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

Drug-induced acanthosis nigricans has been reported in the literature. We present a patient with familial combined hyperlipidemia who developed nicotinic-acid-induced acanthosis nigricans. The literature on the cutaneous side effects of nicotinic acid as well as on the medications that can cause acanthosis nigricans is reviewed. Some hypotheses on the pathogenesis of nicotinic-acid-induced acanthosis are presented.
 ...
PMID:Acanthosis nigricans caused by nicotinic acid: case report and review of the literature. 807 56

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.
 ...
PMID:The effect of nicotinic acid and acipimox on lipoprotein(a) concentration and turnover. 821 3

Fourteen patients with familial hypercholesterolaemia were managed with dietary advice and simvastatin for 12 months. Either nicotinic acid or cholestyramine resin was added to the regimen if serum cholesterol was not less than 5.5 mmol/l within 18 weeks. After dietary advice but before commencing pharmacotherapy for hyperlipidaemia, arterial stiffness was measured in the common carotid and common femoral arteries. These studies were repeated after 12 months on pharmacotherapy. The primary objective of this study was to determine whether arterial stiffness could be altered with total cholesterol and low density lipoprotein (LDL) cholesterol lowering. Over the 12 month interval, serum total cholesterol, LDL cholesterol and triglycerides fell significantly, whereas high density lipoprotein (HDL) cholesterol and body mass index (BMI) rose significantly. Mean supine blood pressure did not change significantly. Arterial stiffness in the common carotid artery decreased from 1.04 +/- 0.21 x 10(5) N/m2 to 0.63 +/- 0.06 x 10(5) N/m2 (T = -2.67, P < 0.01) over the interval. Stiffness of the common femoral artery decreased from 2.10 +/- 0.57 x 10(5) N/m2 to 0.83 +/- 0.15 x 10(5) N/m2 (T = -2.73, P < 0.01). The change in arterial stiffness was not directly related to changes in circulating lipids or supine blood pressure. Increase in BMI, however, correlated with change in arterial stiffness in the common femoral artery (Rs = 0.53, P < 0.05) but not in the common carotid artery. An increase in BMI was associated with a smaller decrease in common femoral arterial stiffness. Aggressive hypolipidaemic therapy was therefore associated with a favourable effect on arterial wall stiffness.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Improvement in arterial stiffness during hypolipidaemic therapy is offset by weight gain. 824 26

Triglycerides and cholesteryl esters are non-polar molecules and, therefore, insoluble in aqueous fluids such as blood. Lipid transport in blood is only possible the formation of lipoproteins. This article proposes a concept for the treatment of hyperlipidemias that is based on lipoprotein pathology. The liver secretes the triglycerides and cholesteryl esters in the form of very-low-density lipoproteins (VLDL). Lipolysis hydrolyzes VLDL triglycerides, providing tissues with fatty acids. and gives rise to relatively cholesterol-enriched intermediate-density lipo- proteins (IDL) and low-density lipoproteins (LDL). IDL and LDL are removed from plasma by receptor-mediated cellular uptake. An increased plasma concentration of VLDL ensues in predominant hypertriglyceridemia (e.g. triglycerides 9 mmol/l, cholesterol 7 mmol/l). VLDL are not considered to be directly atherogenic, but increased levels of VLDL often occur together with an atherogenic decrease of high-density lipoproteins (HDL). Elevated VLDL levels respond well to dietary measures; fibric acid derivatives, nicotinic acid and omega-3-fatty acids also effectively lower VLDL. An increase in IDL leads to both hypertriglyceridemia (e.g. 3 mmol/l) and hypercholesterolemia (e.g. 7 mmol/l). IDL are considered directly atherogenic. Hyperlipidemias due to IDL respond to the same interventions as those due to VLDL. An increased blood level of LDL leads to hypercholesterolemia (e.g. 7 mmol/l) with normal triglyceride levels (e.g. 1 mmol/l); LDL are considered directly atherogenic. Dietary measures can reduce LDL levels by about 10%, but pharmacological treatment by inhibitors of cholesterol synthesis ('statins') and by ion exchange resins is much more effective.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Therapy of hyperlipoproteinemia]. 849 37

Swedish guidelines on treatment of hyperlipidemia recommend higher cut-off levels for initiating treatment than do American guidelines, but are virtually identical for instituting and performing therapy. The aim of this study was to compare family physicians' reported practices in Sweden and Minnesota. We selected random samples of family physicians in southern Sweden and Minnesota for telephone interviews. Participation rates were 236/264 (89%) and 183/209 (88%), respectively. Swedish and Minnesota physicians adhered to their guidelines on cut-off levels in a case describing a 48-year-old man but, contrary to guidelines, reported higher cut-off levels for a 65-year-old man and a 65-year-old woman. In all cases described, Swedish physicians reported significantly higher cut-off levels. Swedish physicians were less prone to institute medication in older patients and less familiar with drugs. Minnesota physicians were more inclined to advise nicotinic acid derivatives (P < .0001 for all patient categories). Swedish physicians more frequently preferred resins (P = .00029) or fibrates (P = .0028) for the 48-year-old man and resins for the 65-year-old man (P = .0026). Despite common medical knowledge, the two medical communities are directed by different guidelines. Although adherence to cut-off levels was equally high in both groups, the use of lipid-lowering drugs has not become a familiar part of the therapeutic armamentarium for Swedish family physicians.
 ...
PMID:Reported treatment of hypercholesterolemia by family physicians in Sweden and Minnesota. 857 63

We attempted to determine the mechanism(s) of poloxamer (P)-407-induced hyperlipidemia in rats by administering a lipid-lowering drug with a known mechanism of action. Five weight-matched animals were assigned to each of four treatment groups. Two groups received P-407 300 mg/ml and two received saline 1 ml. One of the P-407 and one of the saline groups were administered nicotinic acid 100 mg/kg by intraperitoneal injection at 6-96 hours after blood sampling. Blood samples were collected at 7 points from time zero to 120 hours and analyzed for triglyceride and cholesterol concentrations. The detergent produces hypertriglyceridemia (HTG) increasing from 53.4 +/- 7.0 mg/dl (time zero) to 4026.9 +/- 42.1 mg/dl by 24 hours. The HTG response was significantly attenuated by nicotinic acid (at t = 24 hrs). This, however, was followed by an average triglyceride concentration increase of 2.8-fold from 72 to 120 hours. The detergent produces a dramatic hypercholesterolemia (HCHO), increasing cholesterol from 47.5 +/- 1.8 mg/dl to 468.5 +/- 27.9 mg/dl by 48 hours. The HCHO was significantly affected by nicotinic acid administration during the accumulation phase. Nicotinic acid reduced cholesterol concentration from 364.4 +/- 16.1 mg/dl to 276.8 +/- 16.4 mg/dl at 24 hours (p < 0.05). It is a potent antilipolytic agent, limiting the free fatty acids available for the synthesis of triglyceride and cholesterol. These data suggest that P-407 may act by stimulating the release of free fatty acids from the adipocyte for at least 24 hours after injection.
 ...
PMID:Effects of nicotinic acid on poloxamer 407-induced hyperlipidemia. 870 Jul 87

The beneficial effect of cholesterol-lowering therapy for secondary prevention in patients with coronary artery disease (CAD) is well established. The therapeutic goal in this situation is a low-density lipoprotein (LDL) cholesterol level of 100 mg/dl. Cholesterol-lowering therapy will not only lead to a reduction in the progression of lesions but also and probably more importantly will reduce lesion activation and rupture and improve endothelial vasomotor function. Depending on the underlying hyperlipoproteinemia, the first choice for single drug therapy is a bile acid-binding resin or a hepatic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitor in isolated LDL hypercholesterolemia, and nicotinic acid, a fibric acid, or a HMG-CoA reductase inhibitor in combined hyperlipidemia. Combination therapy usually consists of a bile acid-binding resin with either an HMG-CoA reductase inhibitor, a fibric acid, or nicotinic acid in LDL hypercholesterolemia and nicotinic acid with a fibric acid in combined hyperlipidemia.
 ...
PMID:Drug therapy of severe hypercholesterolemia in patients with coronary artery disease. 886 Jul 8

The distal enzymatic step in the process of glucose output is catalyzed by the glucose-6-phosphatase (Glc-6-Pase) complex. The recently cloned catalytic unit of this complex has been shown to be regulated by insulin, dexamethasone, cAMP, and glucose. Using a combination of intralipid and/or nicotinic acid infusions and a pancreatic clamp technique, we maintained plasma free fatty acids (FFAs) at three different levels (0.26 +/- 0.07, 0.56 +/- 0.09, and 1.59 +/- 0.12 mmol/l) in the presence of well-controlled hormonal and metabolic conditions. An increase in the plasma FFA concentration within the physiological range caused a rapid, greater than threefold increase in the mRNA and protein levels of the catalytic subunit of Glc-6-Pase in the liver. These data indicate that the in vivo gene expression of Glc-6-Pase in the liver is regulated by circulating lipids independent of insulin and thus that prolonged hyperlipidemia may contribute to the increased production of glucose via increased expression of this protein.
 ...
PMID:Induction of hepatic glucose-6-phosphatase gene expression by lipid infusion. 897 Oct 97

Atorvastatin is a synthetic HMG-CoA reductase inhibitor which lowers plasma cholesterol levels by inhibiting endogenous cholesterol synthesis. It also reduces triglyceride levels through an as yet unproven mechanism. Dose-dependent reductions in total cholesterol, low density lipoprotein (LDL)-cholesterol and triglyceride levels have been observed with atorvastatin in patients with hypercholesterolaemia and in patients with hypertriglyceridaemia. In large trials involving patients with hypercholesterolaemia, atorvastatin produced greater reductions in total cholesterol, LDL-cholesterol, apolipoprotein B and triglyceride levels than lovastatin, pravastatin and simvastatin. In patients with primary hypercholesterolaemia, the combination of atorvastatin and colestipol tended to produce larger reductions in LDL-cholesterol levels and smaller reductions in triglyceride levels than atorvastatin monotherapy. Although atorvastatin induced smaller reductions in triglyceride levels and more modest increases in high density lipoprotein (HDL)-cholesterol levels than either fenofibrate or nicotinic acid in patients with combined hyperlipidaemia, it produced larger reductions in total cholesterol and LDL-cholesterol. As with other HMG-CoA reductase inhibitors, the most frequently reported adverse events associated with atorvastatin are gastrointestinal effects. In comparative trials, atorvastatin had a similar adverse event profile to that of other HMG-CoA reductase inhibitors. Clinical data with atorvastatin are limited at present. However, with its ability to markedly reduce LDL-cholesterol levels, atorvastatin is likely to join other members of its class as a first-line agent for the treatment of patients with hypercholesterolaemia, if changes in lipid levels with atorvastatin convert to reductions in CHD mortality and morbidity. Atorvastatin may be particularly suitable for patients with heterozygous or homozygous familial hypercholesterolaemia because of the marked reductions in LDL-cholesterol experienced with the drug. Additionally, because of its triglyceride-lowering properties, atorvastatin appears to have the potential to become an appropriate treatment for patients with combined hyperlipidaemia or hypertriglyceridaemia.
 ...
PMID:Atorvastatin. A review of its pharmacology and therapeutic potential in the management of hyperlipidaemias. 912 69

This review article examines the mode of action, the efficacy and the side effects of the various types of hypolipidemic agents (fibrates, bile acid sequestrants, statins, nicotinic acid and acipimox) currently available in Belgium. It also summarizes the recent guidelines recommended by the Belgian Lipid Club in the management of hyperlipidemia for the primary and secondary prevention of cardiovascular diseases as well as the therapeutic strategy.
 ...
PMID:[Pharmacology of hypolipidemic agents]. 913 14


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>