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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As part of our occasional series highlighting advances in drug therapy, this article discusses the mechanisms of hyperlipidaemia and the main groups of drugs used to treat the condition including bile acid-binding agents, fibrates, nicotinic acid and its derivatives, statins and fish oils.
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PMID:Drugs used to lower high lipid levels. 781 17

In a retrospective survey of patients taking medication for hyperlipidaemia, those taking niacin (nicotinic acid) were more likely (p < 0.05) to report sicca syndromes, blurred vision, eyelid oedema, and macular oedema compared with those who never took niacin. Additionally, 7% of those taking niacin discontinued the drug owing to adverse ocular side effects, while none of the other lipid lowering agents were found to cause these side effects (p = 0.016). Data from spontaneous reporting systems support a possible association of decreased vision, cystoid macular oedema, sicca-like symptoms, discoloration of the eyelids with or without periorbital or eyelid oedema, proptosis, loss of eyebrow or eyelashes, and superficial punctate keratitis with the use of niacin in high doses. Decreased vision may be marked, and if the drug is not discontinued, may progress to cystoid macular oedema. All ocular side effects listed above are reversible if the association with niacin is recognised and the drug is discontinued; both the incidence and severity of the ocular side effects seem to be dose dependent.
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PMID:Adverse ocular effects associated with niacin therapy. 788 Jul 95

Patients with non-insulin-dependent diabetes mellitus (NIDDM) are at high risk of cardiovascular disease for many reasons and especially due to the fact that dyslipidemias are more frequent in this group of patients. Fibrate derivatives are the drugs of choice when hypertriglyceridemia is the main lipid anomaly. When hypercholesterolemia is predominant, the use of resins and nicotinic acid has been advocated but these drugs are poorly tolerated on a long-term basis. We assessed the effect of simvastatin, a recent HMG-CoA reductase inhibitor in 12 NIDDM patients with hypercholesterolemia. After 4 weeks of placebo, which did not significantly modify the lipid values, patients were given simvastatin at increasing dosages (from 10 to a maximum of 40 mg daily) during 24 weeks. Compliance and clinical tolerance were excellent. There was no major biological side effect, but a significant deterioration of glucose control was noted at the end of the study. Simvastatin reduced total cholesterol by 28%, LDL-cholesterol by 36% and apo B by 31%. Concomitantly, there was an increase of HDL-cholesterol by 15%. This improvement of lipid profile persisted during the 24 weeks of treatment. Comparing the patients with pure hypercholesterolemia to those presenting combined hyperlipidemia, it was evident that the hypolipidemic effect was more marked in the diabetic subjects with combined hyperlipidemia.
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PMID:Efficacy of simvastatin for lowering cholesterol in non-insulin dependent diabetic patients with hypercholesterolemia. 806 75

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.
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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.
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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)
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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)
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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.
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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.
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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.
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PMID:Drug therapy of severe hypercholesterolemia in patients with coronary artery disease. 886 Jul 8


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