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

THE POSITIVE IMPACT OF TREATMENT: Antihypertensive treatments have clearly demonstrated their capacity to reduce cardiovascular mortality. The limits to the reduction in risk are imputable to insufficient early management, morbidity and poor compleance insufficiency of pharmacological treatments, absence of individualised adaptation to the causal pathology and inappropriate management of other cardiovascular risk factors. TO IMPROVE MANAGEMENT: Rather than creating more cardiovascular prevention Centres which only concern specific cases and research, it is fundamental to provide physicians, nurses and other health care workers with greater competence in hypertension and the management of cardiovascular risks. Conceptual changes are also necessary, particularly in that which concerns the end of the dichotomy between normotension and hypertension, hypercholesterolemia and normocholesterolemia and its individual and populational impact. PROMOTION OF NUTRITIONAL MEANS: Nutritional means should not be forgotten applied to accompany the whole pharmacological treatment of hypertension, they can be used for individual prevention and for reduction of the incidence of high blood pressure in the general population. NEW THERAPEUTIC STRATEGIES: Other than the search for antihypertensive drugs with greater efficacy and improved tolerance, several targets should be envisaged such as optimising the blockage of the renin-angiotensin-aldosterone system, inihibiting aldo-synthase. A CONSERVATIVE ATTITUDE: Although attractive, the individualisation of treatment based on genetic analysis will not be accessible to the majority of hypertensive patients. The attitude to be considered in 2004 consists above all in improving the use of available drugs at appropriate doses and especially in combinations at fixed-doses to allow for an easier therapeutic schedule.
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PMID:[What progress can be expected in the management of hypertension? Forecast from 1974 to 2034]. 1525 30

THREE DEFINITIONS: The metabolic or X syndrome is defined by an association of metabolic anomalies leading to an increased risk of cardiovascular complications. Today, there are at least 3 definitions of X syndrome: those of WHO, EGIR and NCEP. To varying degrees they associate increased abdominal fat, hypertension, glucose tolerance abnormality (ranging from hyperinsulinism to diabetes), and hypertriglyceridemia with low HDL cholesterol. FROM AN EPIDEMIOLOGICAL POINT OF VIEW: The prevalence of metabolic syndrome depends on the definition used and varies with the country or ethnic group considered. About 25% of the US and 10% of the French adult populations are concerned. THE RISK OF COMPLICATIONS: According to clinical trials, people with metabolic syndrome have a 2 to 4-fold increase in risk for coronary heart disease. Some of them have a particularly high risk (association of most features of the syndrome, association of an increased waist circumference and hypertriglyceridemia, presence of biological markers such as elevated C-reactive protein or microalbuminuria). Metabolic syndrome is also associated with a 4-fold increase in risk for developing diabetes.
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PMID:[Epidemiological data and screening criteria of the metabolic syndrome]. 1525 40

Our knowledge about risk factors of atherosclerosis and their associations has considerably changed and improved. The importance of type 2 diabetes and hypertension was detected earlier, hyperlipidemia and dyslipidemia (disturbance of lipoprotein composition) have been recently implemented. We have learnt that the android obesity form and especially visceral fat serve as central trigger-factor of the resulting "metabolic syndrome" and other related disturbances like acute phase proteins, inflammation markers and procoagulatory state. Altogether atherothrombotic events are increased and result in clinically relevant macrovascular disease (myocardial infarction, cerebrovascular und peripheral arterial disease), blood glucose itself causing additionally microvascular disease. The newest comprehensive guidelines of European Associations try to use most of the known factors for treatment guidelines but will fail due to the fact that they cannot be easily used in clinical practice. In additon, visceral fat, that central factor, and body fat mass have not been integrated. We suggest that the risk should be evaluated in the context of body mass index (BMI) and especially of waist circumference which could be THE central intervention factor in the treatment of our patients.
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PMID:[Metabolic syndrome--a high cardiovascular risk?]. 1551 78

In mineralocorticoid target tissues such as the cortical collecting duct in the kidney, the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) is responsible for the peripheral inactivation of cortisol to cortisone, thereby protecting the mineralocorticoid receptor from inappropriate activation by cortisol. Mutations in the HSD11B2 gene cause the syndrome of apparent mineralocorticoid excess, an autosomal recessive form of inherited hypertension in which cortisol acts as a potent mineralocorticoid. Herein are described six new families with mutations in the HSD11B2 gene causing hypokalemic hypertension, with low plasma aldosterone and low renin levels in affected individuals, indicating mineralocorticoid hypertension. Profiling of urinary steroid metabolites showed decreased cortisol inactivation, with urinary tetrahydrocortisol and tetrahydrocortisone ratio (THF + 5alphaTHF)/THE ranging 2.4 to 40 and nearly absent urinary free cortisone in all but one case. Genetic analysis of the HSD11B2 gene from these patients with apparent mineralocorticoid excess revealed distinct homozygous point mutations in four families, a compound heterozygous mutation in one family, and a large 23-bp exonic insert with frameshift and disruption of the amino acid sequence in another family. Expression studies of mutants that were expressed in HEK-293 cells showed marked reduction or abolition of 11betaHSD2 enzymatic activity. These cases are reviewed along with previous ones from the authors' extensive personal experience to highlight the importance of 11betaHSD2 in the understanding of a new biologic principle in hormone action, demonstrating that local metabolism of the glucocorticoid hormones into inactive derivatives by the enzyme 11betaHSD2 is one of the mechanisms that intervene to allow specific aldosterone regulatory effects.
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PMID:Apparent mineralocorticoid excess: report of six new cases and extensive personal experience. 1703 6

This report concerns a case of cortisol-producing adrenocortical adenoma without the phenotype of Cushing's syndrome. A left adrenal tumor was incidentally detected in this patient. A diagnosis of adrenal Cushing's syndrome was based on the results of endocrinological and radiological examinations, although she showed none of the physical signs of Cushing's syndrome, glucose intolerance, hypertension or dyslipidermia. After a successful laparoscopic left adrenalectomy, the pathological diagnosis was adrenocortical adenoma. Slow tapering of glucocorticoids was needed to prevent adrenal insufficiency after surgery, and the plasma ACTH level remained high even though the serum cortisol level had reached the upper limit of the normal range. Further examination showed a urinary THF + allo-THF/THE ratio of 0.63, which was lower than that of control (0.90 +/- 0.13, mean +/- SD). Serum cortisol/cortisone ratios after the cortisone acetate administration were also decreased, and the serum half-life of cortisol was shorter than the normal range which has been reported. These findings indicated a partial defect in 11beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1) activity, which converts cortisone to cortisol. Our case suggests that a change in 11beta-HSD1 activity results in inter-individual differences in glucocorticoid efficacy.
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PMID:A case of cortisol producing adrenal adenoma without phenotype of Cushing's syndrome due to impaired 11beta-hydroxysteroid dehydrogenase 1 activity. 1849 11

IT IS POSSIBLE TO PREDICT THE POPULATION AT RISK FOR ATHEROTHROMBOTIC DISEASE (ATD) WITH HIGH ACCURACY USING ONLY THREE RISK FACTORS: dyslipidemia, cigarette smoking and hypertension. Using a global risk factor graph with the cholesterol retention fraction (CRF, or [low-density lipoprotein cholesterol - high-density lipoprotein cholesterol]/low-density lipoprotein cholesterol) on the vertical axis and systolic blood pressure (SBP) on the horizontal axis, a threshold line can be drawn using CRF-SBP plots (0.74, 100) and (0.49, 140). Eighty-five per cent of all ATD patients in the Bowling Green Study database were observed to lie above this threshold line. Of the 15% of ATD patients with CRF-SBP plots below the threshold line, most were cigarette smokers, leaving only 6% of patients with ATD in the Bowling Green Study database whose risk for ATD could not be predicted by CRF-SBP plot position above the threshold line and/or cigarette smoking status.
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PMID:Prediction of the population at risk for atherothrombotic disease. 1964 14

THE EFFECT OF AN ABNORMAL RENAL CIRCULATION AND A RESULTING HYPERTENSION ON THE DISTRIBUTION OF WATER AND ELECTROLYTES IN SKELETAL MUSCLE OF DOGS WAS AS FOLLOWS: (1) By analysis of the muscle the total content of sodium and chloride was found increased and the total potassium content decreased. (2) A redistribution of water occurred in the muscle involving a shift of water from the muscle cells to the extracellular phase. The calculated mean values per kilo of muscle were, extracellular phase (F) = 254, +/- 54 gm.; intracellular water (H(2)O)(C) = 532, +/- 47 gm., and total solids (S) = 214, +/- 8 gm. This extracellular phase volume of 254 gm. represents an increase of 65 per cent over that found in normal dog muscle. After subjecting the hypertensive dogs to large increases in total body water produced by the intravenous injection of normal isotonic salt solution, the total bulk of 1 kilo of muscle increased a mean average of 103 gm. of which one half was attributed to the extracellular phase and the other half to the swelling of the muscle cells. Whether the changes found in this study are the result of the functional disturbances caused by the experimental renal abnormalities, or the hypertension, or a combination of both is uncertain at this time. The significance of the results is that there is quantitative evidence that a redistribution of water has occurred in skeletal muscle so that a real extracellular edema exists.
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PMID:THE DISTRIBUTION OF WATER AND ELECTROLYTES BETWEEN BLOOD AND SKELETAL MUSCLE IN EXPERIMENTAL HYPERTENSION. 1987 Dec 77

11Beta-hydroxysteroid dehydrogenase isoform 2 (11beta-HSD2) is responsible for conversion of cortisol (F) to inactive cortisone (E). Disturbance of its activity can cause hypertension. To estimate 11beta-HSD2 activity, besides F and E, their tetrahydro- (THF, THE) as well allo-tetrahydro- (allo-THF, allo-THE) metabolites should be determined. This study describes HPLC-FLD method for the quantitative determination of endogenous glucocorticoids (GCs) in plasma and urine (total and free) and their metabolites in urine. Following extraction at pH 7.4 using dichloromethane, GCs (F, E, THF, allo-THF, THE, allo-THE and internal standard--prednisolone) were derivatized with 9-anthroyl nitrile and purified by SPE using C(18) cartridges. The enzymatic hydrolysis of conjugated steroids was provided using beta-glucuronidase. The influence of organic bases on 9-AN derivatization of steroids was investigated. The best yield of the derivatization was obtained in presence of the mixture of 10.0% triethylamine (TEA) and 0.1% quinuclidine (Q). Chromatographic separation was accomplished in the Chromolith RP-18e monolithic column. The elaborated method was validated. Calibration curves were linear in the ranges: for F, E and THF 5.0-1000.0 ng mL(-1), for allo-THF and THE + allo-THE 10.0-1000.0 ng mL(-1). LOD (S/N=3:1) for all analytes amounted 3.0 ng mL(-1). Recoveries of GCs exceeded 90%. The method was precise and accurate, intra- and inter-day precision were 3.0-12.1% and 9.2-14.0%, respectively. Accuracy ranged from 0.2 to 15.1%. The method was applied for estimating endogenous GCs in plasma and urine. Plasma levels of F and E were in the ranges: 133.0-174.5 ng mL(-1) and 17.4-35.9 ng mL(-1), respectively. Free urinary steroids were in the ranges: 12.0-54.1 microg/24 h (UFF) and 37.8-76.2 microg/24 h (UFE). The ratio of (THF + allo-THF)/(THE + allo-THE) amounted from 1.01 to 1.23. The obtained results confirmed utility of the elaborated method in the assessment of 11beta-HSD2 activity in man.
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PMID:HPLC method for determination of fluorescence derivatives of cortisol, cortisone and their tetrahydro- and allo-tetrahydro-metabolites in biological fluids. 2001 71

BACKGROUND: We present the case of a 64-year-old patient who presented to his primary care physician with fatigue, worsening shortness of breath, abdominal discomfort and a rapidly growing abdominal girth, although he had lost 5 kg of weight within 3 months. He had a history of untreated hypertension, compensated renal insufficiency and COPD. Despite weight loss and fatigue, the patient did not experience any other constitutional symptoms such as fever, night sweats or loss of appetite. Investigations: Physical examination, blood tests, CT scan of the abdomen, MRI scan of the abdomen, fine needle biopsy, excisional biopsy, Video Capsule Endoscopy, histology, PET scan. Diagnosis: Inflammatory myofibroblastic tumor, chylous ascites, chyloperitoneum. Management: Systemic chemotherapy, total parenteral nutrition and octreotide therapy. CONCLUSION: WE DESCRIBE THE CASE OF A PATIENT IN WHOM TWO EXTREMELY RARE PHENOMENA ARE PRESENT IN COMBINATION: the diagnosis of an inflammatory myofibroblastic tumor and chylous ascites. While the tumor could be stabilized by different regimens of chemotherapy, the chyloperitoneum was treated with parenteral nutrition and subcutaneous octreotide injections, which resulted in a significant reduction of the amount of chylous ascites drained during regular paracentesis.
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PMID:Chylous Ascites in a Patient with Inflammatory Myofibroblastic Tumor. 2074 Jan 78

THE DEVELOPMENT OF HYPERTENSION CAN BE PREDICTED BY SUCH FACTORS AS: age, salt, alcohol and fiber intake, obesity, physical activity, psychosocial factors, and family history of hypertension or premature cardiovascular disease. Blood pressure response to stressful stimuli is also an important predictor. Research should focus on better assessment and management of predictors including psychosocial factors which increase blood pressure, and personality characteristics that increase sensitivity to stressful stimuli. Since inheritance of blood pressure may be considerable, detecting a hypertensive patient should stimulate the family physician to measure blood pressure of other family members. Future management of hypertension may involve increased public health activity to improve detection, education and management in the community while more efficient office management integrates the patient into the decision making process.
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PMID:Predicting and preventing hypertension and associated cardiovascular disease. 2127 10


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