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)

Tuberculous infection of the oesophagus is rare. This is confirmed by our present review of cases managed in our teaching hospitals over a period of 18 years which uncovered only 11 patients. The main presentation is that of dysphagia whose algorithm of investigation should seek to differentiate tuberculosis from carcinoma, the more common cause of this symptom. Of the 11 patients, 9 presented with dysphagia while 2 had haemorrhage; 7 had an abnormal plain chest radiograph, of whom 4 had a mediastinal mass lesion (3 were lymphadenopathy and one an abscess). All but one had an abnormal radio-contrast oesophagogram, including a mediastinal sinus in two and a traction diverticulum in another two. The mainstay of investigation was oesophagoscopy through which diagnostic biopsy material was obtained in half of the patients. In the other half diagnosis was by either biopsy of associated mediastinal (3) or cervical (1) lymph node masses or by acid fast bacilli positive sputum (1). The diagnosis was established post-mortem in one patient. Treatment was primarily non-operative with standard anti-tuberculosis drug therapy. Two patients underwent a diagnostic thoracotomy and one a drainage of mediastinal abscess together with resection and repair of oesophago-mediastinal sinus during the early part of the series. Outcome of management was very rewarding in 9 patients and death occurred in 2 patients, one of whom had his anti-tuberculosis drug therapy interrupted by severe hepatitis B virus infection. The other death occurred in a patient whose haemorrhage from an aorta-oesophageal fistula was not established ante-mortem. It is recommended that when biopsy material of the oesophagus is unobtainable or non-diagnostic in patients with dysphagia, especially with an abnormal chest radiograph or human immunodeficiency virus infection, effort should be made to obtain biopsy material from associated lymph nodes, even by thoracotomy if necessary, or culture of biopsy from the radiologically abnormal part oesophagus and sputum for mycobacteria, in order to establish the diagnosis of this rare but eminently treatable cause of dysphagia. Clinicians should be aware of tuberculosis of the oesophagus as a possible cause of haematemesis in patients with otherwise unexplained upper gastrointestinal haemorrhage.
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PMID:Oesophageal tuberculosis: a review of eleven cases. 157 Feb 50

Fifty consecutive patients presenting with upper gastrointestinal haemorrhage caused by oesophageal varices were subjected to endoscopic sclerotherapy during the period April 1989 to December 1991. Portal hypertension was caused by alcoholic liver cirrhosis in 22 (44pc), Hepatitis B induced liver cirrhosis in seven (14pc), cryptogenic liver cirrhosis in three (six pc), bilharzial portal fibrosis in 17 (34pc) and extrahepatic portal obstruction in one (two pc). Acute bleeding was controlled in 12 out of 13 patients, five of whom with a fresh bleed and eight who rebled while on the endoscopic sclerotherapy regimen. All patients were treated on a weekly sclerotherapy regimen. Reduction in variceal size of two or more grades was achieved in all 30 patients who had completed at least four or more endoscopic sclerotherapy courses with total eradication of varices in 27 (90pc). Three patients died. All deaths were caused by progressive hepatic encephalopathy. Complications usually seen were retrosternal pain, fever, dysphagia and oesophageal ulceration. There were no fatal complications. The study shows that endoscopic sclerotherapy is effective not only in controlling acute bleeding but also in preventing rebleeding. We recommend a weekly schedule for the early eradication of varices.
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PMID:Endoscopic sclerotherapy in Zimbabwe. 802 85

We report a 79-year-old man who developed progressive gait disturbance and sensory loss. He had been doing well except for hepatitis B virus hepatitis until 72 years of age when he developed angina pectoris for which aorto-coronary bypass operation was performed when he was 73-year-old (1986). In 1990, he developed pulmonary fibrosis for which prednisolone was prescribed. His liver function deteriorated, and the liver function tests suggested liver cirrhosis. He noted an onset of gait disturbance in the middle of June in 1992 when he was 79-year-old. His gait disturbance deteriorated progressively, and he developed edema and loss of sensation in his both legs. He became unable to walk unassisted in the beginning of July. He fractured his right external malleolus after falling down from a chair. He became unable to stand by himself, and he was admitted to the cardiology service of our hospital on July 18, 1992, and the neurology service was asked to see the patient on July 30 of the same month. The patient was well developed and well nourished man in no acute distress. General physical examination revealed slight jaundice, left carotid bruit, and slight pitting pretibial edema. His temperature was 37.3 degrees C. On neurologic examination, he was alert and mentally sound without dementia. He showed a slight weakness in the facial muscles bilaterally and mild dysarthria and dysphagia, however, the other cranial nerves appeared intact. He was unable to stand unassisted. The muscle tone was hypotonic, however, no focal muscle atrophy was noted, nor was observed fasciculatory twitches.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 79-year-old man with rapidly progressive tetraparesis]. 829 70

A 74-year-old man presented sudden onset hoarseness and dysphagia. Two months before this event, he had developed arthralgia of the shoulders, elbows, hands and foot and pleuritis which had been alleviated by a treatment with prednisolone. On admission, the patient could not phonate nor swallow at all. His soft palate was elevated at the right side. The uvula moved left when the patient tried to speak. Laryngoscopic examination revealed the paralysis of right vocal cord. The erythrocyte sedimentation rate (79mm/1h), C-reactive protein (5.3mg/dl), rheumatoid factor (310 IU/ml) and Clq-binding immune complex (4.5 micrograms/ml) were elevated. Hepatitis C virus antibody titer was more than 10.8 IU/l. Anti-nuclear antibody was 1:20 (normal < 1:20) and anti-neutrophil cytoplasmic antibody (p-ANCA) was positive. Blood study also revealed the evidences of hemolytic anemia and hypoproteinemia. Hepatitis B virus markers, cryoglobulin, anti-ds DNA, anti-Sm, anti-RNP, anti-SS-A, anti-SS-B antibodies were negative. Magnetic resonance imaging of the brainstem was normal. A sural nerve biopsy revealed patchy demyelination of the fascicles. The teasing of nerve fibers showed segmental demyelination. Chest X-ray showed the interstitial pneumonia and pleuritis in the right lower lung. Otological examination revealed the bilateral secretory otitis media. A treatment with high dose prednisolone, ciclosporin and cyclophosphamide was partially effective. However we could not continue these medication because of the induction of liver damage. The patient died of multi-organ failure around a year after the emergence of aphonia and dysphagia. The autopsy specimen of the right vagus nerve showed the similar patchy damage of nerve fibers as was observed in the biopsied sural nerve. The present case was diagnosed as systemic rheumatoid vasculitis. The syndrome of aphonia and dysphagia due to paralysis of the unilateral soft palate and vocal cord is called Avellis syndrome. This syndrome has been reported mainly in relation with the infarction of lateral medulla. The present case shows that Avellis syndrome can be produced by mononeuritis of the vagus nerve.
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PMID:[Avellis syndrome in systemic rheumatoid vasculitis]. 882 3

We presented a case of acute inflammatory demyelinating polyneuropathy associated with autoimmune chronic active hepatitis (AI-CAH). This is the third case report of neuropathy in AI-CAH. A 64-year-old male with chronic liver dysfunction was admitted to the hospital because of high fever, distal weakness and sensory disturbance of all extremities, bilateral facial weakness and dysphagia. On neurologic examination, there was bilateral weakness of the upper and lower facial muscles, bulbar palsy and severe distal weakness of all extremities. The deep tendon reflexes were absent and the sensation of touch, pinprick, temperature, and vibration was impaired bilaterally symmetrically in all extremities. Serum biochemistry revealed hyperproteinemia, hypergammaglobulinemia and elevated liver enzymes. Rheumatoid factor, antinuclear antibody anti-smooth muscle antibody were positive. Serological tests for hepatitis B surface antigen and its antibody hepatitis B core antibody, and hepatitis C antibody were all negative. Serum anti-GM1, anti-GD1b, anti-GQ1b and anti-MAG antibodies were negative. Liver biopsy findings were consistent with AI-CAH with marked lymphocytic infiltration in the portal tracts. Albuminocytologic dissociation was noted in CSF. Motorconduction velocity of the median, ulnar and facial nerves were markedly reduced with temporal dispersion. No motor response was evoked in the lower extremities. Needle electromyography revealed denervation and reinnervation potentials in the arm and leg. The sural nerve biopsy showed segmental de- and re-myelination and deposition of IgG components in endoneurium. Neurological symptoms and liver dysfunction improved with corticosteroid treatment. In this case, hypergammaglobulinemia associated with an exacerbation of AI-CAH may be responsible for the acute inflammatory demyelinating neuropathy through an unknown autoimmune mechanism.
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PMID:[A case of acute inflammatory demyelinating neuropathy associated with autoimmune-type chronic active hepatitis]. 950 66

Cerebral cavernous malformations are common vascular anomalies consisting of a cluster of capillaries without intervening brain tissue.1 A variety of approaches for resection have been undertaken,2 and a handful of case reports have described the endoscopic, endonasal, transclival approach.3 We present a case of a 51-yr-old woman with lupus and hepatitis B-associated cirrhosis who presented with diplopia, dysphagia, and ataxia. She had a left abducens nerve palsy and magnetic resonance imaging (MRI) showed a left pontine cavernous malformation. After a repeat hemorrhage, she consented to surgical resection. The lesion appeared to come to the medial pontine pial surface. Tractography indicated a rightward displacement of the left corticospinal tract. Therefore, an endoscopic, transnasal, transclival approach was chosen. A lumbar drain was placed preoperatively. The clivus and ventral petrous bone were drilled using the vidian canal to help identify the anterior genu of the petrous carotid artery. The clival dura was opened, revealing the abducens nerve exiting the ventral pons. The cavernoma was visible on the surface lateral to the nerve. It was removed using blunt dissection and the remaining cavity inspected. The skull base was reconstructed using an abdominal dermal-fat graft and Alloderm covered by a nasoseptal flap. Postoperatively she had transient swallowing difficulty. The lumbar drain was kept open for 5 d. Cerebrospinal fluid (CSF) leak was ruled out using an intrathecal fluorescein injection. She was discharged home, but presented 2 wk postoperatively with aseptic meningitis, which was treated supportively. Postoperative imaging did not show residual cavernoma.
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PMID:Transclival Approach for Resection of a Pontine Cavernous Malformation: 2-Dimensional Operative Video. 3204 6