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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors present the results of the long-term follow up of nine patients with prehepatic portal hypertension treated by a portosystemic anastomosis. The evaluation was made 5-21 years after operation, according to criteria focused on the therapeutic effect of the anastomosis and its possible pathophysiological sequelae. In the authors' opinion the anastomosis is the operation of choice suited for patients lacking a tendency of normalization of the portal circulation and with dangerous manifestations of portal overpressure. The indication is restricted to early age of the patients (for technical reasons). Conversely the patient should not attain adult age without unresolved hypertension. For correct timing of the operation knowledge of the development of the disease is essential. Primarily infact livers do not undergo pathological changes even after years of hypertension nor several years after an anastomosis. This is consistent with the fact that these patients lack clinical manifestations of portosystemic encephalopathy. Investigations of the course of flow curves during semiquantitative evaluation of hepatobiliary sequential scintigraphy supported the previous view that establishment of the anastomosis and elimination of portal overpressure improves hepatic perfusion. Hepatobiliary sequential scintigraphy not previously used in this indication may be of value in the follow up of the disease and evidence of the anastomosis. This preliminary conclusion is being tested in a prospective study.
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PMID:[Life prognosis in patients with prehepatic portal hypertension treated with portosystemic shunts]. 192 90

Hepatic encephalopathy is a major complication of portal-systemic shunts with an incidence ranging up to 52%. A small fraction of these patients are refractory to medical therapy. Shunt ligation and colonic procedures are the main surgical approaches. The goal of the latter is to diminish the colonic absorption of nitrogenous substances which are involved in the pathophysiology of hepatic encephalopathy. Six patients, whose average age was 55.7 +/- 2.6 years, were operated for severe postshunt encephalopathy requiring 4.3 +/- 0.9 admissions for a total duration of 76 +/- 26 days over 1-11 years. One patient had undergone a splenoral shunt and 5 had a portacaval shunt. One ligation of the shunt and 5 colon exclusions were performed. The average postoperative hospital stay was 21.5 +/- 3.9 days. The mean follow-up was 47 +/- 20 months. The patient with the shunt ligation remains free of encephalopathy 94 months after the procedure and has not bled from his esophageal varices. Among the 5 colon exclusion patients, there were 1 death and 3 complications. Three patients were completely relieved of their hepatic encephalopathy. One of those 3 died of a subarachnoid hemorrhage 28 months after the surgery. The fourth still needs medication to control a persistent, although improved, encephalopathy that required 2 further hospitalizations. Colon exclusion is a useful intervention in very selected cases. It has a lower operative mortality than total colectomy and the advantage over shunt ligation of not reestablishing hypertension in the portal system.
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PMID:Surgical treatment of severe postshunt hepatic encephalopathy. 199 94

Vascular dementia is the second most common type of dementia in the elderly after the dementia of Alzheimer's disease. Six forms of vascular dementia have been described: multi-infarct dementia, lacunar dementia, Binswanger's subcortical encephalopathy, cerebral amyloid angiopathy, white-matter lesions associated with dementias, and single-infarct dementia. Each is described. Severe dementia is found in 5% of persons over age 65 and in 15% to 20% of persons over age 80 years. Alzheimer's disease accounts for 50% to 60% of cases of severe dementia and vascular dementia for 10% to 20%; 20% of the patients have both disorders. The incidence of vascular dementia, which seems to be declining, is about 7/1,000 persons/year. Hypertension is the most powerful risk factor for all vascular dementias. Vascular dementias can be accurately diagnosed by using clinical and mental state examinations, Diagnostic and Statistical Manual of Mental Disorders criteria, ischemic scores, and computed tomography or magnetic resonance imaging. The most successful treatment of vascular dementia is the prevention of cerebral infarcts. Study of the incidence of vascular dementias and their treatment will be included in the European Trial on Systolic Hypertension in the Elderly (SYST-EUR) of 3,000 elderly hypertensive patients.
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PMID:Hypertension and the risk of dementia in the elderly. 200 54

Regular drug treatment in mild hypertension (diastolic blood pressure 90-104 mm Hg) reduces death from stroke, and other non-coronary vascular events. The optimum strategy remains sequential monotherapy with the lowest effective dose, with drug combinations as an option. A beta-adrenoceptor blocker or low-dose thiazide is good value treatment for many patients. beta-Blockers are good for young (under 50 years), anxious non-smoking men, men after myocardial infarction, and renal failure patients. Older persons over about 65 years, women, smokers, stroke victims, and liver disease patients should generally take a thiazide or calcium ion-channel blocker. Pregnant women and untreated gouty patients should avoid diuretics. Calcium blockers and angiotensin-converting enzyme inhibitors are preferable in severe or insulin-dependent diabetes and renal failure, and angiotensin manipulators or thiazides in heart failure or peripheral vessel disease. Hyperlipidaemia should not generally exclude thiazides or beta-blockers. Some hypertensive stroke patients without encephalopathy may not need antihypertensive drug treatment for the first 24-48 hours. Drug treatment should be tailored to individuals according to their general condition, physiological age, and any concurrent disease or medication. Unwanted drug reactions should not deter patients from fulfilling social and economic goals. The desired treatment end-point is a diastolic pressure of 85-89 mm Hg, but a compromise is usual in poorly motivated young men, and the elderly.
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PMID:Optimising drug management of individuals with cryptogenic hypertension. 202 55

Three nonelderly patients without hypertension whose clinical and radiologic features otherwise resembled Binswanger's subcortical arteriosclerotic encephalopathy underwent biopsy of the hyperintense periventricular lesions seen on magnetic resonance imaging. The pathologic findings of the periventricular lesions consisted of gliosis with mild rarefaction and edema of the white matter. All patients had a sclerosing vasculopathy of unknown cause, which involved numerous small vessels within the periventricular lesions. The vessels stained negatively for amyloid, amyloid precursors, desmin, vimentin, keratin, immunoglobulin, and complement. On electron microscopy, small arteries, arterioles, venules, and capillaries were characterized by swollen astrocytic foot processes surrounding the vessels; dense, perivascular collagen packing; crystalline arrays of filaments within basement membrane; giant lipid-laden lysosomes within perivascular cells; and narrowing of the vascular lumina. Similar changes were not seen in a control group of 19 patients. The pathologic features of the vessels in these cases are distinct from the vasculopathy associated with Binswanger's subcortical arteriosclerotic encephalopathy. We suggest that a spectrum of vasculopathies may be associated with dementia and periventricular hyperintense lesions on magnetic resonance imaging.
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PMID:Sclerosing vasculopathy of the central nervous system in nonelderly demented patients. 203 86

Recombinant human erythropoietin may improve hemostasis of uremic patients by correcting anemia. However, a complete correction of renal anemia carries the risk of hypertension, encephalopathy, thrombosis, and hyperkalemia. Our aim was to establish the minimum level of packed cell volume (PCV) achieved with recombinant human erythropoietin that corrects the prolonged bleeding time in uremia. Twenty patients with chronic renal failure, anemia, and very prolonged bleeding time (greater than or equal to 15 minutes) were randomly allocated to erythropoietin or no specific treatment. The initial dose of erythropoietin was 50 U/kg intravenously (IV) three times a week. Every 4 weeks, the dose was increased by 25 U/kg until a normalization of bleeding time was achieved. Erythropoietin at a dose ranging from 150 to 300 U/kg/wk induced an increase in PCV to a range of 27% to 32% in all patients but one, and normalized bleeding time in all patients. A significant negative correlation (r = 0.898, P less than 0.001) was found between PCV and bleeding time measurements. Erythropoietin also significantly (P less than 0.01) increased values for red blood cell (RBC) distribution width (basal, 11.3 +/- 0.6; 12 weeks, 13.1 +/- 1.3). Platelet count and platelet function parameters did not significantly change. In untreated patients, no changes were recorded in all the parameters considered. These results establish in a controlled fashion that erythropoietin shortens bleeding time of uremic patients and indicate that a partial correction of renal anemia is enough to normalize bleeding time.
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PMID:Recombinant human erythropoietin to correct uremic bleeding. 206 54

The electrophysiological recordings (E.R.G. associated with C.V.E.P.) performed on 101 children suffering from encephalopathy of different origins demonstrate a trend towards retinal integrity for subjects with encephalopathy and no suspicion of acid-base disorders. However a functional macular deficiency is frequently observed in encephalopathy with suspicion of acid-base disorders (encephalopathy due to intracranial hypertension or cardio-vascular disorders or metabolic deficiencies with acid-base disturbance). In these cases, a common pathophysiological substratum with disturbance of the acute or chronic acid-base equilibrium has been assumed. Over a period of time, in fixed encephalopathy, the electrophysiological results reflect a real but slow maturation of the visual pathways.
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PMID:[Visual electrophysiology in 101 children with encephalopathy]. 208 56

Eclampsia is the most serious manifestation of a toxaemic encephalopathy which may also have nonconvulsive manifestations, such as headache, visual disorders or retinal or cortical origin, confusion or disturbances of consciousness. Some authors consider eclampsia as being only one particular aspect of hypertensive encephalopathy. However, recent studies have drawn attention to the importance of angiospasm which might not be a pure reaction to hypertension but might result from a relative deficiency in vascular prostacyclin. These physiopathological factors, to which must sometimes be added disseminated intravascular coagulation, account for computerized tomographic and neuropathological findings showing cerebral oedema and, in complicated cases, ischaemic or haemorrhagic lesions. Medical treatment must rapidly control the convulsive attacks as well as the arterial hypertension. Magnesium sulfate is not much used outside the United States where it is now strongly controverted. The obstetrical management depends on the time when eclampsia occurs and on the efficacy of the medical treatment.
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PMID:[Eclampsia]. 214 84

A case of fulminant hepatitis in a patient taking lisinopril for 5 weeks for arterial hypertension is reported. Jaundice, fever, myalgia, and marked increase in serum aminotransferase activities occurred after 2 weeks of treatment. Continuation of lisinopril administration for 3 weeks after the onset of jaundice was associated with the development of grade III encephalopathy and a marked decrease in prothrombin and proaccelerin levels. This case strongly suggests that lisinopril may induce acute hepatitis and that continuation of the treatment after the onset of jaundice can lead to life-threatening hepatic failure.
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PMID:Fulminant hepatitis after lisinopril administration. 217 73

Surgically confirmed pheochromocytoma was the cause of arterial hypertension in 6 out of 668 (0.8%) children with significant hypertension admitted to Child Health Centre in Warsaw. Among clinical features most characteristic was sustained hypertension observed in all patients, often complicated by the accelerated phase of malignant hypertension and encephalopathy. Sustained tachycardia was also found in all patients. Elevated sedimentation rate and electrocardiographic changes were observed in each child while other abnormal laboratory findings such as hyperglycemia, etc. occurred at similar rate as in adults. Increased urinary excretion of catecholamines and their metabolites confirmed the diagnosis. In our study the most sensitive methods for tumor localization were ultrasonography and computed tomography of the adrenals while scintigraphy with iodo-131-metabenzylguanidine gave a high percentage of false negative results. Clinical presentation of pheochromocytomas in children is different than in adults and all pediatric patients with severe hypertension should be screened for this disease.
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PMID:Pheochromocytoma in children: difficulties in diagnosis and localization. 219 28


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