had severe erosive esophagitis unresponsive to medical therapy; 16 with esophageal motility disorders were used as symptomatic controls. Twenty-eight of 63 patients studied experienced NOD during the 24-h pH study; 22 had esophagitis and six had esophageal dysmotility without esophagitis. NOD was noted with similar frequency in the two groups; 22/47 (46.8%) of patients with esophagitis and 6/16 (37.5%) with esophageal dysmotility experienced NOD during the period of study. NOD correlated with pH less than 4.0 in 88.6% of patients with esophagitis but in only 7% of patients with esophageal dysmotility (p less than 0.001). There was no difference in acid reflux patterns in esophagitis patients who experienced NOD (22/47), and in those who did not (25/47). There was no correlation between NOD and baseline esophageal motility abnormalities. In summary, 1) NOD is a common, intermittent symptom that occurred in up to 46.8% of esophagitis patients and 37.5% of symptomatic controls during the 24-h period of this study; 2) NOD correlates with esophageal pH less than 4.0 in patients with esophagitis and not in patients with esophageal dysmotility. These data strongly suggest that acid in the distal esophagus frequently triggers the sensation of dysphagia in esophagitis patients, but not in patients with esophageal motility disorders. Combined ambulatory intraesophageal motility and pH monitoring may further elucidate the mechanism of dysphagia in these patients.
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PMID:Nonobstructive dysphagia in reflux esophagitis. 272 32

The Nissen fundoplication is the most common anti-reflux operation performed. Gas bloat and inability to vomit after repair may be severe, but infrequently require reoperation; in contrast, other complications can be very debilitating or life-threatening. One hundred and sixteen patients who required reoperation for serious complications after Nissen repair are presented and classified according to the cause of the failed repair. Nissen complications resulted in recurrent reflux (86 per cent), severe dysphagia (60 per cent), esophageal dysmotility (48 per cent) and gastric perforation and fistualization (5 per cent). The "classic" Nissen fundoplication involves a blind 360 degree wrap, which includes the acid-producing parietal cell mass. The resulting pouch drains poorly and is, therefore, subject to gastric ulceration. Reoperation at our institution, using principally the Hill antireflux procedure, gave excellent or good results in 86 per cent, fair in 9 per cent and poor in 5 per cent. Three operative deaths (2.6 per cent) and one late death (0.9 per cent) occurred.
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PMID:Post Nissen syndrome. 328 31

Esophageal motility disorders consist of a complex array of disturbances in normal esophageal function associated with dysphagia, gastroesophageal reflux, and noncardiac chest pain. A thorough knowledge of normal esophageal anatomy and physiology is important to a full understanding of these motility derangements. Through a complicated interaction of neuromuscular and hormonal influences, the voluntary act of swallowing transforms into an automated sequence of peristaltic waves propelling food and liquids into the stomach in concert with coordinated relaxation of the sphincters. Anatomic and physiologic barriers exist within the esophagus protecting against gastroesophageal reflux and aspiration. With improvements in diagnostic tools such as barium contrast radiography, scintigraphy, pH measurements, and esophageal manometrics with provocative testing, motility disorders have become better defined and understood. Primary motility disorders consist of achalasia, diffuse esophageal spasm (DES), "nutcracker esophagus," hypertensive lower esophageal sphincter, and nonspecific esophageal motility dysfunction (NEMD). A host of secondary and miscellaneous motility disorders also affect the esophagus, including scleroderma and other connective tissue diseases, diabetes mellitus, Chagas' disease, chronic idiopathic intestinal pseudo-obstruction, and neuromuscular disorders of striated muscle. Gastroesophageal reflux disease (GERD) may also be promoted by associated motility disturbances. Treatment modalities include surgical myotomy; dilatation; and pharmacologic manipulations, including use of nitrates, calcium-channel blockers, H2-blockers, and psychotropic drugs where appropriate.
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PMID:Esophageal motility disorders. 329 77

Three families including five subjects with the G or Opitz-Frias syndrome are added to 23 published cases who had dysphagia; characteristics of the two affected relatives were added to 19 well documented published reports. The data from index cases support the concept of the G syndrome as a constellation of midline defects, which include hypertelorism or telecanthus (89%), oesophageal dysmotility (69%), laryngotracheal clefts (44%), cleft palate or bifid uvula (34%), heart defects (29%), hypospadias (100% of males), renal or ureteral anomalies (42%), and mental retardation (38%). Affected relatives, often identified by hypertelorism, dysphagia, or hypospadias, had a much lower incidence of associated defects and mental retardation. They provide a more rounded but still biased view of a syndrome compatible with normal intelligence and life span. The data do not support a highly characteristic face in the G syndrome, which discriminates it from the phenotypically similar BBB syndrome. The variable expressivity and five cases of male to male transmission observed in 18 families are consistent with autosomal dominant inheritance. Vigilance for the morphological characteristics of G syndrome in patients with dysphagia is underscored by the potential for normal development with appropriate intervention.
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PMID:Further delineation of the G syndrome: a manageable genetic cause of infantile dysphagia. 335 1

Gastroesophageal reflux is frequently associated with esophageal atresia and tracheoesophageal fistula repair. Following unsuccessful medical treatment, 14 (45%) of 31 patients underwent a Nissen fundoplication. Five of these 14 patients had prolonged dysphagia requiring supplemental gastrostomy feeding. Four of these five patients underwent postoperative manometry and extended pH monitoring, which revealed a normal lower-esophageal sphincter pressure (greater than 15 mm Hg), normal pH results, and marked esophageal dysmotility. The fundoplication creates a mechanical obstruction for those patients with a dyskinetic esophagus who cannot generate the pressure to open the "new sphincter". To avoid this complication, antireflux surgery should be deferred, if possible, in those patients with severe gastroesophageal reflux and marked esophageal motility abnormalities.
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PMID:Problems associated with a Nissen fundoplication following tracheoesophageal fistula and esophageal atresia repair. 335 88

Sudden esophageal obstruction after eating poorly chewed meat has been called the Steakhouse syndrome. Some cases have demonstrable esophageal narrowing above which food impacts, but in many patients with identical symptoms no underlying obstruction is demonstrated. We report four patients with acute dysphagia who were unable to swallow liquids or solids for as long as 72-96 h. Onset occurred after eating meat in three patients and after taking psyllium in one. All had a structurally normal esophagus demonstrated by x-ray and endoscopy, but motor disorders were defined by manometry in three. We hypothesize that an underlying motor abnormality led to food impaction and call this presumed spastic variant "Steakhouse spasm." We suspect that this is a common but frequently unrecognized manifestation of esophageal dysmotility.
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PMID:Steakhouse spasm. 361 82

Patients who have undergone repair of esophageal atresia and tracehoesophageal fistula as infants have been noted to have residual esophageal dysmotility and pulmonary dysfunction during their childhood years. However, limited information is available about the long-term follow-up of these patients. In this study we performed esophageal and pulmonary function studies on 12 adults who had required surgical repair of these defects in the first week of life. Most patients had symptoms of dysphagia and heartburn at time of evaluation. Pathologic gastroesophageal reflux was documented in 67% of patients and esophagitis was noted in 34%. All patients had esophageal motility abnormalities characterized by low-amplitude nonperistaltic waves throughout most of the esophagus. In addition, although most patients had no respiratory symptoms, mild restrictive lung volumes were noted in many patients. However, airflow obstruction and airway hyperreactivity were not present. These data demonstrate that clinical symptoms and abnormal esophageal manometry and pulmonary function persist well into the third and beginning of the fourth decade after repair of esophageal atresia and tracheoesophageal fistula in infancy.
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PMID:Long-term evaluation of esophageal and pulmonary function in patients with repaired esophageal atresia and tracheoesophageal fistula. 362 93


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