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)

Stroke represents a major health burden in our country. Ischaemic stroke has got several risk factors associated with increased chance of atherosclerosis. A small hospital-based study was done to look into the risk factors associated with ischaemic stroke. Forty patients with CT-confirmed cerebral infarction were taken for the study and detailed history and clinical findings were obtained. Investigations like complete haemogram, fasting blood glucose, urea, creatinine, lipid profile, serum Lp(a), homocysteine, fibrinogen, ECG, chest x-ray, echocardiography, MRI/MRA where indicated, were done to identify the risk factors as well. Results indicated that hypertension was the most prevalent (87.5%) risk factor followed by ischaemic heart disease (35%) and diabetes. Dyslipidaemia was also found in a significant number of cases, mostly elevated LDL, low HDL and elevated Lp(a). Fibrinogen and homocysteine were of less significance.
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PMID:Risk factor analysis in ischaemic stroke: a hospital-based study. 1657 Jul 59

Dyslipidemia is a potent cardiovascular (CV) risk factor in the general population. Elevated low-density lipoprotein cholesterol (LDL-C) and/or low high-density lipoprotein (HDL-C) are well-established CV risk factors, but more precise determinants of risk include increased apoprotein B (ApoB), lipoprotein(a) [Lp(a)], intermediate and very low-density lipoprotein (IDL-C, VLDL-C; "remnant particles"), and small dense LDL particles. Lipoprotein metabolism is altered in association with declining glomerular filtration rate such that patients with non dialysis-dependent chronic kidney disease (CKD) have lower levels of HDL-C, higher triglyceride, ApoB, remnant IDL-C, remnant VLDL-C, and Lp(a), and a greater proportion of oxidized LDL-C. Similar abnormalities are prevalent in hemodialysis (HD) patients, who often manifest proatherogenic changes in LDL-C in the absence of increased levels. Patients treated with peritoneal dialysis (PD) have a similar but more severe dyslipidemia compared to HD patients due to stimulation of hepatic lipoprotein synthesis by glucose absorption from dialysate, increased insulin levels, and selective protein loss in the dialysate analogous to the nephrotic syndrome. In the dialysis-dependent CKD population, total cholesterol is directly associated with increased mortality after controlling for the presence of malnutrition-inflammation. Treatment with statins reduces CV mortality in the general population by approximately one third, irrespective of baseline LDL-C or prior CV events. Statins have similar, if not greater, efficacy in altering the lipid profile in patients with dialysis-dependent CKD (HD and PD) compared to those with normal renal function, and are well tolerated in CKD patients at moderate doses (<or=20 mg/day atorvastatin or simvastatin). Statins reduce C-reactive protein as well as lipid moieties such as ApoB, remnants IDL and VLDL-C, and oxidized and small dense LDL-C fraction. Large observational studies demonstrate that statin treatment is independently associated with a 30%-50% mortality reduction in patients with dialysis-dependent CKD (similar between HD- and PD-treated patients). One recent randomized controlled trial evaluated the ability of statin treatment to reduce mortality in type II diabetics treated with HD ("4D"); the primary end point of death from cardiac cause, myocardial infarction, and stroke was not significantly reduced. However, results of this trial may not apply to other end-stage renal disease populations. Two ongoing randomized controlled trials (SHARP and AURORA) are underway evaluating the effect of statins on CV events and death in patients with CKD (including patients treated with HD and PD). Recruitment to future trials should be given a high priority by nephrologists and, until more data are available, consideration should be given to following published guidelines for the treatment of dyslipidemia in CKD. Additional consideration could be given to treating all dialysis patients felt to be at risk of CV disease (irrespective of cholesterol level), given the safety and potential efficacy of statins. This is especially relevant in patients treated with PD, given their more atherogenic lipid profile and the lack of randomized controlled trials in this population.
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PMID:Statins for treatment of dyslipidemia in chronic kidney disease. 1729 64

Hyperlipidemia (HLP), a common complication, is very prevalent in children with primary nephrotic syndrome (PNS). HLP not only significantly increases the cardiovascular risk in adulthood, but also accelerates the progression of renal disease. Proteinuria as the most important pathophysiological change can reduce serum colloid osmotic pressure, which leads to an increase in the synthesis of serum proteins including lipoproteins in the liver for export to the serum. Thus, the severity of lipid abnormalities may correlate with the degree of proteinuria. A total of 378 children with PNS were divided into three groups according to their urinary protein excretion (UPE), group A (50 mg/kg/d < or = proteinuria <100 mg/kg/d, 125 cases), group B (100 mg/kg/d < or = proteinuria <200 mg/kg/d, 132 cases) and group C (proteinuria > or =200 mg/kg/d, 121 cases). In addition, 200 healthy volunteers with neither allergic nor renal disease between 3 and 14 years of age were recruited as the control group. Fasting serum levels of lipoprotein (a) [Lp(a)], total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (apoA1), apoB, and albumin (Alb) were measured. Serum low density lipoprotein cholesterol (LDL-C) was calculated by the Friedewald formula. As expected, when all patients were compared with healthy children in this study, UPE and the serum concentrations of Lp(a), TC, TG, HDL-C, LDL-C, and apoB were higher in the PNS than in the control group (p<0.01), whereas for apoA1/B ratio the opposite was observed (p<0.01). Furthermore, patients in group C exhibited significantly higher Lp(a), TC, TG, LDL-C, and apoB concentrations than those in group A or B (p<0.01), whereas for apoA1/B ratio the opposite was found (p<0.01). The increase in serum lipids was accompanied by a significant augmented UPE in all patients (p<0.05). More specifically, positive correlations were observed between serum levels of TC (r=+0.80, p<0.01), HDL (r=+0.49, p<0.01), LDL (r=+0.79, p<0.01), ApoB (r=+0.62, p<0.01) and log proteinuria in group B; additionally, a negative correlation was observed between apoA1/B ratio and log proteinuria in group B (r=-0.38, p<0.01). However, no correlation of serum lipid profiles with UPE was determined in group A and C, respectively (p>0.05). Serum Alb was negatively correlated with Lp(a) (r=-0.96, p<0.01), TC (r=-0.78, p<0.01), TG (r=-0.78, p<0.01), LDL-C (r=-0.88, p<0.01), apoA1 (r=-0.26, p<0.01), and apoB (r=-0.71, p<0.01), while positively correlated with apoA1/B (r=+0.27, p<0.01) in all nephrotic children. Furthermore, no correlation existed between serum lipid profiles and Alb in group A, B and C, respectively (p>0.05). In Conclusion, secondary dyslipidemia in children with PNS is in parallel with the degree of UPE. There are diverse characteristics of lipid metabolism under different UPE. As for the patients with medium-UPE, positive correlation between serum lipids and proteinuria is presented.
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PMID:Characteristics of lipid metabolism under different urinary protein excretion in children with primary nephrotic syndrome. 1946 31

Although high serum total cholesterol and LDL cholesterol levels are predictive of cardiovascular diseases in the general population, this association is more complex in the dialysis patients. Two recent randomized trials failed to show significant beneficial effects of statins on the primary cardiovascular outcomes in these patients. The reasons for this lack of benefits are unclear. The postulates include the possibilities that LDL cholesterol is not important in atherogenesis and that atherosclerosis is not a major contributor to cardiovascular diseases in the dialysis population. It is important to note that high serum LDL cholesterol level is not a prominent feature of uremic dyslipidemia. Instead, the hallmark dyslipidemias in the dialysis population are hypertriglyceridemia as a result of the accumulation of lipoprotein remnant particles, low serum HDL cholesterol levels, high serum levels of lipoprotein(a) [Lp(a)], and the modification of LDL cholesterol by oxidation and carbamylation. In vitro and epidemiologic studies have further suggested that these abnormal lipoproteins or aberrant serum lipoprotein levels are atherogenic. More research efforts should be directed toward these dyslipidemic states and the multitude of other putative cardiovascular risk factors in dialysis patients.
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PMID:Is lipid control necessary in hemodialysis patients? 1999 12

Niacin has profound and unique effects on lipid metabolism. In addition to increasing high-density lipoprotein cholesterol, it is also known to decrease total cholesterol, low-density lipoprotein cholesterol, and triglyceride. Interestingly, the plasma concentration of lipoprotein(a) [Lp(a)], which has been suggested to play a role as an independent risk factor for coronary heart disease, is also decreased by niacin. Therefore, it is not surprising that in the literature it was given unique description as broad-spectrum lipid drug. Its impact is referred to as desirable normalization of a range of cardiovascular risk factors. However, its clinical use is limited due to harmless but unpleasant unique side effect of cutaneous flushing. Interestingly, recent experimental and clinical studies suggest the potential benefit of niacin as a treatment of dyslipidemia and high plasma phosphate associated with chronic kidney disease (CKD). Both dyslipidemia and high serum phosphate levels are shown to be associated with higher cardiovascular mortality. Furthermore, niacin administration improves renal tissue lipid metabolism, renal function and structure, hypertension, proteinuria, and histological tubulointerstitial injury. Further studies are required before the use of niacin for the treatment of both dyslipidemia and hyperphosphatemia with CKD advocated.
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PMID:Niacin as potential treatment for dyslipidemia and hyperphosphatemia associated with chronic renal failure: the need for clinical trials. 2048 51

Cardiovascular diseases remain the most important cause of death worldwide. The situation in the Czech Republic is one of the best when compared to the other countries of the former socialist block; on the other hand, we significantly lack behind when the comparison is made to south and southwest European countries. The concept of risk factors (RF) and multifactorial character of atherosclerosis as the main cause of cardiovascular diseases (CVD) is fully accepted at present. Hyperlipoproteinaemia (HLP) and dyslipidemia (DLP) are a group of high incidence metabolic diseases characterised by increased levels of lipids and lipoproteins in plasma or, in case of DLP, by unsuitable, atherogenic composition of lipids and lipoproteins in plasma. HLP and DLP are among the most important RF for the development of CVD. Mainly LDL-cholesterol (LDL-C) is perceived as a very important risk factor; successful reduction of LDL-C is linked to a reduction in cardiovascular risk. Even when LDL-C is decreased and the so-called "target values" achieved, patients are still at risk ofa CV event. This remnant risk is the so called "residual risk". The most important "rival" to LDL-cholesterol among the risk factors is the metabolic syndrome, or rather the DLP associated with the metabolic syndrome, characterised from the perspective of DLP by low levels of HDL-cholesterol and increased triglycerides with concurrent occurrence of "small dense LDL". The issue of heterogeneity and atherogenicity oflipoprotein particles in general then becomes topical. Lipoprotein (a)--Lp(a) is another important lipid risk factor that is getting a significant attention.
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PMID:[Hyperlipoproteinaemia and dyslipoproteinaemia I. Classification, diagnostics, cardiovascular, cardiometabolic and residual risk]. 2068 65

Women with diabetes are faced with a higher risk of dyslipidemia and cardiovascular disorders than men with diabetes. We aimed to study the role of gender and menopausal status in serum Lp(a) levels in patients with type 2 diabetes. We quantified serum Lp(a) levels in a group of 477 patients with type 2 diabetes (men, premenopausal and postmenopausal women with diabetes), as well as in 105 controls. We stratified the patients into two groups of low Lp(a) levels (Lp(a) <35 mg/dl) and elevated Lp(a) levels (Lp(a) >35 mg/dl). Patients with diabetes had higher serum Lp(a) levels than the controls. Serum Lp(a) levels was significantly higher in women with diabetes than men with diabetes. Lp(a) levels did not differ between male and females in the control group. Premenopausal and postmenopausal women with diabetes did not differ significantly in serum Lp(a) levels. The odds ratio of having a serum Lp(a) level higher than 35 was 5.85 in premenopausal women with diabetes, 5.08 in postmenopausal women with diabetes, 2.41 in men with diabetes and 1.9 in the women in the control group compared to the men in the control group, after adjustment for age and BMI. This observational study clearly indicated that serum Lp(a) levels were significantly higher in women and men with diabetes. The increase in women was independent of menopause. The level of serum Lp(a) had no correlation with lipid parameters in men or women.
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PMID:Serum lipoprotein(a) levels are greater in female than male patients with type-2 diabetes. 2115 71

Dyslipidemia is the most important risk factor for atherosclerosis. LDL, VLDL remnants, chylomicron remnants, small dense LDL(sdLDL), Lp(a), and oxidized LDL are pro-atherogenic and HDLs are anti-atherogenic lipoproteins. Not native LDL but modified LDL causes to the formation of foam cells. Among LDL particles, smaller denser LDLs are more susceptible to oxidation, and have longer residence time and higher affinity to the extracellular matrix. Delayed clearance of triglyceride-rich lipoproteins results in the formation of sdLDL which is associated with insulin resistance and postprandial hyperlipidemia. HDL plays an important role in the reverse cholesterol transport as well as having antiinflammatory and antioxidative effects. Dysfunction of HDL is an independent pro-atherogenic factor. In addition, decreased HDL-cholesterol is a feature of the metabolic dyslipidemia.
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PMID:[Dyslipidemia and atherosclerosis]. 2122 74

We investigated the hypolipidemic effect of glycyrrhizic acid (GA) focused on the mRNA expression and hepatic HMG-CoA reductase (HMGR) activity in hamsters fed a high-fat diet. Male Syrian Golden hamsters were fed a high fat diet for 8 weeks for induction of dyslipidemia and were treated with GA and fenofibrate. The concentrations of plasma total cholesterol and triglyceride were significantly lower in the GA-treated group than in the control group. The GA treatment significantly decreased Apo B, Lp(a), and cholesterol-ester-transport protein (CETP) concentrations, but increased Apo A-I levels and the Apo A-I/ Apo B ratio. The contents of cholesterol and triglyceride in hepatic tissue were significantly lower in the GA group than in the control group. Real-time PCR analysis revealed that HMGR mRNA expression was significantly lower in the GA group than in the control group. These results indicate that GA treatment reduces plasma cholesterol by down-regulating hepatic HMGR mRNA expression in hamsters fed a high fructose-fat diet.
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PMID:Glycyrrhizic acid attenuates the expression of HMG-CoA reductase mRNA in high fructose diet induced dyslipidemic hamsters. 2147 Apr 96

LDL apheresis (LDLa) is an invasive therapeutic tool to control qualitative and quantitative disorders of lipid metabolism. It is aimed at achieving a metabolic balance in association with lipid-lowering drugs in patients with severe, genetically determined or acquired dyslipidemia who do not reach clinically adequate LDL-cholesterol (LDL-C) levels (<70 mg/dL) despite appropriate lipid-lowering drug treatment. A poorly known dyslipidemia is constituted by elevation of lipoprotein (a) [Lp(a)], which appears to be genetically determined and not influenced by diet or lipid-lowering medication. An Lp(a) level exceeding 30 mg/dL is an independent risk factor for premature cardiovascular disease and cerebrovascular disease. Numerous data support the notion that cardiovascular risk reduction is related to the degree of reduction of LDL-C, and the progression of atherosclerosis can be delayed or reversed by intensive and continuous cholesterol-lowering treatment. After the introduction of HMG-CoA reductase inhibitors (statins), the clinical benefit of cholesterol-lowering treatment has received significant confirmation. However, this treatment has shown poor results in the most severe, genetically determined forms. LDLa is an intensive extracorporeal cholesterol-lowering treatment approach with well documented efficacy and safety. It has also shown effects not directly correlated with its lipid-lowering activity, such as antioxidant effects on oxidized LDL and antiinflammatory effects on the cytokine network, the endothelium and the coagulation system. Finally, data acquired by the Italian Multicenter Study on LDLa Working Group were highlighted and the new evidence in the literature discussed.
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PMID:[LDL apheresis: an update and overview. LDL apheresis in Sardinia, Italy (SMILDLa)]. 2238 23


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