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

A 61-year-old parkinsonian patient ingested up to 100 gm of levodopa during a period of 12 hours. Signs of parkinsonism were completely alleviated. Adverse effects included initial hypertension followed rapidly by hypotension of a few hours' duration, prolonged symptomatic postural hypotension, sinus tachycardia, mental confusion, insomnia, and anorexia. The effects of the overdose gradually subsided over 1 week. Analyses of serum and urine for dopa and its metabolites confirmed the overdose, which biochemically resulted in apparent saturation of two enzymatic pathways that inactivate dopamine: conjugation with sulfuric acid and O-methylation.
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PMID:Acute overdose with levodopa. Clinical and biochemical consequences. 117 16

Clinical diabetic nephropathy in man is the consequence of the development of a specific constellation of glomerular, tubular, vascular, and interstitial structural abnormalities accompanied by highly characteristic immunohistochemical alterations that, together, are unique to diabetes. Because changes resembling the specific pathology of diabetes do not develop in patients with conditions that lead to long-standing glomerular hyperfunction (such as unilateral nephrectomy), it is unlikely that glomerular hemodynamic abnormalities per se can be the cause of diabetic nephropathy. Whether hemodynamic abnormalities represent a risk factor that, in the presence of the diabetic state, can accelerate the rate of development of the basic lesions of diabetic nephropathy is currently unclear. However, there is considerable evidence that when the renal lesions of diabetes are far advanced, factors such as systemic hypertension can determine the rate of renal functional deterioration in diabetes as in other disorders. Although the diabetic rat may be a useful model for the study of aspects of the pathogenesis of diabetic nephropathy, much confusion has resulted from the inclusion of focal segmental glomerular sclerosis as a diabetic lesion. Similarly, the acceptance of all increases in urinary protein excretions in this model as resulting from or reflecting of diabetic nephropathology can be misleading. It is concluded that treatment aimed at manipulating renal hemodynamics in diabetic patients without evidence of renal disease should remain in the realm of clinical research.
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PMID:An overview of renal pathology in insulin-dependent diabetes mellitus in relationship to altered glomerular hemodynamics. 146 81

The clinico-tomographic correlations in 30 patients hospitalized for primary thalamic hemorrhage were studied. Arterial hypertension, observed in 90% of patients, represented the most important risk factor. Twenty-six subjects showed a sensory-motor hemisyndrome contralaterally to the lesion, nineteen showed alteration in level of consciousness from confusion to stupor and coma. Twelve subjects had poorly reactive pupils and eleven speech disturbances with involvement of the left thalamus. Seven patients died following hemorrhage; all subjects presented ventricular bleeding, severe disturbance of consciousness and arterial hypertension. On admission to hospital impairment of consciousness was the most significant unfavourable prognostic factor.
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PMID:Thalamic hemorrhage. 30 cases studied: clinico-tomodensitometric correlations. 158 Feb 1

We reviewed the clinical features of 26 children with Takayasu's arteritis. In contrast to what is often seen in adults, in this age group inflammation of different systems is a conspicuous feature. Eighty five percent of cases had arterial hypertension. The high incidence of arthritis and heart failure provoked confusion with rheumatic fever. There was a high frequency of positive purified protein derivative (73%) and lymphadenopathy (38%) with a histological picture of caseating granulomas, suggesting a link between Takayasu's arteritis and an atypical mycobacterial infection. No improvement of the arterial obstruction was observed with corticosteroid therapy. Takayasu's arteritis in children presents as an aggressive often lethal disease. The mortality rate was 35% over an observation period of 5 years.
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PMID:Takayasu's arteritis in children. 168 Nov 2

Atheroembolism, a systemic vascular disease. Cholesterol crystal embolization (CCE) is an infrequent but serious disorder that is often an unrecognized medical problem. CCE may occur spontaneously from eroded atherosclerotic plaques or most frequently following procedures such as angiography, angioplasty, cardiac catheterization, anticoagulant therapy and aortic surgery. CCE predominantly affects elderly males with a frequent history of hypertension, atherosclerotic vascular diseases and renal insufficiency. CCE may result in protean clinical manifestations and may produce a spectrum of functional impairment. Confusion over the disease's natural history arises because the difficulty of establishing an antemortem diagnosis, and because the laboratory findings are non-diagnostic and non-specific. The mortality was 81% and the causes of death was most often due to multiorgan failure especially renal involvement. The definitive diagnosis depends upon finding the presence of intravascular cholesterol crystal in biopsy or autopsy specimens. The skin, muscle and kidney were the three most common sites for obtaining a premortem diagnostic biopsy.
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PMID:[Atheroembolism: a form of systemic vascular disease]. 174 76

Cardiac remodeling constitutes a risk factor in cardiovascular disease. It may occur in a variety of circumstances. In hypertension and following myocardial infarction, pharmacological intervention in the remodeling process has been the subject of several studies. But the mechanisms of action of drugs that do contribute to regression of the remodeling response are still a matter of debate. Much of the confusion around the subject comes from the fact that classic arteriolar vasodilators do not result in such regression in hypertensive cardiac hypertrophy. This paper reviews some of the literature to examine whether there is indeed an exceptional position for vasodilators in hypertensive heart disease. Although, conceptually, arteriolar dilatation, and thus afterload reduction, might also have favorable effects on the remodeling response following myocardial infarction, clinical studies suggest the opposite. In the present paper, possible mechanisms are discussed, and evidence is presented that shows that hydralazine has an unexpected effect on the remodeling response at the level of the extracellular matrix.
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PMID:Cardiac remodeling in hypertension and following myocardial infarction: effects of arteriolar vasodilators. 182 79

A 34-year-old black male with hemoglobin AS was admitted for renal failure, polydipsia, hypertension, schizophrenia, mental confusion, and visual hallucinations. Abnormal electrolytes were corrected by dialysis, but blood specimens were reported as hemolyzed with hyperkalemia. Peaked T waves on electrocardiographic analysis were followed by cardiac arrest. An autopsy revealed sickled cells in the visual cortex and other symptomatic organs, but normal erythrocytes in most of the vascular tree. These findings suggest true progressive sickle cell crisis in a hemoglobin AS patient.
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PMID:Crisis in sickle cell trait. 186 94

Neurologic manifestations of pregnancy-induced hypertension (PIH) vary from diffuse symptoms such as headache and confusion to focal signs such as paralysis and visual loss. Recognition of the neurologic symptoms associated with PIH is essential for early diagnosis of severe preeclampsia and eclampsia. The recent advances in neuroradiologic imaging, including the use of computed tomography (CT) scans and magnetic resonance imaging (MRI), have greatly enhanced our understanding of the correlation between neurologic complaints and neuroanatomic pathological changes characteristic of preeclampsia and eclampsia. The aim of this review is to summarize the current knowledge on the pathophysiologic changes in the central nervous system (CNS) caused by PIH. The diagnostic possibilities offered by new imaging techniques are emphasized.
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PMID:Neurologic involvement in hypertensive disease of pregnancy. 194 96

Twenty-eight patients (19 females, 9 males) were evaluated pre- and posttransplant to determine the frequency and find predictors of excessive weight gain after orthotopic liver transplant. Posttransplant, 21 patients gained and 7 patients lost weight as compared with their pretransplant dry weight. The majority of weight gain occurred between 2 and 16 months; 64.3% of patients (18/28 pts.) became overweight. All patients overweight prior to transplant (11 pts.) were more overweight posttransplant (P less than 0.005). Overweight and nonoverweight patients were similar in age, female predominance, etiology of liver disease, hypercholesterolemia, and hypertriglyceridemia pretransplant, as well as diabetes mellitus and medications including prednisone posttransplant. Overweight patients more commonly had a family history of diabetes mellitus, arteriosclerotic heart disease, and hypertension. They also had more hypertension, hypercholesterolemia, hypertriglyceridemia, abnormal physical findings related to the liver, and abnormal results of hepatic tests posttransplant. Mean rate of weight gain for overweight patients compared with nonoverweight ones during the first 16 months after transplant was 1.5 kg/month +/- 0.9 vs 0.4 kg/month +/- 0.4 for those not overweight. After 16 months mean rate of increase was slower for overweight patients (0.3 kg/month +/- 0.3), whereas weight appeared to stabilize in the nonoverweight ones. We conclude that excessive weight gain after liver transplant is common and occurs early. Since obesity may contribute to, as well as be a separate cause, of hepatic abnormalities, confusion may result when interpreting abnormal results of hepatic tests. Obesity prior to transplant predicts excessive weight gain posttransplant, although all patients may be at risk.
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PMID:Excessive weight gain after liver transplantation. 201 32

Severe complications involving the central nervous system occurred in 7 of 36 children (19%) after renal transplantation. The children, aged 1.6-13.1 years at transplantation were treated with ciclosporin and prednisolone. Six of them had azathioprine as well. The neurological symptoms consisted of seizures, drowsiness, confusion, hallucinations, visual disturbances, and mental changes. In all cases electroencephalograms were severely pathological, showing diffuse abnormalities with or without focal abnormalities and epileptic activity. In all but one case the ciclosporin trough blood levels were within the therapeutic range. Blood glucose and electrolytes were normal. Several factors might contribute to the central nervous system complications: ciclosporin, corticosteroids, hypertension, rejection, and as yet unknown ones.
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PMID:Central nervous system complications in children treated with ciclosporin after renal transplantation. 208 97


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