Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated plasma homocysteine (Hcy), dyslipidemia and hemorheological abnormalities all occur commonly in end-stage renal disease (ESRD) and are recognized risk factors for arteriosclerosis. To study the effect of folate supplementation on these factors we conducted a randomized controlled trial. Thirteen hemodialysis (HD) and 8 continuous ambulatory peritoneal dialysis (CAPD) patients received either 5 mg folic acid daily or placebo for 3 months. After 1 and 3 months, fasting blood samples were taken for Hcy, lipid profile, blood and plasma viscosity, red blood cell (RBC) osmotic fragility, plasma fibrinogen concentration and in vivo platelet aggregability. At baseline, the CAPD patients had a higher mean plasma fibrinogen concentration than the HD patients and they also tended to have higher mean plasma viscosity. Folate-treated patients showed marked increases in RBC folate and an average decrease in plasma Hcy concentration of 33%. Mean total cholesterol, LDL cholesterol and triglyceride concentrations decreased significantly in the CAPD patients who took folate. Folate had no significant effect on hemorheology. In conclusion, folate supplements in ESRD reduce plasma Hcy concentrations and may improve lipid profiles. In our patients, hemorheological abnormalities were more marked in patients on CAPD than in those on HD and were not improved by folate supplementation.
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PMID:A controlled trial of the effect of folate supplements on homocysteine, lipids and hemorheology in end-stage renal disease. 1086 36

The Framingham Study was initiated in 1948 to investigate an epidemic of coronary disease in the USA, using a prospective epidemiological approach. Insights were provided into the prevalence, incidence, full clinical spectrum and predisposing factors. The major "risk factors" (a term coined by the Framingham Study) for coronary disease, stroke, peripheral artery disease and heart failure were identified and clinical misconceptions dispelled about isolated systolic hypertension, left ventricular hypertrophy, dyslipidemia, atrial fibrillation and glucose intolerance. Average values for blood lipids, blood pressure, body weight, glucose and fibrinogen were shown to be dangerously suboptimal and to have a continuous graded relationship to cardiovascular disease without critical values. Dyslipidemia, glucose intolerance and elevated fibrinogen were shown to have smaller hazard ratios in the elderly, but this was offset by a higher absolute risk. Diabetes was shown to operate more strongly in women, eliminating their advantage over men. Serum total cholesterol was shown to derive its atherogenic potential from its LDL component and also to reflect cholesterol being removed in the HDL fraction. The total/HDL-cholesterol ratio was demonstrated to be the most efficient lipid profile for predicting coronary disease. LDL was shown to be correlated with hemostatic factors, suggesting that there would be additional benefits to lowering LDL. High triglyceride associated with reduced HDL, indicating insulin resistance and small dense LDL, was shown to be associated with excess coronary disease. All the risk factors tended to cluster, and this was shown to be promoted by insulin resistance induced by weight gain. Multivariate risk profiles were produced to facilitate risk stratification of candidates for coronary disease, stroke, peripheral artery disease and heart failure. The Framingham Study is now engaged in quantifying the independent contributions of homocysteine Lp(a), insulin resistance, small dense LDL, C reactive protein, clotting factors and genetic determinants of cardiovascular disease. We are now able to estimate the lifetime risk of all the atherosclerotic cardiovascular disease outcomes.
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PMID:The Framingham Study: ITS 50-year legacy and future promise. 1087 16

Patients with chronic uremia have a substantially elevated risk of death from cardiovascular disease than do the general population. Although uremic and nonuremic groups share some of the risk factors for cardiovascular mortality, such as older age, diabetes, and inflammation, other factors appear to affect cardiovascular mortality in the opposite direction. For example, being overweight and having hyperlipidemia are established risk factors in the general population, whereas lower body mass index and lower plasma cholesterol have been shown to be risk factors for cardiovascular mortality in end-stage renal disease (ESRD). This paradoxical phenomenon is explained by two facts: (1) that malnutrition is a strong predictor of cardiovascular mortality in ESRD and (2) that plasma lipid levels are lowered in malnutrition. However, it is not known whether atherosclerosis is promoted by malnutrition or by low cholesterol level. Because the cardiovascular mortality rate is theoretically the product of event rate and fatality rate after an event, risk factors for cardiovascular mortality could fall into two categories: those raising the event rate and those affecting the fatality rate. Some factors could work both ways. Patients with ESRD show a significant increase in both event rate and fatality rate. Dyslipidemia is an independent factor affecting atherosclerotic arterial wall changes and cardiovascular events in ESRD. Other factors affecting the cardiovascular event rate in ESRD include diabetes and an elevated homocysteine level. In contrast, factors associated with poor survival after an event include diabetes and anemia. Malnutrition could be a factor causing the fatality rate to rise, although there is no direct evidence supporting this possibility. Further studies are needed to show the differential effects of a risk factor on event rate and fatality rate. Patients with ESRD would have a better chance of living longer by better management of the two categories of risk factors.
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PMID:Paradox of risk factors for cardiovascular mortality in uremia: is a higher cholesterol level better for atherosclerosis in uremia? 1157 13

This review briefly summarises the scientific evidence for the child's future risk of ischemic heart diseases (IHD). The conventional risk factors such as dyslipidemia, hypertension, diabetes and smoking can not account for all the cases of cardiovascular diseases. Therefore other risk factors such as fibrinogen, homocysteine, paraoxonaze and abnormality in antioxidant defence systems are included. Among the lipids parameters the level of lipoprotein (a) and increased plasma cholesterol, specifically LDL-cholesterol may be used as a marker of family history of IHD and hypercholesterolemia. Additionally, low level of HDL-cholesterol is also related with endothelial dysfunction and increased oxidative stress. It has been hypothesised that free radicals mediate in the development of IHD and that antioxidants play a protective role in prevention of this pathology. Many of the major risk factors can be modified through diet, body mass control, exercise and (if necessary) through pharmacological intervention. Therefore, the efficacious prevention should be related with the early detection of risk factors particularly in children with familial dyslipidemia, hypertension and IHD.
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PMID:[Selected independent risk factors of atherosclerosis in children as the basis of early detection of premature ischemic heart disease]. 1157 34

Insulin resistance syndrome (IRS) is a cluster of prevalent conditions including glucose intolerance, hypertension and dyslipidemia, which commonly predispose to cardiovascular disease. However, the mechanism by which IRS is related with cardiovascular disease is not yet settled. Recently, it has been hypothesized that atherosclerosis is an inflammatory disease and that an increase in oxidative stress plays a key role in causing endothelial dysfunction associated with atherosclerosis. There has been, however, no study directly relating IRS with oxidative stress in human subjects. We measured various markers of oxidative stress among subjects who participated in a population-based epidemiological study performed in 1996. IRS was defined as non-diabetic subjects having more than two of three salient features of the syndrome (glucose intolerance, hypertriglyceridemia/low high density lipoprotein (HDL)-cholesterol and hypertension). The subjects with IRS (n=70) showed higher plasma malondialdehyde (MDA; 2.10+/-1.43 vs. 1.63+/-1.21 micromol/ml, P=0.009), homocysteine (16.32+/-8.34 vs. 13.06+/-6.49 micromol/l, P=0.002) and ceruloplasmin concentrations (29.80+/-5.28 vs. 27.39+/-5.10 mg/dl, P=0.002) than control subjects (n=196). Plasma MDA concentration was positively correlated with waist-to-hip ratio (r=0.124, P=0.044), and with plasma triglyceride (TG; r=0.163, P=0.008), ferritin (r=0.200, P=0.002) and homocysteine concentrations (r=0.136, P=0.032). These results suggest that increase in oxidative stress may contribute to the development of cardiovascular disease in IRS.
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PMID:Oxidative stress markers in Korean subjects with insulin resistance syndrome. 1173 6

The pathophysiology of coronary atherosclerosis is complex and multifactorial. The probability of the development of symptomatic coronary heart disease may be predicted by standard risk factor stratification involving hypertension, dyslipidemia, age, positive family history, and diabetes. However, risk factor stratification has been demonstrated to have significant limitations in the individual patient, which has generated a search for more specific and sensitive markers. Evidence is increasing that atherosclerosis is a disease characterized by inflammation, beginning with the earliest identifiable lesion (fatty streak) to the advanced vulnerable plaque. Clinical markers of inflammation, including C-reactive protein, modified low-density lipoprotein, homocysteine, tumor necrosis factor, and thermogenicity, have been identified as emerging risk factors that may add prognostic information in patient management. This review centers on inflammation as a potential pathogenetic factor in atherosclerosis and the role that clinical markers may play in the identification of patients at risk.
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PMID:Atherosclerosis and inflammation. 1182 71

Hypertension, dyslipidemia, impaired glucose tolerance, and obesity remain the major modifiable risk factors for most of the coronary disease afflicting the elderly. The relative risk associated with these established risk factors diminishes with advancing age, but this is offset by a greater absolute and attributable risk. Diabetes is increasing alarmingly in prevalence and operates more powerfully in women, eliminating their coronary disease resistance (relative to men). Interest in this entity now focuses on the insulin resistance syndrome promoted by abdominal obesity that has become so common in the elderly. The isolated systolic hypertension and large pulse pressure that predominate in the elderly is now recognized as a coronary disease hazard. Dyslipidemia, characterized by a high total to high-density lipoprotein cholesterol ratio, is the most predictive lipid profile for coronary disease in the elderly. High triglycerides, accompanied by low high-density lipoprotein cholesterol usually signifies insulin resistance and more atherogenic, small, dense low-density lipoprotein. Left ventricular hypertrophy is an ominous harbinger of coronary disease. Fibrinogen and the leukocyte count are correlated coronary disease risk factors that may indicate unstable lesions. Novel risk factors, such as hemostatic factors, homocysteine, lipoprotein(a), C-reactive protein, and hyperinsulinemia, are worthy of attention, but the efficacy of correcting them in the elderly has not yet been demonstrated. Nor has the efficacy of hormone replacement therapy in women. All the coronary risk factors tend to cluster, and the hazard posed by each is greatly influenced by the burden of coexisting risk factors. High-risk elderly candidates for coronary disease can be efficiently targeted for treatment by global risk assessment, using only the major established risk factors. The distinction between primary and secondary prevention in the elderly is less clear than in the middle-aged because they often have advanced presymptomatic vascular pathology that imposes a coronary event rate comparable to that of the middle-aged who have already sustained a clinical event. Declines in coronary mortality rates in the United States have included the elderly, justifying optimism about the efficacy of preventive measures. Most of the elderly have sufficient remaining life expectancy to warrant vigorous preventive management. Trials of risk factor modification in the elderly indicate that decades of exposure to modifiable risk factors can be countered by measures implemented late in life.
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PMID:Coronary heart disease risk factors in the elderly. 1187 68

To determine whether there is a correlation between fibrinolytic activity and dyslipidemia, we performed a study of 72 subjects (20 patients with hypercholesterolemia, 20 with hypertriglyceridemia, 12 with isolated low high-density lipoprotein (HDL)-cholesterol (mean age 47.7 +/- 6.3, body mass index 24.7 +/- 0.4) and 20 healthy controls. Plasminogen activator inhibitor-1 (PAI-1), tissue-plasminogen activator activity and plasmin-antiplasmin complexes (PAP) were detected at baseline and after venous occlusion test. We also measured at baseline lipidic pattern, soluble E and P selectins (sE-sel, sP-sel), prothrombin factor 1+2 (F1+2), lipoprotein(a), factor VII, plasma insulin, fibrinogen, homocysteine, and thrombin activable fibrinolysis inhibitor (TAFI) activity. Fibrinolysis was significantly reduced in hypertriglyceridemic patients compared with hypercholesterolemic patients and control subjects (PAP, p < 0.01 and p < 0.001) and was associated with increased PAI-1 (at baseline and after venous occlusion test, p < 0.001). sP-sel, F1 +2 and TAFI were not significantly different compared with controls, while hypercholesterolemic subjects showed a significant increase in these parameters (p < 0.001), which were related to decreased PAP only at the upper low-density lipoprotein (LDL)-cholesterol levels (>160 mg/dl) (p < 0.001, r = -0.76). Moreover, there was no significant difference in PAI-1 activity (at baseline and after venous occlusion test) compared with controls. In conclusion, endothelial dysfunction was the main mechanism of decreased fibrinolysis in subjects with hypertriglyceridemia and low HDL-cholesterol, while enhanced thrombin generation and TAFI activity were the main determinants in hypercholesterolemia.
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PMID:Different mechanisms of fibrinolysis impairment among dyslipidemic subjects. 1206 44

Hyperhomocysteinemia is now recognized as an independent risk factor for atherosclerotic cardiovascular disease in patients with normal renal function. Hyperhomocysteinemia is common in patients with chronic renal failure. Kidney transplant recipients have a high risk of cardiovascular death. Recently, attention has been paid to the association between homocysteine and cardiovascular disease. Dyslipidemia is also common in kidney transplant recipients. The purpose of this study was to assess whether fluvastatin in a dose of 20 mg affects homocysteine concentration in 10 stable renal transplant recipients. We evaluated Hcy, lipoprotein (a) by the use of commercially available kits as well as plasma fibrinogen and cholesterol, triglycerides and albumin levels. All the parameters were studied before and after 1, 2 and 3 months of fluvastatin treatment. Cholesterol and LDL decreased significantly as early as after 1 month and remained lowered during the therapy. No significant changes in Hcy, lipoprotein (a) and fibrinogen were found during therapy with fluvastatin. Fluvastatin is an effective hypolipemic agent and has no effect on Hcy and fibrinogen concentration in kidney transplant recipients.
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PMID:Effects of fluvastatin on homocysteine and serum lipids in kidney allograft recipients. 1222 4

Renal disease is often associated with an increased risk of vascular events. Moreover, an accelerated form of atherosclerosis commonly occurs in these patients. The reasons for these associations are not clearly defined but include the widespread presence of several established risk factors (eg, dyslipidemia, hypertension, and diabetes). Other predictors of atherosclerotic disease may also be abnormally elevated (eg, homocysteine, fibrinogen, and lipoprotein a). In addition, there is evidence that impaired renal function per se predicts vascular risk. Despite this high-risk background, the potential benefit of treatment with statins has not been widely investigated in these patients. The present review considers the evidence (experimental and clinical) that statins exert beneficial effects in patients with different types of renal disease. This includes improved renal function, decreased microalbuminuria, and a fall in blood pressure. Statins may also improve renal allograft survival. The potential mechanisms mediating these effects are considered. The interactions between statins and several risk factors that may be present in patients with impaired renal function are also considered. There is an urgent need to define the role of statins in these high-risk patients. Which is the statin of choice? This question is relevant because impaired renal function can interfere with statin pharmacokinetics. Furthermore, other drugs administered to these patients may cause serious interactions with statins.
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PMID:Statins and renal function. 1236 55


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