Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Dopamine beta-hydroxylase is stored and released with catecholamines by exocytosis from secretory vesicles in noradrenergic neurons and chromaffin cells. Although dopamine beta-hydroxylase enzymic activity is measurable in cerebrospinal fluid, such activity is unstable, and its relationship to central noradrenergic neuronal activity in humans is not clearly established. To explore the significance of cerebrospinal fluid dopamine beta-hydroxylase, we applied a homologous human dopamine beta-hydroxylase radioimmunoassay to cerebrospinal fluid, in order to characterize the properties and stability of cerebrospinal fluid dopamine beta-hydroxylase, as well as its relationship to central noradrenergic neuronal activity and its variation in disease states such as hypertension, renal failure, Parkinsonism and congenital dopamine beta-hydroxylase deficiency. 2. Authentic, physically stable dopamine beta-hydroxylase immunoreactivity was present in normal human cerebrospinal fluid at a concentration of 31.3 +/- 1.4 ng/ml (range: 18.5-52.5 ng/ml), but at a 283 +/- 27-fold lower concentration than that found in plasma. Cerebrospinal fluid and plasma dopamine beta-hydroxylase concentrations were correlated (r = 0.67, P = 0.001). Some degree of local central nervous system control of cerebrospinal fluid dopamine beta-hydroxylase was suggested by incomplete correlation with plasma dopamine beta-hydroxylase (with an especially marked dissociation in renal disease) as well as the lack of a ventricular/lumbar cerebrospinal dopamine beta-hydroxylase concentration gradient. 3. Cerebrospinal fluid dopamine beta-hydroxylase was not changed by the central alpha 2-agonist clonidine at a dose that diminished cerebrospinal fluid noradrenaline, nor did cerebrospinal fluid dopamine beta-hydroxylase correspond between subjects to cerebrospinal fluid concentrations of noradrenaline or methoxyhydroxyphenylglycol; thus, cerebrospinal fluid dopamine beta-hydroxylase concentration was not closely linked either pharmacologically or biochemically to central noradrenergic neuronal activity. 4. Cerebrospinal fluid dopamine beta-hydroxylase was not changed in essential hypertension. In Parkinson's disease, cerebrospinal fluid dopamine beta-hydroxylase was markedly diminished (16.3 +/- 2.9 versus 31.3 +/- 1.4 ng/ml, P < 0.001) and rose by 58 +/- 21% (P = 0.02) after adrenal-to-caudate chromaffin cell autografts. In congenital dopamine beta-hydroxylase deficiency, lack of detectable dopamine beta-hydroxylase immunoreactivity in cerebrospinal fluid or plasma suggests absent enzyme (rather than a catalytically defective enzyme) as the origin of the disorder. 5. We conclude that cerebrospinal fluid dopamine beta-hydroxylase immunoreactivity, while not closely linked to central noradrenergic neuronal activity, is at least in part derived from the central nervous system, and that its measurement may be useful in both the diagnosis and treatment of neurological disease.
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PMID:Dopamine beta-hydroxylase immunoreactivity in human cerebrospinal fluid: properties, relationship to central noradrenergic neuronal activity and variation in Parkinson's disease and congenital dopamine beta-hydroxylase deficiency. 814 25

We report the findings of a total population survey of Thugbah community in the Eastern Province of Saudi Arabia (SA) to determine its point prevalence of neurological diseases. During this two-phase door-to-door study, all Saudi nationals living in Thugbah were first screened by trained interviewers using a pretested questionnaire (sensitivity 98%, specificity 89%) administered at a face-to-face interview. Individuals with abnormal responses were then evaluated by a neurologist using specific guidelines and defined diagnostic criteria to document neurological disease. The questionnaire was readministered blind by a neurologist to all those with abnormal responses and a 1-in-20 random sample of those without abnormal responses, respectively. The family members of an individual with an abnormal response were also screened to improve accuracy. A total of 23,227 Saudis (98% of the eligible subjects) were screened and those residing in Thugbah on the reference date (22,630) were used to calculate the point prevalence rates. Forty-two percent of those screened were in the first decade of life and only 1.5% were more than 60 years old. There were marginally more females (50.2%) than males (49.8%). Consanguineous marriages especially between first cousins were present in 54.6%. The demographic characteristics of Thugbah community were similar to those in other parts of SA. The overall crude prevalence ratio (PR) for all forms of neurological disease was 131/1,000 population. All subsequent PRs are per 1,000 population. Headache syndromes were the most prevalent disorder (PR 20.7). The PR for all seizure disorders was 7.60, and the epilepsies (6.54) were more frequent than febrile convulsions (0.84). Mental retardation, cerebral palsy syndrome, and microcephaly were common pediatric problems with PRs of 6.27, 5.30 and 1.99, respectively. Stroke, Parkinson's disease, and Alzheimer's disease were uncommon with respective PRs of 1.8, 0.27 and 0.22. Central nervous system (CNS) malformations (0.49) such as hydrocephalus and meningomyelocele were more prevalent than spinal muscular atrophy (0.13), congenital brachial palsy (0.13) and narcolepsy (0.04). Multiple sclerosis was rare (0.04). Osteoarthritis and low back pain syndromes were the main non-neurological conditions seen. The major medical diseases that may be neurologically relevant were diabetes mellitus, hypertension, and connective tissue disorders.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A community survey of neurological disorders in Saudi Arabia: the Thugbah study. 827 77

Isoflurane anaesthesia was proposed instead of electro-convulsive therapy (ECT) in patients with treatment-refractory depression. This open study compared burst-suppression-isoflurane-anaesthesia (BSIA) and ECT in 12 severely depressed patients. A series of 6 BSIA was administered in every patient. If improvement was insufficient or only temporary, a series of up to 12 ECT was given. A marked improvement of the depression was shown after both BSIA and ECT. Three patients were discharged from hospital after BSIA, nine patients were treated with BSIA and then ECT. The therapeutic effect of both regimens was equal as evidenced by the Hamilton-depression-rating-scale, a visual-analog-scale and the clinical global impression. BSIA requires more time and monitoring than ECT. Our exclusions of coronary, cerebral and peripheral vascular disease, untreated hypertension and focal neurological disease are strongly recommended. Due to the ease of application, ECT remains the standard treatment in depressed patients, but we consider BSIA a valuable alternative at least in patients who object to ECT.
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PMID:Intra-individual open comparison of burst-suppression-isoflurane-anaesthesia versus electroconvulsive therapy in the treatment of severe depression. 846 36

Although much has been learned about cerebral physiology during CPB in the past decade, the role of alterations in CBF and CMRO2 during CPB and the unfortunately common occurrence of neuropsychologic injury still is understood incompletely. It is apparent that during CPB temperature, anesthetic depth, CMRO2, and PaCO2 are the major factors that effect CBF. The systemic pressure, pump flow, and flow character (pulsatile versus nonpulsatile) have little influence on CBF within the bounds of usual clinical practice. Although cerebral autoregulation is characteristically preserved during CPB, untreated hypertension, profound hypothermia, pH-stat blood gas management, diabetes, and certain neurologic disorders may impair this important link between cerebral blood flow nutrient supply and metabolic demand (Figure 5). During stable moderate hypothermic CPB with alpha-stat management of arterial blood gases, hypothermia is the most important factor altering cerebral metabolic parameters. Autoregulation is intact and CBF follows cerebral metabolism. Despite wide variations in perfusion flow and systemic arterial pressure, CBF is unchanged. Populations of patients have been identified with altered cerebral autoregulation. To what degree the impairment of cerebral autoregulation contributes to postoperative neuropsychologic dysfunction is unknown. It must be emphasized that not the absolute level of CBF, but the appropriateness of oxygen delivery to demand is paramount. However, the assumption that the control of cerebral oxygen and nutrient supply and demand will prevent neurologic injury during CPB is simplistic. A better understanding of CBF, CMRO2, autoregulation and mechanism(s) of cerebral injury during CPB has lead to a scientific basis for many of the decisions made regarding extracorporeal perfusion.
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PMID:Cerebral blood flow and metabolism during cardiopulmonary bypass. 846 2

Stroke is a partly preventable neurological disease associated with excessive economic cost. Adequate prevention of stroke and sufficient therapy in the acute phase will help to reduce the heavy burden of morbidity and severe economic impact. Hypertension as such, and even more so stroke itself, are known to influence cerebral autoregulation in a negative sense. With respect to the prevention of stroke, antihypertensive therapy should be accompanied by attempts to inhibit of atherogenesis, for instance via improvements of the lipid profile (lowering of LDL, elevation of HDL) or via inhibition of platelet aggregation. In conditions of acute stroke, a pharmacologically induced rise in intracranial pressure should be avoided, whereas cerebral perfusion pressure must be maintained. If possible, ischaemic tolerance should be increased. Also with respect to the secondary prevention of stroke, antihypertensive therapy should be aiming at maintaining cerebral blood flow, whereas the progression of atherosclerotic lesions should be impaired as much as possible. Urapidil may be characterised as a peripheral alpha 1-adrenoceptor blocker with additional sympathoinhibitory effect, triggered by the stimulation of central 5HT1A-receptors. Urapidil, well documented as an effective antihypertensive agent in short- and long-term trials, also showed beneficial influence in the acute phase of stroke. After 3 years of treatment with urapidil (60 mg b.i.d.), the total cardiovascular risk proved reduced by 26%. In addition, urapidil influenced lipid profile, glucose metabolism, and platelet aggregation favourably in hypertensive patients. In animal experiments, urapidil improved the ischaemic tolerance of the brain. Taken together it would seem worthwhile to investigate urapidil as a possibly beneficial agent in the treatment of acute stroke, as well as in secondary prevention of this condition.
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PMID:Potential beneficial effects of urapidil in primary and secondary prevention of stroke. 853 45

The serum concentration of lipoprotein(a) [Lp(a)], lipids, lipoproteins, apolipoprotein A-I, and apolipoprotein B were determined in 228 patients with cerebral infarction, composed of 87 cases of asymptomatic lacunar infarction, 99 cases of lacunar infarction, and 42 cases of atherothrombotic infarction, and in a control group of 138 healthy subjects with normal MRI. Observations were made on the distribution of Lp(a), Lp(a) and other risk factors for cerebral infarction and these were statistically analyzed, primarily by multiple logistic regression analysis. The diagnosis of these cases was based on the Classification of Cerebrovascular Diseases III of the National Institute of Neurological Disorders and Stroke. The following results were obtained. 1) Lipoprotein (a) (1) Lp(a) did not show a normal distribution with the curve showing a gradual declining slope to the right. It was therefore considered not appropriate in our analysis to use as a means or standard deviation. (2) The 25th percentile, 50th percentile, and 75th percentile of the control group were 5.0 mg/dl, 11.0 mg/dl, and 22.4 mg/dl, respectively. In studying the distribution in these percentile ranges by subtypes of infarction, an increase in cases showing values greater than the median of the control group was observed in asymptomatic lacunar infarction, lacunar infarction, and atherothrombotic infarction, when compared to the control group. In asymptomatic lacunar infarction and lacunar infarction in particular, Lp(a) showed a significantly higher value compared to the control group. (3) However, by multiple logistic regression analysis to adjust for age and sex, Lp(a) did not show a significant odds ratio for asymptomatic lacunar infarction, lacunar infarction and atherothrombotic infarction. 2) Various serum lipids and other parameters (1) The various serum lipids did not show any involvement in asymptomatic lacunar infarction. However, involvement of HDLC and Apo A-I in lacunar infarction and atherothrombotic infarction was observed with the odds ratios in lacunar infarction being 4.2 with a confidence interval of 2.9-9.4 and 4.7 with a confidence interval of 2.2-10.1, and the odds ratios in atherothrombotic infarction being 3.1 with a confidence interval of 1.1-9.0 and 9.6 with a confidence interval of 3.0-30.5, respectively. (2) Involvement of diabetes mellitus in asymptomatic lacunar infarction and lacunar infarction was small, but a strong involvement in atherothrombotic infarction was observed with the odds ratio being 4.3 with a confidence interval of 1.2-16.2. (3) Involvement of hypertension in asymptomatic lacunar infarction and lacunar infarction was observed with the odds ratios being 2.6 with a confidence interval of 1.4-5.2 and 5.6 with a confidence interval of 2.4-13.0, respectively, but the involvement in atherothrombotic infarction was low. The foregoing results indicated that there was no involvement of Lp(a) as a risk factor for any type of cerebral infarction, unlike its involvement in coronary heart diseases. Only blood pressure was involved as a risk factor for asymptomatic lacunar infarction, but for lacunar infarction not only blood pressure but also HDLC and Apo A-I were involved as risk factors. HDLC, Apo A-I, and diabetes mellitus were involved as risk factors for atherothrombotic infarction, but the involvement of hypertension was minimal.
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PMID:Lipoprotein(a) and other risk factors for cerebral infarction. 856 15

Prevention of stroke caused by carotid bifurcation stenosis can be achieved by accurate identification and evaluation of patients at risk. A consensus report from the National Institute of Neurologic Disorders and Stroke has standardized diagnostic criteria and symptoms related to this disease. Recent prospective, randomized trials have identified effective treatment for both asymptomatic and symptomatic carotid stenosis. The risk factors for carotid stenosis are similar to those for atherosclerosis--hypertension, diabetes, cigarette smoking and hyperlipidemia. A carotid bruit is the most common clinical finding, although its positive predictive value is only about 60 to 70 percent. Recent clinical trials have identified patient groups that benefit from surgical and medical therapy, depending on the degree of carotid stenosis and the presence or absence of symptoms. Symptomatic patients with carotid stenosis greater than 70 percent benefit from surgical therapy. Asymptomatic patients who have carotid stenosis greater than 60 percent and are good surgical candidates should be referred for surgical consultation.
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PMID:Prevention of stroke caused by carotid bifurcation stenosis. 862 32

Systemic lupus erythematosus (SLE) patients, specially those with antiphospholipid antibodies, have a high incidence of arterial and venous thrombotic manifestations. However, renal infarction has been rarely reported in these patients. The case of a young female with renal infarction, diagnosed by renal arteriography and scintigraphy, and arterial hypertension (AH) is described. In subsequent years she also suffered several cerebrovascular accidents with important neurological sequelae. No evidence of systemic disease was observed at this time. Fourteen years after the renal infarction a diagnosis of SLE was established. Despite therapy with prednisone, acetylsalicylic acid, azathioprine and antihypertensive drugs the progression of the neurological disease led to death. The sudden appearance of severe AH in a young woman with a renal infarction should alert the clinician about a possible underlying renal artery thrombosis in association with SLE and antiphospholipid antibodies.
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PMID:Renal infarction in a severely hypertensive patient with lupus erythematosus and antiphospholipid antibodies. 868 43

We report the results of a systematic study on the association of antiphospholipid antibodies (aPLs) with some neurological disease other than stroke in a childhood population. Patients affected by migraine, benign intracranial hypertension (BIH) or unilateral movement disorders, such as hemichorea and hemidystonia with acute-subacute onset, were screened for aPLs. None of them had clinical or serological evidence of Systemic Lupus Erythematosus (SLE) or other connective tissue disease. Moderate to high levels of anticardiolipin antibodies (aCL) and/or positive Lupus Anticoagulant (LA) were demonstrated in 6 out of 17 patients with migraine, in 3 out of 4 patients with BIH and in all of the 5 patients showing unilateral movement disorders. The association between aPLs and these neurological conditions, usually regarded as cryptogenic, may suggest a possible pathogenetic mechanism.
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PMID:Neurological disorders, other than stroke, associated with antiphospholipid antibodies in childhood. 883 75

This two-stage epidemiologic study was to investigate the prevalence and types of dementia among elderly people in the Saa-Min district of Kaohsiung City in Taiwan. In stage one, the Chinese Mini-Mental Status Examination (CMMSE) and Blessed Dementia Rating Scale were employed. In stage two, a comprehensive neurobehavioral examination and neuropsychologic tests were administered by neurologists and neuropsychologists. Dementia was defined by DSM-III-R criteria. The National Institute of Neurological and Communication Disorders and Stroke-Alzheimer's Disease and Related Disorders Association guidelines for Alzheimer's disease (AD) and the National Institute of Neurological Disorder and Stroke-Association international pour la Recherche et l'Enseignement en Neurosciences criteria for vascular dementia (VaD) were applied. A total of 1,016 randomly selected elderly people participated in phase one: 131 people with CMMSE below cutoff values participated in phase two, of whom 45 were confirmed to have a form of dementia. The prevalence of dementia in this sample was 4.4% (3.2% in men and 5.8% in women): 2.0% for those 65 to 74 years old, 8.3% for those 75 to 84 and 24.4% for those > or = 85 years old; 6.0% for those who were illiterate, 3.3% for those who attended grade-school; and 2.8% for those who finished junior-high-school. AD (22 cases, 48.9%) was the most common cause of dementia, followed by VaD (11 cases, 24.4%) and mixed dementia (MIX: 5 cases, 11.1%). Old age and being female were significant high risk factors for AD. Medical history indicated that stroke and hypertension were significant risk factors for VaD. A relatively high prevalence of dementia was observed in this study, probably because we assessed neurobehavior in great detail. Although AD was the leading cause of dementia in the present population sample. VaD and MIX also comprised an important proportion, reflecting the high prevalence of stroke in Taiwan. Older women had high risk for AD, not for VaD; and those with a history of stroke and hypertension had high risk for VaD, not for AD.
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PMID:Prevalence of dementia in an urban area in taiwan. 896 73


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