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 62 year old woman admitted with a history suggesting acute myocardial infarction had thrombolytic treatment with anisoylated plasminogen-streptokinase activator complex, which resulted in submucosal haemorrhage in the oesophagus; this caused dissection of the wall of the oesophagus and complete dysphagia. The haematoma resolved spontaneously, leaving behind a diverticulum, with reduced peristalsis and delayed emptying but no obstruction.
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PMID:Oesophageal dissection after thrombolytic treatment for myocardial infarction. 148 Nov 88

Spontaneous intramural haematoma of the oesophagus (SIHO) is an uncommon disorder. It presents usually with acute chest pain followed by dysphagia. This condition may mimic spontaneous rupture of the oesophagus (Boerhaave Syndrome), dissection of the thoracic aorta or acute myocardial infarction. Hence early accurate confirmation of the diagnosis by radiology is vital for the appropriate acute management. The condition is frequently mistaken for acute myocardial infarction which may prompt inappropriate thrombolytic therapy. The appearances on contrast studies of oesophagus and on CT scanning are characteristic. Despite this, the diagnosis may easily be missed, if appropriate careful radiological technique is not used. This paper reports three consecutive cases of SIHO managed in one institution. These cases illustrate that early gastrografin contrast radiology followed by barium contrast radiology and if necessary by thoracic CT is diagnostic in all cases of this condition.
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PMID:Spontaneous intramural haematoma of the oesophagus: radiologic recognition. 882 33

We report a 49-year-old man with progressive bulbar palsy and respiratory failure. He was well until his 48 years of the age (December 1994) when he noted a difficulty in speaking in loud voice. In February, 1995, he noted regurgitation of foods to his nose and difficulty in his speech. He was admitted to our service in May 29, 1995. On admission, he was alert and oriented to all spheres and he was not demented. His higher cerebral functions were normal. In cranial nerves, he showed dysarthria and dysphagia; muscle atrophies were seen in the tongue, the bilateral sternocleidomastoid, supraspinatus, and infraspinatus muscles. Fasciculations were seen in these muscles. He showed no muscle weakness in his limbs except for the upper limb girdle muscles, no ataxia, no reflex abnormalities, nor sensory changes. EMG showed neurogenic changes in the affected muscles. MRI of the brain and the spinal cord was entirely normal. He was discharged for out patient follow-up, however, in October of 1995, he noted difficulty in swallowing solid foods. Gastrostomy was placed and he was discharged to his home. In February 11th of 1996, he was found unresponsive and brought into the ER of our hospital. On admission, he was comatose without spontaneous respiration. BP could not be obtained. He was immediately intubated and artificial ventilation was started. On the following morning, he became alert and he was not demented. He continued to show marked dysarthria and dysphagia; again no weakness was noted in the distal parts of the upper and lower extremities. Laboratory examination showed increase in serum CK to 2,173 IU/L and amylase to 2,032 IU/L. He was extubated on February 15th, however, his spontaneous respiration was not suffice to maintain his blood gas. According to his will, he was not placed on respirator and he died on February 24th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had ALS. Although no upper neuron signs were observed clinically, it is not uncommon to see degeneration in the corticospinal tract in post-mortem examination. The question was what might have been the cause of increase in CK and amylase. Many participants thought that they were secondary to multiple organ failure due to prolonged hypoxic state at his last admission; other possibilities raised included acute myocardial infarction and acute bowel necrosis. Post-mortem examination revealed muscle atrophy in the facial, lingual, cervical, intercostal, and the upper limb girdle areas. The lungs were unremarkable except for old organized pneumonic foci in the right middle and lower lobes. Marked to moderate congestion was seen in many internal organs, however, no other gross abnormality was found. It was thought that respiratory palsy itself was the direct cause of his agonal event. In the spinal cord, the anterior horns showed various degree of neuronal loss and gliosis. No clear evidence of pyramidal tract degeneration was seen at the light microscope level. Lower brain stem motor neurons were markedly reduced. But no Bunina body was found. The substantia nigra showed moderate degree of neuronal loss and extraneuronal neuromelanins. The locus coeruleus showed similar but milder changes. The degree of nigral degeneration appeared to be well beyond those which could be seen in usual ALS patients. The question was whether or not this patient might have been in an early stage of the extended form of ALS.
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PMID:[A 49-year-old man with progressive bulbar palsy and respiratory failure]. 949 5

Imidapril hydrochloride (imidapril) is a long-acting, non-sulfhydryl angiotensin-converting enzyme (ACE) inhibitor, which has been used clinically in the treatment of hypertension, chronic congestive heart failure (CHF), acute myocardial infarction (AMI), and diabetic nephropathy. It has the unique advantage over other ACE inhibitors in causing a lower incidence of dry cough. After oral administration, imidapril is rapidly converted in the liver to its active metabolite imidaprilat. The plasma levels of imidaprilat gradually increase in proportion to the dose, and decline slowly. The time to reach the maximum plasma concentration (T(max)) is 2.0 h for imidapril and 9.3 h for imidaprilat. The elimination half-lives (t(1/2)) of imidapril and imidaprilat is 1.7 and 14.8 h, respectively. Imidapril and its metabolites are excreted chiefly in the urine. As an ACE inhibitor, imidaprilat is as potent as enalaprilat, an active metabolite of enalapril, and about twice as potent as captopril. In patients with hypertension, blood pressure was still decreased at 24 h after imidapril administration. The antihypertensive effect of imidapril was dose-dependent. The maximal reduction of blood pressure and plasma ACE was achieved with imidapril, 10 mg once daily, and the additional effect was not prominent with higher doses. When administered to patients with AMI, imidapril improved left ventricular ejection fraction and reduced plasma brain natriuretic peptide (BNP) levels. In patients with mild-to-moderate CHF [New York Heart Association (NYHA) functional class II-III], imidapril increased exercise time and physical working capacity and decreased plasma atrial natriuretic peptide (ANP) and BNP levels in a dose-related manner. In patients with diabetic nephropathy, imidapril decreased urinary albumin excretion. Interestingly, imidapril improved asymptomatic dysphagia in patients with a history of stroke. In the same patients it increased serum substance P levels, while the angiotensin II receptor antagonist losartan was ineffective. These studies indicate that imidapril is a versatile ACE inhibitor. In addition to its effectiveness in the treatment of hypertension, CHF, and AMI, imidapril has beneficial effects in the treatment of diabetic nephropathy and asymptomatic dysphagia. Good tissue penetration and inhibition of tissue ACE by imidapril contributes to its effectiveness in preventing cardiovascular complications of hypertension. The major advantages of imidapril are its activity in the treatment of various cardiovascular diseases and lower incidence of cough compared with some of the older ACE inhibitors.
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PMID:Protection of the cardiovascular system by imidapril, a versatile angiotensin-converting enzyme inhibitor. 1217 88

Intramural hematoma of the esophagus (IHE) is a rare but well-documented condition that is part of the spectrum of esophageal injuries which includes the more common Mallory-Weiss tear and Boerhaave's syndrome. Acute retrosternal or epigastric pain is a common clinical feature, which can be accompanied by dysphagia, odynophagia, or hematemesis. An early differentiation from Mallory-Weiss tear, Boerhaave syndrome, ruptured aortic aneurysm, aortic dissection, acute myocardial infarction, or pulmonary pathology can be difficult. Computed tomography (CT) is the imaging modality of choice and characteristically reveals a concentric or eccentric thickening of the esophageal wall with well-defined borders and variable degree of obliteration of the lumen. Measurement of the attenuation values within the lesion will reveal blood density which varies according to the age of the hematoma. CT should be considered the preferred diagnostic technique, thereby facilitating proper clinical management. Early diagnosis is crucial as most patients may be treated conservatively with good outcome.
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PMID:Intramural hematoma of the esophagus: a pictorial essay. 1795 75

An 82-year-old man was admitted for recurrent and unresectable esophageal cancer. His performance status was grade 2, although he was on hemodialysis due to chronic renal failure since 2003. Esophagogastroduodenoscopy revealed stenosis of esophagus by the recurrent tumor. After percutaneous endoscopic gastrostomy, he received biweekly combination chemotherapy with docetaxel (18 mg/m(2)) and nedaplatin (16 mg/m(2)). Hemodialysis was carried out one hour after termination of nedaplatin infusion. As severe adverse reactions due to anticancer-chemotherapy were not encountered, he could receive four courses of chemotherapy in our outpatient clinic. Difficulty in swallowing improved after the second course was finished. Finally, he died of acute myocardial infarction. In conclusion, combination chemotherapy with docetaxel and nedaplatin can be safely carried out for a patient with recurrent and unresectable esophageal cancer even on hemodialysis by appropriate down-dosing of anticancer agents.
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PMID:[An elderly hemodialytic case of recurrent esophageal cancer given combination chemotherapy with docetaxel and nedaplatin who showed temporal relief of swallowing disturbance]. 2049 20

INTRODUCTION. Takotsubo syndrome (TTS) is a rare condition that mimics an acute myocardial infarction. It is associated with precordial pain, ST segment elevation, absence of coronary occlusion and reversible deformation of the left ventricle due to anteroapical dyskinesia that is reminiscent of a Japanese art of fishing octopuses (tako-tsubo). It is related with emotional and physical stress, and is thought to be mediated by an acute release of catecholamines. CASE REPORT. An 83-year-old woman with hypertension. She was admitted to the heart unit with a suspected acute coronary syndrome and respiratory failure, and thus required mechanical ventilation. An echocardiography scan showed severe ventricular dysfunction with apical dyskinesia. Cardiac catheterisation ruled out heart disease and a ventriculography scan revealed a bloated systolic deformation of the anterior and apical segments (TTS). Attempts to withdraw ventilation were unsuccessful and the neurology department was consulted. A directed medical history revealed that the patient had been suffering from generalised weakness, and progressive dysphagia and dyspnoea for several months. Results of an edrophonium test were positive. Single-fibre electromyography showed a pathological jitter and acetylcholine anti-receptor antibodies were positive. The patient was treated with immunoglobulins, corticoids and pyridostigmine. A control echocardiogram showed resolution of the TTS. CONCLUSIONS. TTS must be considered within the extra-neurological complications arising from myasthenic crisis. The neurologist must take this into account when faced with any symptom or sign of a potentially cardiac origin in myasthenic crisis and other neurocritical conditions.
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PMID:[Myasthenic crisis and Takotsubo syndrome: a non-chance relationship]. 2323 40

Sarcopenic dysphagia is characterized by the loss of swallowing muscle mass and function associated with generalized loss of skeletal muscle mass and function. In this report, the authors describe a patient with possible sarcopenic dysphagia after lung cancer surgery and was treated subsequently by rehabilitation nutrition. A 71-year-old man with lung cancer experienced complications of an acute myocardial infarction and pneumonia after surgery. He was ventilated artificially, and a tracheotomy was performed. The patient received diagnoses of malnutrition, severe sarcopenia, and possible sarcopenic dysphagia. His dysphagia was improved by a combination of dysphagia rehabilitation including physical and speech therapy and an improvement in nutrition initiated by a nutrition support team. Finally, he no longer had dysphagia and malnutrition. Sarcopenic dysphagia should be considered in patients with sarcopenia and dysphagia. Rehabilitation nutrition using a combination of both rehabilitation and nutritional care management is presumptively useful for treating sarcopenic dysphagia.
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PMID:Rehabilitation Nutrition for Possible Sarcopenic Dysphagia After Lung Cancer Surgery: A Case Report. 2682 95

Intramural hematoma of the esophagus is a rare injury causing esophageal mucosal dissection. Forceful vomiting and coagulopathy are common underlying causes in the elderly population taking antiplatelets or anticoagulation agents. Acute retrosternal pain followed by hematemesis and dysphagia differentiates the hematoma from other cardiac or thoracic emergencies, including acute myocardial infarction or aortic dissection. Direct inspection by endoscopy is useful, but chest computed tomography best assesses the degree of obliteration of the lumen and excludes other differential diagnoses. Intramural hematoma of the esophagus is generally benign and most patients recover fully with conservative treatment. Bleeding can be managed medically unless in hemodynamically unstable patients, for whom surgical or angiographic treatment may be attempted; only rarely esophageal obstruction requires endoscopic decompression. We report an unusual case of esophageal hematoma, presenting in a young preeclamptic woman after surgical delivery of a preterm twin pregnancy, with a favorable outcome following medical management.
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PMID:Intramural Hematoma of the Esophagus Complicating Severe Preeclampsia. 2860 83

Peri-procedural management of dual antiplatelet therapy following percutaneous coronary intervention for esophagogastroduodenoscopy and intervention is not clearly defined. We describe a case of a patient with a drug-eluting stent implanted in the setting of an acute myocardial infarction six weeks earlier who was bridged with cangrelor after interruption of ticagrelor for esophageal balloon dilatation because of dysphagia. The patient tolerated the procedure well and was transitioned back to ticagrelor without any complications.
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PMID:Use of intravenous cangrelor as antiplatelet bridge therapy in a patient undergoing esophageal dilation procedure. 3193 70


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