Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In five patients who had been on chronic maintenance haemodialysis for more than eight months a syndrome involving altered consciousness, asterixis, and abnormal electroencephalogram developed after they had been given flurazepam and diazepam. All five patients were adequately treated by haemodialysis. Hepatic, pulmonary, and cardiac decompensation were not present. The encephalopathy and other abnormalities cleared when the drugs were withdrawn. Symptoms were also produced by accidental rechallenge.
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PMID:Drug-induced encephalopathy in patients on maintenance haemodialysis. 6 91

The treatment of high blood pressure prevents death from congestive heart failure, hypertensive nephropathy, and encephalopathy, and strokes from cerebral arteriolar disease (lacunes, hemorrhage from microaneurysms). However, atherosclerosis, manifested as coronary artery disease is just as frequent a cause of death in well-controlled hypertensives as in poorly-controlled patients. Increasing evidence suggests that increased blood velocity, by causing turbulence and high shear rates at the endothelial surface of arteries, may be important in the pathogenesis of atherosclerosis. Turbulence has been observed in cerebral berry aneurysms. In order to measure the effects of antihypertensive agents on blood velocity, a new method of analysing Doppler ultrasound velocity recordings has been developed. Studies in Rhesus monkeys show the following: In doses which reduce diastolic pressure by 13-28%, propranolol decreased mean blood velocity (MV) by 17%, clonidine decreased MV by 14%, while methyldopa increased MV 12%, and hydralazine increased MV by 52%. (p less than .00001). It is hypothesized that enlargement of berry aneurysms, the progression of cerebral atherosclerosis, and embolism from carotid lesions might all be decreased by the selection of antihypertensive agents which decrease blood velocity.
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PMID:Effects of antihypertensive drugs on blood velocity: implications for prevention of cerebral vascular disease. 40 9

Sudden withdrawal of oral therapy with hydralazine for reduction of afterload in a patient precipitated severe congestive heart failure. Signs of metabolic encephalopathy evolved due to low cardiac output. Reinstitution of therapy with hydralazine resulted in prompt improvement in cardiac and neurologic status. This case underscores the need for careful follow-up of such patients and argues against sudden withdrawal of vasodilator therapy.
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PMID:Precipitation of heart failure following sudden withdrawal of hydralazine. 43 28

In this patient with long-standing cardiomyopathy and congestive heart failure the syndrome of fulminant hepatic failure developed on two occasions; he recovered both times. There was no evidence of viral or toxic hepatitis as a cause of his liver failure. We conclude that in this case, aggravation of long-standing congestive heart failure may have led to severe hepatocellular necrosis with signs of encephalopathy not commonly observed.
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PMID:Congestive heart failure as cause of fulminant hepatic failure. 68 25

Previous reports have described 5-20% prevalence of hyponatremia in extended care facilities, due largely to drugs or inappropriate antidiuretic hormone secretion. In our 400 bed VA extended care facility, 15 men with organic brain syndrome (Alzheimer's, multi-infarct dementia, anoxic encephalopathy or alcoholism) currently receive Isocal via gastrostomy as the sole source of nutrition. We noted intermittent hyponatremia in about half of these patients, and conducted a chart review to investigate the cause. Mean age was 68 yr (range 46-92); tube feeding duration was 3 mo.-3 yr; 266 Na concentrations were obtained from the charts. Simultaneous with these Na analyses, one of three diets prevailed: (A) mixed foods (3-6 g Na/day) orally before gastrostomy; (B) Isocal supplemented with NaCl to give 2 g Na/day; (C) unsupplemented Isocal providing 1 g Na/day. (B) and (C) had been randomly varied by rotating physicians. Serum Na was directly related to Na intake. On (A), Na was within normal range (135-145 mEq/l) in all men. One patient was hyponatremic during diet (B). During (C), eight patients were hyponatremic. Na was less than 135 mEq/l in 40% of all samples during diet (C) and less than 130 mEq/l in 14%. Changing from diet (A) or (B) to diet (C) caused nearly equivalent declines in Na and Cl; K and HCO-3 were unaffected. No hyponatremic patient took drugs known to cause hyponatremia, or had congestive heart failure, hypoalbuminemia, lipemia or fasting hyperglycemia. At the end of the study, four hyponatremic men were changed from (C) to (B); serum Na became normal in all four patients, without edema or hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyponatremia in tube-fed elderly men. 308 Apr 61

Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease) is an autosomal dominant, systemic fibrovascular dysplasia in which telangiectases, arteriovenous malformations, and aneurysms may be widely distributed throughout the body vasculature. Major clinical manifestations include: recurrent bleeding from mucosal telangiectases and arteriovenous malformations; hypoxemia, cerebral embolism, and brain abscess due to pulmonary arteriovenous fistulas; high-output congestive heart failure and portosystemic encephalopathy from hepatic arteriovenous malformations; and a variety of neurologic symptoms due to central nervous system angiodysplasia. Therapy is primarily supportive, consisting of iron supplementation and blood transfusion. Septal dermoplasty and oral estrogens may allow prolonged remission of epistaxis, but permanent surgical cure of gastrointestinal bleeding is rarely feasible because of diffuse angiodysplasia of the alimentary tract. Ligation, resection, or embolization may be indicated for pulmonary arteriovenous fistulas. The prognosis and survival of patients with hereditary hemorrhagic telangiectasia are favorable, providing treatable complications are accurately diagnosed.
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PMID:Clinical spectrum of hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease). 355 68

We treated a Japanese man with Rendu-Osler-Weber disease and a recurrent encephalopathy with hyperammonemia concomitant with recurrent epistaxis, G-I bleeding, congestive heart failure with aortic and mitral regurgitation, and chronic renal failure. At peritoneoscopy, several telangiectasia were noted on the surface of the liver. Angiographical studies revealed widened and tortuous hepatic arteries with early filling of hepatic veins and small pools of contrast medium scattered throughout the parenchyma. The recurrent encephalopathy was attributed to the porto-systemic shunt formed in the liver.
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PMID:Rendu-Osler-Weber disease with portosystemic encephalopathy. 369 24

The antihypertensive effects of intravenous labetalol were evaluated in 59 patients with hypertensive crises or severe hypertension in need of rapid lowering of blood pressure in a multicenter study. Patients appearing with a supine diastolic blood pressure 125 mm Hg or greater, or a supine systolic blood pressure of more than 200 mm Hg received an initial mini-bolus injection (20 mg) of labetalol. This was followed by repeated incremental doses of 20 to 80 mg given at 10 minute intervals to achieve a supine diastolic blood pressure of less than 95 mm Hg or decrease 30 mm Hg or greater, or a satisfactory decrease in systolic blood pressure. Patients were stratified into those who had taken antihypertensive medication within 24 hours and those who had not. The initial mini-bolus injection caused rapid but not abrupt reduction in blood pressure; the baseline mean blood pressure decreased 23/14 mm Hg. Further injections were needed in the majority of patients (mean: 197 mg). The blood pressure reduction after the last dose of labetalol was 55/33 mm Hg. In pretreated patients and in those who had no medication for 24 hours prior to the intravenous labetalol, the response was similar. Heart rate decreased 10 beats per minute in the total population. In patients pretreated with beta-adrenergic blockers, blood pressure response was similar to that in the total group (59/35 versus 55/33 mm Hg), but heart rate remained essentially unchanged. The dose required to achieve the therapeutic effect was less in pretreated patients than in untreated patients, but the duration of action was shorter. No serious adverse effects were encountered even in patients with concomitant diagnoses of acute left ventricular failure, myocardial infarction, stable congestive heart failure, atrial fibrillation, angina pectoris, acute stroke, transient ischemic attack or encephalopathy. Labetalol is a safe and effective treatment for a rapid blood pressure reduction in hypertensive emergencies.
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PMID:Intravenous labetalol in the treatment of severe hypertension and hypertensive emergencies. 613 20

The most important complications of intravascular administration of contrast agents include idiosyncratic (anaphylactoid) reactions, shock, congestive heart failure, cardiac arrhythmias, acute renal failure, and neurotoxic effects. The incidence of serious neurotoxic effects is low. Entry of contrast agents into the central nervous system normally is limited but may be increased by osmotic opening of the blood-brain barrier with cerebral arteriography or arch aortography. Most neurotoxic effects are thought to represent direct effects of the contrast agent on brain or spinal cord. Adverse effects with arteriography include seizures, transient cortical blindness, brain edema, and spinal cord injury. Most cases of focal brain deficit (other than cortical blindness) are attributed to embolism secondary to the catheter. Seizures may occur with intravenous administration, especially in patients with brain tumors or other processes disrupting the blood-brain barrier. The most important adverse effects observed with myelographic agents include acute and chronic meningeal reactions with iophendylate, and seizures and transient encephalopathy with metrizamide.
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PMID:Neurotoxicity of radiological contrast agents. 634 33

Fulminant hepatic failure has been reported in patients with chronic congestive heart failure. Two patients in whom jaundice and coma followed cardiac surgery were studied to find the possible etiology. Clinical, biochemical, and histologic evaluations revealed low cardiac output; elevated levels of bilirubin, lactic dehydrogenase, serum glutamic oxaloacetic transaminase, and alkaline phosphatase; prolonged prothrombin time; and centrizonal necrosis of hepatocytes with sinusoidal dilatation. No other possible causes of hapatic dysfunction and coma were identified. We conclude that acute postoperative congestive heart failure may cause fulminant hepatic failure and metabolic encephalopathy.
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PMID:Hepatic coma after open heart surgery. 738 54


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