Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examines the effect of nicotinic acid (1 g t.d.s.) on serum Lp(a) concentration in a group of patients with type II hyperlipidaemia selected on the basis of a plasma Lp(a) concentration greater than 30 mg/dl. Reductions in total cholesterol, triglyceride, LDL-cholesterol and Lp(a) were 16.3%, 25.5%, 23.7% and 36.4%, respectively, with an increase in HDL cholesterol of 37.3%. The reduction in Lp(a) concentration did not correlate with any other lipoprotein changes. In order to establish the mechanism of the fall in Lp(a) concentration, in vivo turnover of autologous Lp(a) was studied in three subjects before and whilst taking nicotinic acid. The fractional catabolic rate in Lp(a) was unaltered in the subjects on therapy, indicating that nicotinic acid did not increase catabolism of Lp(a) but decreased the synthetic rate. Since nicotinic acid was poorly tolerated we examined the effect of acipimox, an analogue of nicotinic acid on lipoproteins using a placebo controlled double-blind crossover design in a group of hyperlipidaemic patients again selected with plasma Lp(a) concentration greater than 30 mg/dl. Acipimox was better tolerated than nicotinic acid but the percentage changes in lipoprotein concentrations were smaller.
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PMID:The effect of nicotinic acid and acipimox on lipoprotein(a) concentration and turnover. 821 3

Exploratory data analysis (EDA) software facilitates unstructured, iterative open exploration of complex datasets with the aid of multiple linked graphical displays. We are investigating relationships between plasma lipoproteins and coronary artery disease by retrospective analysis of 1677 consecutive UCSF Lipid Clinic patients. Our preliminary experience is with Data Deck 3.0 although several additional software programs (JMP 2.0, Systat 5.1, Minitab 8.0, StatView 4.0) are mentioned. Lipid diagnosis (751 women and 925 men) was 22% primary hypercholesterolemia, 19% combined hyperlipidemia, 3% dysbetalipoproteinemia, 15% endogenous lipemia, 4% mixed lipemia, 5% elevated Lp(a) and 32% with no major lipid abnormality. We found the Macintosh platform (68030) to be flexible and powerful for analysis of moderate size (less than 1 Mb) clinical datasets. High resolution color monitors (1024 x 768 pixels), fast hard disks (< 18 msec) and moderate amounts of system memory (8 + Mb) facilitate exploratory analysis.
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PMID:Exploratory data analysis of hyperlipidemia on the Macintosh: software tools for analysis of biochemical, clinical, and genetic variables in 1677 consecutive lipid clinic patients. 825 63

The relationship between lipoprotein(a) [Lp(a)] and metabolism of triglyceride-rich lipoproteins (TRL) was studied in 58 untreated patients with familial combined hyperlipidemia (FCH) from eight different kindreds, 17 spouse controls, and 17 unrelated controls. Lp(a) plasma concentrations were not significantly different between FCH subjects (343 +/- 61 mg/L, mean +/- SEM) and controls (249 +/- 52 mg/L). In FCH, log-transformed Lp(a) levels correlated positively with postheparin lipoprotein lipase ([LPL] r = .61, P = .0002) and hepatic lipase ([HL] r = .46, P = .008) activities and total plasma cholesterol level (r = .30, P = .03). In controls, Lp(a) correlated with LPL (r = .50, P = .04) and total plasma cholesterol level (r = .51, P = .003). In eight FCH patients, treatment with the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin resulted in significantly increased mean LPL activities and plasma Lp(a) concentrations. In three of these FCH patients, repeated measurements during 1 year demonstrated that changes in Lp(a) concentrations were paralleled by similar changes in LPL activity, but not HL activity. The observed correlation between postheparin plasma lipolytic activities and Lp(a) plasma concentrations suggests a connection between the metabolism of TRL and Lp(a).
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PMID:Lipoprotein(a) plasma concentrations associated with lipolytic activities in eight kindreds with familial combined hyperlipidemia and normolipidemic subjects. 851 May 21

Hyperlipidemia and elevated lipoprotein (a) [Lp(a)] levels have been linked to the development and progression of premature atherosclerosis. Two male caucasian patients (36 and 42 years old) with heterozygous familial hypercholesterolemia and extremely elevated Lp(a) concentrations, resistant to diet regimen and lipid lowering drugs, were treated with LDL-apheresis for 55 months (liposorber system, Kaneka, Japan) and 15 months (immunoadsorption system, special Lp(a) columns, Lipopak, Pocard, Russia). Lp(a) dropped on average by 50%, total cholesterol by 27%, LDL-cholesterol by 42%, triglycerides by 43% and the fibrinogen concentration by 16%. Prior to treatment, both patients had suffered three myocardial infarctions. Four and six coronary angiographies with two and four percutaneous transluminal angioplasties (PTCA) were necessary. Since the treatment with LDL-apheresis neither myocardial infarctions nor cardiac complaints have been observed, and both patients have reported better performance. Available data suggest that LDL-apheresis may be effective in the treatment of patients with extremely high Lp(a) concentration.
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PMID:LDL-apheresis in two patients with extremely elevated lipoprotein (a) levels. 856 5

The hypothesis that increased cholesterol synthesis provides a mechanism that contributes to nephrotic syndrome-associated hyperlipidemia is mainly based on experimental evidence. The serum level of the cholesterol precursor, lathosterol (expressed per millimole cholesterol), is a reliable marker of whole-body cholesterol synthesis in normocholesterolemia and primary hypercholesterolemia. Serum lathosterol and lipoprotein levels were measured in 11 moderately hyperlipidemic patients with nephrotic-range proteinuria and 22 matched controls. The proteinuric patients were evaluated before and during three antiproteinuric treatment periods with angiotensin-converting enzyme (ACE) inhibition therapy (n = 6) or a low-protein diet (n = 5) alone, in combination, and again as a single treatment. In untreated patients, serum total cholesterol, very-low-density (VLDL) and low-density (LDL) lipoprotein cholesterol, apolipoprotein B (apo B), and lipoprotein (a) [Lp(a)] levels were higher than in controls (P < .01 to P < .001), but the lathosterol to cholesterol ratio tended to be lower in patients (0.99 +/- 0.43 micromol/mmol) as compared with controls (1.29 +/- 0.41 micromol/mmol, P < .10). During combined antiproteinuric treatment, total and VLDL + LDL cholesterol, apo B, and Lp(a) decreased (P < .02 to P < .01), but remained higher than levels in controls. Yet the serum lathosterol to cholesterol ratio changed little and was even lower (P < .05) in treated patients than in controls. Serum total cholesterol (r = -.82, P < .01) and apo B (r = -.84, P < .01) were inversely correlated with serum albumin in untreated patients, whereas the serum lathosterol to cholesterol ratio was not (r = -.01, NS). In the patient group, multiple regression analysis showed that changes in the lathosterol to cholesterol ratio during the study were only related to changes in the dietary polyunsaturated to saturated fatty acids ratio (P:S) coinciding with the low-protein diet (P < .01). In contrast, the decrease of VLDL + LDL cholesterol, apo B, and Lp(a) was independently related to reduction of proteinuria (P < .02 to P < .001), but not to changes in the lathosterol to cholesterol ratio. In conclusion, the present data, based on the serum lathosterol to cholesterol ratio, do not support the concept that increased cholesterol synthesis plays an important role in the maintenance of human nephrotic syndrome-associated hypercholesterolemia. Moreover, it appears unlikely that the decrease of apo B-containing lipoproteins with antiproteinuric treatment is attributable to inhibition of cholesterogenesis. These findings warrant further documentation of cholesterol synthesis in human nephrotic syndrome by direct methods.
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PMID:The serum lathosterol to cholesterol ratio, an index of cholesterol synthesis, is not elevated in patients with glomerular proteinuria and is not associated with improvement of hyperlipidemia in response to antiproteinuric treatment. 863 47

Hyperlipidemias are grouped according to their lipid levels in hypercholesterolemia, hypertriglyceridemias, and mixed hyperlipidemias. Among these, hypercholesterolemia has the strongest correlation to the risk for coronary heart disease. Based on the results from epidemiologic studies and intervention trials several expert panels have defined cholesterol values with low and high cardiovascular risk and cholesterol target levels for treatment. In the presence of hyperlipidemia additional parameters like LDL cholesterol, HDL cholesterol, and Lp(a) may be determined depending on the individual patient's risk profile. For classification of familial lipid disorders, analysis of relatives and the determination of special parameters may be necessary. These include apolipoproteins (concentration, isoforms, mutants), enzyme activities (lipases, LCAT), LDL receptor activity, oratypical lipoproteins.
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PMID:[Classification of hyperlipoproteinemias and interpretation of laboratory parameters]. 865 Sep 32

We designed a short-term randomized controlled study in 12 adult patients with chronic renal failure to assess the metabolic effects of a low-protein diet (LPD) supplemented or not with ketoacids (Cetolog, Clintec Corp., France). Dietary survey included a monthly 3-day food record and a 24-hour urinary urea measurement. After a baseline period (1.11 g protein, 31.7 kcal/kg BW/day), patients reduced their protein intake (PI) to 0.71 g/kg BW/day. Energy intake (EI) was kept constant (31.4 kcal/kg BW/day) during the 3-month period. Baseline plasma lipids did not show overt hyperlipemia. After reducing PI, a significant increase in apolipoprotein AI and the Apo-AI/Apo-B ratio was observed. Plasma Lp(a) levels were elevated at baseline and did not change during the 3-month LPD period. There was no difference between groups receiving ketoacids or not. Thus, in adult chronic renal failure, under a sufficient EI, reducing PI by 40% had a beneficial effect on plasma lipid profile. This improvement in lipid profile might reduce the high cardiovascular risk in these patients.
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PMID:Effects of low-protein diet supplemented with ketoacids on plasma lipids in adult chronic renal failure. 867 7

Lipoprotein disorders are considered an important cause for the high cardiovascular morbidity and mortality in patients with end-stage renal disease and following renal transplantation. This article reviews the disease-associated changes of lipids and lipoproteins in these patients and, where known, the underlying causes and mechanisms. Further, we discuss the perturbed lipoprotein system in relation to the cardiovascular risk of patients on renal replacement therapy. Patients treated by hemodialysis are often hypertriglyceridemic with increased very low density lipoprotein (VLDL) levels and a type IV Frederickson pattern of hyperlipidemia. Total and LDL cholesterol concentrations are usually normal or subnormal. Treatment of end-stage renal disease by peritoneal dialysis results in increased total, VLDL and LDL cholesterol concentrations. Both treatment modalities are accompanied by a decrease of high density lipoprotein (HDL) cholesterol and apolipoprotein AI, whereas lipoprotein(a) [Lp(a)] concentrations are significantly elevated in both groups. Following renal transplantation a high incidence of hypercholesterolemia and hypertrigylceridemia is observed, which is attributed, at least in part, to the immunosuppressive therapy. Most patients normalize HDL cholesterol values and Lp(a) decreases to pre-disease plasma concentrations. Several studies have described elevated levels of cholesterol, triglycerides and Lp(a) in patients with cardiovascular complications during different phases of renal replacement therapy, which indicates a predictive (causative) role of these parameters for atherosclerotic diseases.
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PMID:Lipoprotein metabolism in renal replacement therapy: a review. 868 43

Renal disease is accompanied by specific alterations of the lipoprotein metabolism. While marked hyperlipidemia is a characteristic finding in the nephrotic syndrome, the dyslipoproteinemia of renal insufficiency is predominantly reflected in an abnormal apolipoprotein pattern but does not necessarily include elevated plasma lipid concentrations. The specific changes in nephrotic syndrome include increased formation primarily of cholesterol-rich and to a varying extent of triglyceride-rich ApoB-containing lipoproteins in the VLDL-LDL density range with little or no change among the ApoA-containing lipoproteins in HDL. The dyslipoproteinemia of renal failure is, on the other hand, mainly characterized by a decreased catabolism of the triglyceride-rich ApoB-containing lipoproteins with increased concentrations of partially metabolized lipoproteins of intermediate and very low density and a decreased concentration of ApoA-containing lipoproteins in HDL. In addition, increased levels of Lp(a) are found both in the nephrotic syndrome and in renal failure. Dialysis treatment appears to have only a modest influence on the renal dyslipoproteinemia. Due to its atherogenic character, the dyslipidemia of renal disease may be related to the accelerated development of cardiovascular disease in these patients.
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PMID:Diagnosis and classification of dyslipidemia in renal disease. 871 66

The nephrotic syndrome is frequently associated with hyperlipidaemia and hyperfibrinogenaemia, leading to an increased coronary and thrombotic risk, which may be enhanced by high lipoprotein (a) [Lp(a)] concentrations. We followed the quantitative and qualitative pattern of plasma lipoproteins over 18 months in a patient with nephrotic syndrome suffering from premature coronary artery disease and with elevated level of Lp(a) (470 mg dL-1). Analysis of kinetic parameters after heparin-induced extracorporeal plasma apheresis revealed a reduced fractional catabolic rate for both low-density lipoprotein (LDL) and Lp(a). After improvement of the nephrotic syndrome, Lp(a) decreased to 169 mg dL-1 and LDL concentrations were normalized. The decrease of Lp(a) was associated with an increase in plasma albumin concentrations. Analysis of apo(a) isoforms in the patient showed the presence of isoform S2 (alleles 10 and 19). Consequently, the authors' present strategy is to normalize the elevated Lp(a) and fibrinogen levels. For this purpose heparin-mediated extracorporeal LDL precipitation (HELP) apheresis is a promising regimen, helping to reduce the thrombotic risk and prevent coronary and graft atherosclerosis as well as the progression of glomerulosclerosis in our patient.
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PMID:Hyperlipoprotein(a)aemia in nephrotic syndrome. 873 90


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