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)

A 71-year-old woman developed dysphagia and hematemesis with an endoscopic diagnosis of esophageal submucosal hematoma. Post mortem examination demonstrated an aorto-esophageal fistula as the etiology of her hematemesis. The differential diagnosis of upper gastrointestinal bleeding in the elderly patient without cirrhosis is discussed. A review of the literature on aorto-esophageal fistula is included.
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PMID:Aortic aneurysm eroding the esophagus. Case report and review. 30 Feb 22

Endoscopic esophageal variceal sclerotherapy was performed in 301 patients with portal hypertension (emergency, 72 and elective, 229) using 3% aqueous phenol as sclerosant. The cause of portal hypertension was cirrhosis of the liver in 189 patients (Child's class A-48, B-66, and C-75), extrahepatic portal venous obstruction (EHPVO) in 90, and non-cirrhotic portal fibrosis in 22 patients. In the emergency group, active bleeding was controlled in 87% of cases. Re-bleeding occurred in 101 of 290 (35%) surviving patients. Obliteration of varices was achieved in 228 (84%) patients, with a mean of 5.14 +/- 2.27 sclerotherapy sessions. Of 301 patients, 29 (9.6%) had an early in-hospital mortality (30.5% in emergency and 3% in elective group), with 16 deaths due to variceal bleeding. Of the remaining 272 patients, 40 (15%) died during follow-up, of which only 11 died of variceal bleeding. Complications, such as superficial ulcers, dysphagia, and strictures, were observed in 14%, 7% of emergency, and 3% of elective patients. None of the patients developed systemic toxicity. In conclusion, 3% aqueous phenol is an effective, safe, and economical sclerosant for esophageal variceal sclerotherapy.
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PMID:Endoscopic esophageal variceal sclerotherapy using 3% aqueous phenol. 156 12

Two patients with cirrhosis are presented who developed retrosternal pain and dysphagia immediately after sclerotherapy of esophageal varices. Extensive submucosal bleeding of the esophageal wall was demonstrated radiologically and endoscopically. Complete resolution occurred spontaneously and did not lead to residual complications such as strictures. Intramural hematoma of the esophagus is an unusual complication after endoscopic variceal sclerotherapy.
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PMID:Intramural hematoma of the esophagus after variceal sclerotherapy. 174 37

Hepatolenticular degeneration (Wilson's disease) is a hereditary disease in which metabolic disorder of copper leads to its accumulation in the liver, brain, cornea and kidneys with consequent pathologic changes in those organs. Hereditary mechanism of the disease is autosomal recessive with prevalence of 30-100 per 1,000,000 inhabitants. Etiology of this disease is not yet explained. There are two hypotheses. The first one is that it is the disorder of ceruloplasmine metabolism caused by insufficient synthesis of normal ceruloplasmine, or synthesis of functionally abnormal ceruloplasmine. The second one is: the block of copper biliar excretion which is the consequence of the liver lysosomes functional defect. Pathogenetic mechanism of disease is firstly long-term accumulation of copper in the liver, and later, when the liver depo is full, its releasing in circulation and accumulation in the brain, cornea, kidneys and bones, which causes adequate pathologic changes. Toxic activity of copper is the consequence of its activity on enzymes, particularly on those with -SH group. There are two basic clinical forms of the disease: liver disease or neurologic disease. Before puberty the liver damage is more frequent, while in adolescents and young adults neurologic form of the disease is usual. The liver disease is nonspecific and characterized by symptoms of cirrhosis and chronic aggressive hepatitis. The only specificity is hemolytic anemia which, in combination with previous symptoms, is important for diagnosis of the disease. Neurologic symptoms are the most frequent consequence of pathologic changes in the basal ganglia. In our patients the most frequent symptoms were tremor (63%); dysarthria, choreoathetosis and rigor (38%); ataxia and mental disorders (31%); dysphagia and dystonia (12%), diplopia, hypersalivation, nystagmus and Babinski's sign (6%). Among pathologic changes in other tissues and organs the most important is the finding of Kayser-Fleischer ring in the cornea as a result of copper accumulation. Its importance for precise diagnosis is great. The diagnosis of the disease is based on anamnesis, clinical examination, specific and nonspecific laboratory tests. The therapy of choice is penicillamine. If we use it early, the result will be good remission in the majority of patients. Late diagnosis or delay in treatment cause death which is the result of bleeding from esophageal varices or basal ganglia disease. Immunologic damages caused by penicillamine demand interruption of therapy and substitution by three-ethyl-tetra-amine (TETA). We also use zinc salts and tetratiomolibdate in therapy of this disease. Pathogenesis, clinical picture and therapy of the disease are based on our own results.
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PMID:[Hepatolenticular degeneration]. 226 49

Obstructive intramural hematoma of the esophagus is an unusual complication of endoscopic sclerotherapy. We report three patients with liver cirrhosis who experienced such a complication. In our series, the frequency was 1.6 percent. A few hours after sclerotherapy, all three patients complained of low retrosternal pain, dysphagia and hypersialorrhea. Endoscopy was performed in two patients and showed a typical bluish submucosal mass occupying the esophageal lumen. Outcome was favorable in all patients within one week of conservative treatment. We hypothesized that hematoma could be ascribed to variceal puncture. The extension of the hematoma with dissection of the esophageal wall which had been fragilized by previous sclerotherapy sessions could have been facilitated by impaired coagulation.
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PMID:[Obstructive intramural hematoma of the esophagus. A rare complication of endoscopic sclerotherapy of esophageal varices]. 239 66

In 1984 we started a prospective controlled trial comparing endoscopic sclerotherapy (ES) with the distal splenorenal shunt (DSRS) in the elective treatment of variceal hemorrhage in cirrhotic patients. The study population included 40 patients with cirrhosis and portal hypertension referred to our department from October 1984 to March 1988. These patients were drawn from a pool of 173 patients who underwent either elective surgery or endoscopic sclerotherapy during this time. Patients were assigned to one of the two groups according to a random-number table: 20 to DSRS and 20 to ES. During the postoperative period, no DSRS patient died, while one ES patient died of uncontrolled hemorrhage. One DSRS patient had mild recurrent variceal hemorrhage despite an angiographically patent DSRS. Four ES patients suffered at least one episode of gastrointestinal bleeding: two from varices and two from esophageal ulcerations. Five ES patients developed transitory dysphagia. Long-term follow-up was complete in all patients. Two-year survival rates for shunt (95%) and ES (90%) groups were similar. One DSRS patient rebled from duodenal ulcer, while three ES patients had recurrent bleeding from esophagogastric sources (two from varices and one from hypertensive gastropathy). One DSRS and two ES patients have evolved a mild chronic encephalopathy; four DSRS and two ES patients suffered at least one episode of acute encephalopathy. Two ES patients had esophageal stenoses, which were successfully dilated. Preliminary data from this trial seem to indicate that DSRS, in a subgroup of patients with good liver function and a correct portal-azygos disconnection, more effectively prevents variceal rebleeding than ES. However no significant difference in the survival of the two treatment groups was noted.
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PMID:Distal splenorenal shunt versus endoscopic sclerotherapy in the prevention of variceal rebleeding. First stage of a randomized, controlled trial. 240 92

Sclerotherapy of esophageal varices is an effective hemostatic treatment and may also prevent bleeding. In our study, we examined the effects of prophylactic sclerotherapy on esophageal motility in 15 patients with Child's A cirrhosis of the liver. All the patients underwent three manometric measurements, performed respectively before the sclerotherapy, 1 week after the eradication of varices, and 3 months later. The results of our study show that prophylactic sclerotherapy of esophageal varices does not significantly change the resting pressure and length of the lower esophageal sphincter. Neither the amplitude nor the duration of the postswallowing esophageal peristaltic waves is significantly influenced by sclerotherapy. However, sclerotherapy produces a significant increase in tertiary contractions in the distal esophagus, which could explain the onset of dysphagia among patients in whom postsclerotherapy stricture is not evident.
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PMID:Manometric evaluation of esophageal motility in patients submitted to prophylactic variceal sclerosis. 323 49

Thirty-one children with variceal bleeding due to portal hypertension (extrahepatic obstruction 19, non-cirrhotic portal fibrosis five, and cirrhosis of liver seven patients) were treated with endoscopic sclerotherapy with absolute alcohol. Acute variceal bleeding was successfully controlled in 10 patients by emergency sclerotherapy. A 3 weekly schedule of sclerotherapy could achieve obliteration of varices in all the patients. The mean (+/- SD) number of sclerotherapy courses and the time required for variceal eradication was 4.5 +/- 1.7 and 14.4 +/- 3.9 weeks, respectively. During a mean follow-up of 23.3 +/- 11.4 months, variceal recurrence was seen in three (9.7%) patients, two with cirrhosis and one with noncirrhotic portal fibrosis. Recurrence was not seen in any patient with extrahepatic obstruction. Five (16.1%) patients had a rebleed that could be controlled with emergency sclerotherapy. Esophageal stricture developed in four (12.9%) patients and could be dilated easily in all of them. The other complications of sclerotherapy included retrosternal pain, dysphagia, and fever; these were mild and short lasting. Survival in patients with extrahepatic obstruction and noncirrhotic portal fibrosis was 100%. The only death was in a cirrhotic, who died due to terminal hepatic failure. In conclusion, endoscopic sclerotherapy can be recommended as a safe and effective treatment in children for the control of acute variceal bleeding and for variceal obliteration.
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PMID:Endoscopic sclerotherapy for varices in children. 326 87

One hundred one patients, 54 with cirrhosis of liver, 31 with noncirrhotic portal fibrosis (NCPF), and 16 with extrahepatic obstruction (EHO), were followed up at monthly intervals for a mean (+/- SD) period of 17.9 +/- 4.8 months after achieving total variceal eradication with endoscopic sclerotherapy. Recurrence of esophageal varices was seen in 19 (18.8%) patients, 12 with cirrhosis and seven with NCPF, within a mean (+/- SD) period of 5.7 +/- 1.6 months. No patient with EHO showed recurrence. Three (2.9%) patients rebled from the recurred varices. Mean (+/- SD) number of sclerotherapy sessions and the amount of absolute alcohol required for eradication of recurred varices were 1.6 +/- 0.8 and 3.6 +/- 1.8 ml, respectively. Dysphagia and esophageal stricture were present in 15 (14.9%) patients with nearly similar frequency in patients with cirrhosis, NCPF, and EHO. Dysphagia in four patients with stricture improved without dilatation. While there were no deaths in patients with NCPF and EHO, 11 patients with cirrhosis died. There was significant (p less than 0.01) improvement in the liver status of surviving patients with cirrhosis after variceal eradication. It can be concluded that variceal recurrence and rebleeding are not major problems after sclerotherapy. Sclerotherapy probably helps in spontaneous improvement of the liver status of surviving cirrhotics and reduces long-term morbidity and mortality of patients with NCPF and EHO.
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PMID:Follow-up of patients after variceal eradication. A comparison of patients with cirrhosis, noncirrhotic portal fibrosis, and extrahepatic obstruction. 372 86

To assess the efficacy of absolute alcohol as a sclerosant, endoscopic sclerotherapy was carried out using a conventional endoscope and an indigenously designed injector. Forty three patients with portal hypertension who had presented with history of variceal bleeding were included in the study. Portal hypertension was caused by cirrhosis in 30 (69.8%), non-cirrhotic portal fibrosis in eight (18.6%) and extra-hepatic obstruction in five (11.8%). Acute bleeding was successfully controlled in all 11 patients, seven with a fresh bleed and four who rebled while on endoscopic sclerotherapy regimen. All patients with fresh, recent, or old bleeding were treated with a weekly endoscopic sclerotherapy schedule. Reduction in variceal size of two or more grades was achieved in all 20 patients who had completed at least four endoscopic sclerotherapy courses with total eradication of varices in 16 (80%). The mean (+/- SD) number of endoscopic sclerotherapy courses and time required for variceal eradication was 6.06 (+/- 1.87) and 9.1 (+/- 4.69) weeks respectively. None of these patients has shown appearance of fresh varices in a follow up of 18.47 +/- 8.50 weeks (range six to 38 weeks). Six patients died; all deaths were caused by progressive hepatic encephalopathy. Complications usually seen were dysphagia, retrosternal pain and fever; these were mild and easily tolerated by the patients. Rebleeding occurred in four patients who had received less than four endoscopic sclerotherapy courses. Absolute alcohol appears to be an effective, safe, economical, and freely available sclerosant. advocate endoscopic sclerotherapy as the first line of treatment for acute variceal bleeding and recommend a weekly schedule for the early eradication of varices.
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PMID:Endoscopic sclerotherapy using absolute alcohol. 387 16


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