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

Monocyte chemotactic peptide-1 (MCP-1) plays a key role as a mediator of inflammatory infiltration, mainly composed with macrophages. Experimental studies showed that macrophages and their products are pathogenetic factors of chronic renal graft rejection (ch.g.r.). The objective of the present study was to determine the role of MCP-1 in the pathogenesis of human renal ch.g.r. Examined were 34 patients with ch.g.r. (Group I), 50 patients with a stable allograft function (Group II), and 25 healthy subjects (control). Serum and urine levels of MCP-1 were measured by ELISA. The serum level of MCP-1 was found to be higher in transplant patients, than in control group, but this difference was not significant. The serum level of MCP-1 showed a correlation with concentration of triglycerides in both transplant patient groups. This may results from overproduction of MCP-1 through cells of vascular wall affected by hyperlipidemic microenvironment. Considering the lack of relationship between the serum and urine levels of MCP-1, I decided attribute the urine levels of MCP-1 to the secretion through the infiltrating cells and through the kidney cells. In patients with ch.g.r. the urine levels of MCP-1 were significantly higher p < 0.001) than in patients with a stable graft function and control group. MCP-1 levels were particularly high (> 2000 pg/mg creatinine) in patients with enhanced dynamics of ch.g.r. The MCP-1 levels were higher in those patients whose biopsies described cellular infiltration (1385 + 820 pg/mg creatinine vs 680 + 280 pg/mg creatinine). The urine level of MCP-1 showed a correlation with concentration of serum creatinine, cholesterol, level of proteinuria and with arterial pressure in ch.g.r. patients. Increased urine levels of MCP-1 and correlation of MCP-1 with the activity of progressive deterioration of the graft function suggest important role of this chemokine in the pathogenesis of ch.g.r., possibly by activating macrophages and by stimulating their influx into the vascular wall, glomeruli and interstitial tissue. Relationship of urinary MCP-1 excretion with arterial hypertension and lipid disorder suggest that the effect of those risk factors for a progressive deterioration of graft function manifest on the molecular level by affecting the generation of MCP-1.
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PMID:[The role of monocyte chemotactic peptide (MCP-1) in chronic renal allograft rejection]. 976 Aug 14

The clinical outcome of long-term renal allograft recipients in the Chinese population has not been reported previously. We analysed patients from the pre-cyclosporin era who had grafts that functioned for > 10 years. Forty-five patients (31 men, 14 women; mean age 30, follow-up duration 13.3 years), representing a 10-year graft survival of 53%, were included. Thirty-six patients (80%) received living-related allografts and 9 (20%) received cadaveric or living-unrelated renal transplantation. The mean serum creatinine at last follow-up was 1.36 mg/dl (range, 0.83-4.08). Major posttransplantation complications included: hypertension in 25 (56%), infection in 16 (36%), acute rejection in 15 (33%), lipid disorder in 13 (29%), liver disease in 7 (16%), osteonecrosis in 5 (11%), malignancy in 4 (9%), coronary artery disease in 3 (7%), and diabetes mellitus in 3 (7%). Five grafts were lost: 3 to chronic rejection, and 2 to patients with stable function who died of non-renal causes. Proteinuria correlated strongly with graft function and survival, and marginally with hypertension. In hepatitis B carriers, serum alpha-feto protein is useful in the early detection of hepatocellular carcinoma. We conclude that while patients in the pre-cyclosporin era can survive with excellent graft function beyond the first decade, the risk of complications leading to significant morbidity still remains even when patients are receiving minimal doses of immunosuppression in the second decade.
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PMID:Long-term renal allograft recipients from South-east Asia in the pre-cyclosporin era. 1035 40

A fructose-enriched diet promotes hypertension in rats. We thought that an enhancement of the glycolytic and/or lipid disorder (s) that raise blood pressure could be the cause. Therefore, we studied 4 groups of Sprague-Dawley rats (+/-200 g): (1) control rats received a standard diet and tap water; (2) the glycerol group of rats received a standard diet and 0.54 mol/L glycerol in tap water; (3) the fructose group was given a fructose-enhanced diet (chow had 55% fructose instead of dextrin) and tap water; and (4) the fructose-glycerol group was given the fructose-enhanced diet and 0. 54 mol/L glycerol in drinking water. At the end of the second week, the findings were as follows. Blood pressure was 149+/-2 mm Hg in the fructose-glycerol group versus 129+/-2 (P<0.001), 131+/-2 (P<0. 001), and 140+/-3 (P<0.005) mm Hg in the control, glycerol, and fructose groups, respectively. Insulinemia was higher in the fructose-glycerol group than the control (P<0.001), glycerol (P<0. 001), and fructose groups (P<0.001); triglyceridemia was higher in the fructose-glycerol (P<0.02), fructose (P<0.05), and glycerol groups (P<0.02) than the control group. Thoracic aorta rings showed a lower ED(50) to 12,13-phorbol dibutyrate in the fructose-glycerol group than in the control (P<0.001), glycerol (P<0.002), and fructose groups (P<0.001). In conclusion, glycerol-fructose administration resulted in hypertriglyceridemia, hyperinsulinemia, and increased vascular sensitivity to 12,13-phorbol dibutyrate (with respect to the control group), and significantly greater expression of protein kinase C alpha and betaII (with respect to the glycerol group).
Hypertension 1999 Oct
PMID:Potential role of glycerol leading to rat fructose hypertension. 1052 99

Lipid metabolism disorders were proposed to mediate numerous cell membrane alterations in various forms of hypertension. Elevated plasma triglycerides were found to be associated with changes in membrane structure and function related to altered microviscosity in particular domains of the cell membrane. The aim of our study was to determine if an abnormal triglyceride metabolism might play a causal role in these alterations of membrane dynamics. Using genetically hypertensive rats of the Prague hereditary hypertriglyceridemic (HTG) strain we investigated whether the elevation of circulating triglycerides induced by high fructose intake and/or their lowering by chronic gemfibrozil treatment (for 10 weeks starting at the age of 6 weeks) are followed by reciprocal changes in membrane microviscosity. Two different fluorescent probes exploring either the outer membrane leaflet (TMA-DPH anisotropy) or the membrane lipid core (DPH anisotropy) were used in platelets of HTG rats. DPH (diphenylhexatriene) fluorescence anisotropy was decreased in platelets of fructose-treated HTG animals with highly elevated plasma triglyceride levels, whereas it was increased in gemfibrozil-treated HTG rats in which triglyceride levels were almost normalized. On the contrary, TMA-DPH (trimethylamino-diphenylhexatriene) anisotropy was not substantially altered in platelets from HTG rats by the above modifications of circulating triglycerides. No changes of plasma cholesterol or blood pressure were associated with the triglyceride-dependent modifications of membrane core microviscosity. Our interventional study demonstrates a major causal role of circulating triglycerides in the control of the microviscosity of membrane lipid core.
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PMID:Chronic changes in plasma triglyceride levels do modify platelet membrane microviscosity in rats. 1094 55

Genes contributing to common forms of hypertension are largely unknown. A number of studies in humans and in animal models have revealed associations between insulin resistance, dyslipidemia, and elevated hypertension. To identify genes contributing to blood pressure (BP) variation associated with insulin-resistant dyslipidemia, we conducted a genome-wide scan for BP in a set of 18 Dutch families exhibiting the common lipid disorder familial combined hyperlipidemia. Our results reveal a locus on chromosome 4 that exhibits a significant lod score of 3.9 with systolic BP. In addition, this locus also appears to influence plasma free fatty acid levels (lod=2.4). After adjustment for age and gender, the lod score for systolic BP increased to 4.6, whereas the lod score for free fatty acid levels did not change. The chromosome 4 locus contains an attractive candidate gene, alpha-adducin, which has been associated with altered BP in animal studies and in some human populations. However, we found no evidence for an association between 2 intragenic alpha-adducin polymorphisms and systolic BP in this sample. We also observed suggestive evidence for linkage (lod=1.8) of diastolic BP to the lipoprotein lipase gene locus on chromosome 8p, supporting a finding previously observed in a separate insulin-resistant population. In addition, we also obtained suggestive evidence for linkage of systolic BP (lod=2.4) and plasma apolipoprotein B levels (lod=2.0) to a locus on proximal chromosome 19p. In conclusion, our genome scan results support the existence of multiple genetic factors that can influence both BP and plasma lipid parameters.
Hypertension 2001 Oct
PMID:Genome scan for blood pressure in Dutch dyslipidemic families reveals linkage to a locus on chromosome 4p. 1164 Dec 85

Several studies have reported the penetration and impact of national and international recommendations on the management of dyslipidaemia, a major cardiovascular risk factor. Most of them were carried out on patients participating in clinical trials or on in-hospital cases. The PRAGMA study was developed in order to evaluate management of this condition in general practice, at the heart of the health care system. From September to December 1998, 1,717 general practitioners were chosen randomly and included 6,623 patients considered to have a lipid disorder. In this sample, the prevalence of the main risk factors was as follows: hypertension: 39.6%, diabetes: 11.6%, obesity: 19.6%, past or present smokers: 33.8%. The main lines of management consisted in prescribing lipid lowering drugs (96.6%) with dietary recommendations (95.8%) and a fall lipid profile (59.9%). The main factors spontaneously cited by the general practitioners as being decisional were: the total cholesterol level (47.8%), diet (40.8%), body weight (29.4%) and drug therapy (19.2%). The cardiovascular risk factors were rarely taken into account in their totality. These results suggest that the management of dyslipidaemia patients by general practitioners is far from being optimal. Efforts should be made to change attitudes to take into consideration the global cardiovascular risk factors of patients with lipid disorders.
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PMID:[Management of dyslipidemias diagnosed in general practice in France--The PRAGMA Study]. 1172 9

Hyperlipidemia is now established as a major risk factor for causation of coronary heart disease (CHD) in adults; however, there is much debate on the level of coronary risk at which lipid-lowering drugs should be used. These issues of possible harm or lack of benefit from long-term use of lipid-lowering therapy, and cost effectiveness, are also pertinent in the pediatric setting. Evidence from several countries indicates that children have an increasing prevalence of obesity, hyperlipidemia and type 2 diabetes mellitus. Children who have high serum lipids 'track' these increased levels into adulthood. In some countries there is a trend to screen children for hypercholesterolemia. Family history itself is a poor discriminator in determining which children need to be screened and treated. Estimation of apolipoprotein B and/or apolipoprotein E genotype can improve prediction. Measuring high density lipoprotein cholesterol also helps, but obesity appears to be the best marker for screening children at high risk. These considerations should not cloud the need for case finding and treatment of children with genetic disorders. Low fat diets have been shown to be well tolerated and effective in children; however, there are no major long-term studies demonstrating harm or benefit in those on lipid-lowering drugs. Nevertheless, concerns regarding the psychological effect and the theoretical metabolic effects of long-term lipid lowering remain. Lipid-lowering drugs should be generally restricted to children with genetic disorders of lipid metabolism. Children with diabetes mellitus, hypertension or nonlipid-related inherited disorders leading to premature CHD in adults should be treated with diet, and with lipid-lowering drugs when they reach adulthood. Children with secondary hyperlipidemia should be assessed individually. A number of drugs and nutriceuticals are available for use in children, but only a few drugs are licensed for use in children.
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PMID:Should pediatric patients with hyperlipidemia receive drug therapy? 1196 May 11

John Guillebaud, medical director of the Margaret Pyke Family Planning Center in London, and Andrew Kaunitz, MD, professor and assistant chair of obstetrics and gynecology at the University of Florida Health Sciences Center in Jacksonville, make recommendations on how clinicians should prescribe desogestrel-containing oral contraceptives (OC) amid new data which indicate that the risk for venous thromboembolism (VTE) for such OCs may be lower than first reported. John Guillebaud notes that in the UK, young women with no risk factors are typically started on second-generation OCs because some of these clients may be predisposed for VTE. Patients with a VTE risk factor, such as obesity or severe varicose veins, should be taking second-generation OCs. Patients with an arterial risk factor, such as being a heavy smoker, diabetic, having lipid disorder, or high blood pressure should be encouraged to consider switching to third-generation pills as they near age 30 years. Dr. Kaunitz recommends that current users of desogestrel OCs who are doing well remain with their current OC. For clinicians who prefer to start first-time OC users on new progestin OCs and who believe that vascular disease risks may be higher with desogestrel pills, clients should be started on norgestimate-containing OCs. Other clinicians can choose to use desogestrel-containing OCs in first-time clients.
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PMID:2 methods for prescribing third-generation OCs. 1234 20

This study was done to establish the relationship between disorders of lipid metabolism and risk factors of ischemic cerebrovascular stroke, search for correlations between disorders of lipid metabolism and severity of ischemic stroke, and assess the association between fibrinogen levels in serum and risk factors in patients suffering from different types of ischemic stroke. Altogether, 117 patients were enrolled, including 76 males and 41 females aged 20 to 55 years (mean--45.3 years). The patients were divided into three groups depending on the dynamics of neurological symptoms: (1) transient ischemic attacks (TIA); (2) reversible ischemic neurologic deficit (RIND); (3) completed stroke (CS). The diagnosis was based on history-taking, physical examination, laboratory tests and neuro-imaging studies. The tests included a complete blood count, glucose, glucose tolerance, 24-hour glucose profile, coagulation profile, fibrinogen, total cholesterol, triglycerides, HDL and LDL cholesterol fractions, and beta-lipoproteins. Blood was collected on the first day of hospitalization prior to any medication. An ECG, CT, and Doppler USG of carotid vessels were done. Cardiac etiology of stroke was ruled out with Holter ECG and echocardiography. The results were subjected to statistical analysis with Yule's coefficient for two qualitative variables. Lipid disorders usually co-existed with obesity, fat-rich diets and sedentary lifestyle in all ischemic stroke types studied. They were accompanied by elevated blood pressures in every type of stroke and by diabetes in TIA. Lipid disorders were found to co-exist with other risk factors for ischemic stroke predominantly in female patients, while in male patients these disorders were an independent risk factor for ischemic stroke. The extent of lipid disorders correlated with the severity of ischemic stroke. Elevated levels of fibrinogen in serum were detected in female patients in every type of stroke. In male patients, elevated fibrinogen was found only in TIA and co-existed with high blood pressure, diabetes and obesity.
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PMID:[Metabolic disturbances and prognosis in ischemic cerebrovascular stroke in patients up to 55 years of age]. 1460 83

The National Cholesterol Education Program Adult Treatment Panel III has provided a clinical definition for the metabolic syndrome that is practical for use in an office setting. Identification and treatment of the metabolic syndrome is of enormous public health importance because it is associated with a marked elevation in coronary heart disease risk and affects nearly 25% of adults in the United States. First-line therapy is lifestyle modification, which includes body weight reduction, increased physical activity, and moderation of the dietary glycemic load. Drug treatments focusing on the major components of the syndrome (atherogenic dyslipidemia, hypertension, and a prothrombotic state) have demonstrated efficacy for reducing coronary heart disease events. Fibrates seem to be particularly effective in patients for whom a disturbance of the triglyceride-high-density lipoprotein axis is the primary lipid disorder. Fibrates also appear to influence a number of emerging risk factors, including hemostatic and inflammatory markers and indicators of improved vascular wall biology, which may contribute to their cardioprotective effects.
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PMID:Fibrates for treatment of the metabolic syndrome. 1466 7


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