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PubMed1987

Lipid-lowering drugs. An overview of indications and optimum therapeutic use.

Drug treatment of patients with hyperlipoproteinaemia is indicated to reduce the risk of atherosclerosis in patients with increased concentrations of atherogenic lipoproteins, and to lower the plasma concentrations of triglyceride-rich lipoproteins in patients with severe hypertriglyceridaemia who are at risk of abdominal pain and pancreatitis. Such therapy should be initiated only after satisfactory exclusion of secondary causes of hyperlipoproteinaemia, and should be regarded as an adjunct to rather than a substitute for appropriate dietary therapy. Drug therapy should be strongly considered in those patients with concentrations of atherogenic lipoproteins which exceed the 90th to 95th percentile for age. In patients with increased plasma concentrations of low density lipoproteins (LDL), agents which enhance the rate of LDL catabolism (cholestyramine and colestipol) or reduce the rate of LDL synthesis [e.g. nicotinic acid (niacin)] are the 'drugs of choice'. For those patients with concurrent hypertriglyceridaemia, nicotinic acid is the preferred initial drug, and in both patient groups combined drug therapy is often necessary to attain optimal reductions in LDL cholesterol concentrations. Clofibrate remains the 'drug of choice' for the rare patient with type III hyperlipoproteinaemia, whereas the newer agent gemfibrozil should be used in patients with plasma triglyceride concentrations above 1000 mg/dl who are at increased risk of abdominal pain and pancreatitis. Although currently limited to investigational use, mevinolin and related compounds, which are specific inhibitors of the rate-limiting enzyme in cholesterol biosynthesis (HMG Co-A reductase), offer considerable promise in the therapy of patients with primary hypercholesterolaemia due to elevated levels of LDL cholesterol.

Humans↗

PubMed1987

Bezafibrate. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in hyperlipidaemia.

Bezafibrate is a lipid-lowering drug, chemically related to clofibrate. At its recommended dosage of 200 mg 3 times daily, or alternatively 400 mg once daily as a sustained-release preparation, it produces substantial reductions in plasma triglyceride and cholesterol concentrations in patients with hypertriglyceridaemia and hypercholesterolaemia, respectively. Preliminary investigations indicate that a single daily dose of 400 mg in a sustained-release preparation is as effective as 200 mg 3 times daily. In patients with any type of hyperlipoproteinaemia bezafibrate also increases the plasma HDL-cholesterol concentration. These effects are equivalent in patients with primary hyperlipoproteinaemia or hyperlipoproteinaemia secondary to diabetes or renal disease, although dosage adjustment is important in the latter group. During long term therapy (2 to 4 years) the influence of bezafibrate on the lipid profile is sustained. The lipid-lowering effects of bezafibrate are at least equivalent to those of clofibrate, fenofibrate, colestipol, probucol or sustained release etofibrate. In addition, the increase in HDL-cholesterol tends to be at least as great as with all alternative treatments studied. Bezafibrate is rapidly eliminated, and thus does not accumulate during prolonged administration in patients with normal renal function. Experimental studies have shown bezafibrate to have a complex range of effects on lipoproteins and on the enzymes and receptors involved in lipid metabolism. However, its exact mechanism of lipid-lowering action is unclear. Bezafibrate enhances anticoagulation in hyperlipoproteinaemic patients requiring anticoagulant therapy, and preliminary investigations indicate that it reduces the plasma fibrinogen concentration, especially in patients with hyperfibrinogenaemia. These properties of bezafibrate could contribute to an antiatherogenic effect of the drug, but further investigation is required to establish the drug's potential as chronic therapy in patients with hyperfibrinogenaemic atherosclerosis. Adverse reactions to bezafibrate have largely been restricted to gastrointestinal disturbances, with some cutaneous reactions and central nervous system effects. The incidence of side effects has been no greater than with comparative lipid-lowering drugs. In patients with renal disease, a few cases of marked elevation of serum creatine phosphokinase and myoglobin, and associated muscle cramps, have been reported (diagnosed as rhabdomyolysis). Hepatic enzyme induction by bezafibrate in rats results in hepatomegaly, but there has been no case of significant hepatotoxicity in man.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Regression of coronary atherosclerosis. Angiographic perspective.

The influence of dietary or pharmacological intervention on coronary atherosclerosis can best be assessed by performing serial coronary arteriography on patients at high risk for coronary disease progression who are randomised into controlled trials. Changes in coronary artery lesion diameter of less than 20% cannot be accurately assessed by visual interpretation, because of inter- and intra-observer variability. The introduction of quantitative, computer-assisted measurements of coronary lesions has reduced variability and greatly improved the precision of measurements. Both cholestyramine and colestipol-niacin have been shown to reduce the rate of progression of coronary atherosclerosis; however, in both studies coronary lesions were assessed visually and no quantitative measurements were reported. A marked reduction in serum cholesterol appears to be the intervention that is most likely to prevent the progression or induce regression of coronary atherosclerosis. Quantitative angiographic measurement techniques should be used in clinical trials designed to assess cholesterol-lowering interventions.

Angiocardiography↗

PubMed1988

An overview of lipid-lowering drugs.

The long term use of lipid-lowering drugs in the treatment of patients with hyperlipoproteinaemia is aimed at reducing plasma concentrations of known atherogenic lipoproteins with a favourable effect on lipid deposition in the arterial wall. A less common aim is to prevent the adverse sequelae of hyperchylomicronaemia in patients with severe hypertriglyceridaemia. The decision to begin drug therapy should be made only after the exclusion of secondary factors and after an adequate trial of diet has failed to produce acceptable concentrations of plasma lipids and lipoproteins. The bile acid sequestrants (cholestyramine and colestipol), nicotinic acid, fenofibrate and inhibitors of hydroxymethylglutaryl coenzyme A (HMG CoA) reductase (e.g. lovastatin or simvastatin) are the most effective drugs for use in patients with primary hypercholesterolaemia; these agents reduce plasma concentrations of total and LDL-cholesterol by 15 to 45%. For those patients with concurrent hypertriglyceridaemia, nicotinic acid, lovastatin or simvastatin, or fenofibrate are the preferred drugs for initial use; bile acid sequestrants frequently exacerbate hypertriglyceridaemia in these patients. Fibric acid derivatives (e.g. clofibrate, gemfibrozil, bezafibrate or fenofibrate) are all effective in the therapy of patients with type III hyperlipoproteinaemia, as is nicotinic acid and I have found lovastatin to be effective also. Gemfibrozil or nicotinic acid are the most effective agents to use in the treatment of patients with severe hypertriglyceridaemia who are at increased risk of abdominal pain and pancreatitis. Combined therapy with drugs which have different mechanisms of action can be effectively used in the treatment of patients with severe hypercholesterolaemia or combined hyperlipidaemia; for the former group, combinations which use bile acid sequestrants, HMG CoA reductase inhibitors and nicotinic acid are the most effective.

Humans↗

PubMed1997

Atorvastatin. A review of its pharmacology and therapeutic potential in the management of hyperlipidaemias.

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.

Anticholesteremic Agents↗

PubMed1983

The effect of cholesterol feeding and alterations in bile acid homeostasis on de novo sterologenesis in diabetic rats.

Previous studies have demonstrated that de novo cholesterol synthesis is increased two- to threefold in the intestines of diabetic animals. This increase is due to a stimulation of cholesterogenesis in both the small and large intestine but, quantitatively, the small intestine is primarily responsible for the observed increase. The present study examined the effect of cholesterol feeding and alterations of bile acid homeostasis on de novo sterol synthesis in intact normal and diabetic animals. Cholesterol feeding in the control animals did not affect sterol synthesis in the small intestine, but in diabetic animals cholesterol feeding markedly inhibited small intestinal sterologenesis. The threefold stimulation of small intestinal sterol synthesis observed in diabetic animals is completely obliterated by cholesterol ingestion. Moreover, this inhibition of sterol synthesis by cholesterol feeding in the small intestine of diabetic animals occurred very rapidly (within 36 h). In the large intestine, cholesterol feeding did not influence sterol synthesis in either the diabetic or control animals. In the liver, cholesterol feeding markedly inhibited sterol synthesis to similar degrees in the diabetics and controls. Colestipol feeding and biliary drainage, procedures that reduce bile acid pool size, stimulated sterol synthesis in the liver and small intestine of both diabetic and control animals. However, reductions in bile acid pool size increased sterologenesis in the large intestine in control animals but had no effect in the diabetics. Bile acid ingestion did not alter either small or large intestinal sterologenesis in the diabetic or control animals. In conclusion, the present study demonstrates the sterol synthesis is enhanced in the small and large intestine of diabetic animals and, moreover, both the cholesterol- and bile acid-mediated regulation of cholesterol synthesis in the intestines of the diabetic animals is altered from normal.

Animals↗

PubMed1991

Recent trends in the prescribing of cholesterol lowering drugs in Australia. A report from the Drug Utilization Subcommittee of the Pharmaceutical Benefits Advisory Committee.

OBJECTIVE: To determine the recent pattern of use of hypolipidaemic drugs in the Australian community. DESIGN: Drug utilisation study employing prescription data collected during the operation of the Australian Pharmaceutical Benefits Scheme (PBS). SETTING: Non-hospital drug use in Australia. PATIENTS: All patients, pensioners and non-pensioners, who received prescriptions for hypolipidaemic agents under the PBS between January 1987 and December 1989. MAIN OUTCOME MEASURES: The total number of prescriptions, average quantity dispensed with each prescription, defined daily doses (DDD) and Australian population figures for pensioners and non-pensioners were used to express the consumption of hypolipidaemic agents as DDD/1000 individuals/day. RESULTS: Between the March quarter 1987 and the December quarter 1989 prescribing of hypolipidaemics for the Australian community increased from 68,120 to 304,760 prescriptions per quarter, which translates to a rise in use from 1.2 to 5.2 DDD/1000 inhabitants/day. This included a rise in the use of clofibrate from 0.6 to 2.6 DDD/1000 inhabitants/day, and of cholestyramine from 0.6 to 1.9 DDD/1000 inhabitants/day. Prescribing of hypolipidaemics for pensioners increased from 29,569 to 123,440 prescriptions per quarter. This translated into a rise in use from 3.7 to 14.8 DDD/1000 pensioners/day. Notable rises were seen for clofibrate, 1.9 to 8.1 DDD/1000 pensioners/day, and cholestyramine, 1.6 to 4.7 DDD/1000 pensioners/day. In comparison published data from the Nordic countries and the United States showed a lower overall use of hypolipidaemics and declining consumption of clofibrate. CONCLUSIONS: The trend in Australia was unusual in that the use of clofibrate increased to a greater extent than that of the resins, cholestyramine and colestipol which are generally preferred for treatment of hypercholesterolaemia. Possible reasons for this include: the better tolerability of clofibrate; its readier availability during the study period; the recommendation by the Pharmaceutical Benefits Advisory Committee that clofibrate was the preferred drug when triglyceride levels were also elevated and the limited availability of newer hypolipidaemic agents.

Aged↗

PubMed1992

[Pravastatin, a new cholesterol synthesis inhibitor for lowering increased serum cholesterol].

The association between increased risk for coronary artery disease (CAD) and elevated plasma cholesterol has been firmly established. The beneficial effect of cholesterol lowering treatment modalities was confirmed in both primary and secondary intervention trials. Because long-term treatment is usually required for lipid lowering therapies the drugs used for lipid reduction have to be not only efficacious but also safe. Inhibitors of cholesterol synthesis that have become clinically available during the last few years, can reduce plasma levels of total cholesterol and low density lipoprotein (LDL)-cholesterol very effectively. In the Familial Atherosclerosis Treatment Study (FATS) an intensive cholesterol lowering treatment modality consisting of a combination of an inhibitor of cholesterol synthesis and colestipol reduced the progression of coronary lesions and caused a partial regression of such lesions. Among the various inhibitors of cholesterol synthesis developed recently, pravastatin appears to be tissue-specific because of its hydrophilic property.

Cholesterol↗

PubMed1991

[Is regression of atherosclerosis by drugs possible?].

The development of atheromatous wall changes and local thrombotic complications in coronary arteries may be influenced by drug treatment. Calcium antagonists appear to reduce the progression of minimal coronary lesions only, while lipid lowering agents (colestipol, niacin, fibrates and HMG-CoA-reductase inhibitors) can retard the progression of established stenotic lesions or even produce a slight regression in 20-30% of patients within two to four years. In acute stages of coronary artery disease, however, treatment with platelet inhibitors, anti-coagulants and betablockers is required to prevent life-threatening complications. Hence the optimum strategy for secondary prevention in coronary artery disease depends on the clinical presentation in individual patients.

Adrenergic beta-Antagonists↗

PubMed1991

Cholesterol-mediated suppression of alpha 1-inhibitor III, a plasma alpha-macroglobulin family protein.

Using differential hybridization techniques we have isolated a hamster cDNA encoding a cholesterol-regulated protein. By sequence homology we concluded that the isolated cDNA encodes alpha 1-inhibitor III (alpha 1 I3), a protein of the alpha-macroglobulin (alpha M) family. When hamsters were fed diets rich in cholesterol, cholic acid, or chenodeoxycholic acid, the amount of alpha 1I3 RNA was reduced between 5- and 10-fold. Drugs that lower plasma cholesterol levels, such as colestipol and mevinolin, increased alpha 1I3 RNA between 2- and 3-fold. Additionally, plasma alpha 1I3 protein levels, as measured by immunoblotting techniques using an anti-human alpha 2M antibody, correlate well with alpha 1I3 RNA levels in those hamsters. Plasma alpha 1I3 protein was inversely proportional to plasma cholesterol levels in those hamsters. The observed suppression of alpha 1I3 expression by cholesterol mimics the cholesterol-mediated regulation of other genes that maintain cholesterol homeostasis, such as 3-hydroxy-3-methylglutaryl coenzyme A synthase, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and low density lipoprotein receptor. We hypothesize that alpha 1I3 may play a role in the onset of atherosclerosis and may provide a link between cholesterol and the clotting system. Furthermore, the availability of another sterol-regulated gene, like alpha 1I3, should help elucidate the molecular mechanisms of cholesterol-mediated regulation of gene transcription.

Acute-Phase Proteins↗

PubMedDate not supplied

[Critical review of drugs in 1990].

New chemical entities approved abroad (43) and in Yugoslavia (37) were presented. Discussions on several "old" drugs (41) open at the Yugoslav Federal Drug Committee for any reason (new formulation, new dose, new packaging, dosage regimen or indication) and renewal of registration (114) were also included. Special attention was given to the drugs which had been refused the renewal of registration (8). Critical drug re-evaluation as an important element of the improvement of pharmacotherapy was emphasized. A total of 78 drugs was discussed or registered in 1990-1.28% of drugs from the group A (vancomycin), 10.2% from the group B (aclarubicin, dexfenfluramine, warfarin, alprazolam, colestipol, lovastatin, combination: cetrimonium + lidocain and estradiol vag.), 87.1% (the greatest number so far!) from the group C and 1.28% from the group D. Surveys of the most prescribed drugs in Zagreb, in Yugoslavia and in the world were also given having proved largely non-rational drug prescribing in this country. Further development of drug formulary concept was discussed, primarily for the drugs paid by the Health Insurance, as well as the unsatisfactory ADR reporting in Yugoslavia. Presented were also the activities of the Committee for Diagnosis, Pharmacotherapy and ADR of the Yugoslav Federal Institute for Health Protection. Publishing of Yugoslav daily defined doses is, according to the authors essential for further systematic monitoring of drug consumption on different levels in this country. It would be impossible to rationalize pharmacotherapy without these data.

Pharmaceutical Preparations↗

PubMed1990

The National Cholesterol Education program: guidelines and commentaries.

There is overwhelming evidence that atherosclerosis is caused by elevated cholesterol levels and that the process can be prevented, arrested, and even reversed by altering the cholesterol fractions. The National Cholesterol Education program established guidelines for the management of hypercholesterolemia. Classification of cholesterol values are: Desirable 200 mg./dl, Borderline high 200-239 mg./dl high risk 240 mg./dl and above. Total cholesterol is used for case finding and screening, but LDL cholesterol is the key index for decisions requiring treatment. Classification of LDL levels is as follows: High risk 160 mg/.dl and over, Borderline 130 to 159 mg./dl, Acceptable 130 mg./dl and below. Secondary and familiar disorders should be identified. Dietary therapy is the cornerstone of cholesterol reducing interventions. Steps one and two diets are described, with limitations of saturated fats to 10% of total calories and cholesterol to 300 mg./daily in step one; step two diet limits saturated fats to 7% of total calories-and cholesterol to 200 mg./daily. Pharmacotherapy is based on 5 groups of hypolipidemics agents: A--Resins (cholestyramine and colestipol) B--Nicotinic acid C--Probucol D--Fibric acids (gemfibrozil) E--Reductase inhibitors (lovastatin). Some areas of criticism and controversies regarding the guidelines are discussed and identified.

Humans↗

PubMed1990

[Determination of potentially atherogenic triglyceride-rich lipoprotein particles].

Hypertriglyceridemia is a common disorder of lipid transport occurring either as a primary or secondary manifestation of the underlying metabolic derangement. Although most prospective studies have provided no evidence for the independent contribution of plasma triglycerides to atherosclerosis, results of several clinical and metabolic studies have indicated that some modified triglyceride-rich lipoproteins may be as atherogenic as the typical cholesterol-rich low density lipoproteins. Our studies on the sequential fractionation of apolipoprotein B-containing lipoproteins have identified five major apolipoprotein-defined lipoprotein families including cholesterol-rich lipoprotein B and triglyceride-rich lipoproteins B:C, B:C:E, B:E and A-II:B:C:D:E. The evaluation of the results of Cholesterol Lowering Atherosclerosis Study has shown that some triglyceride-rich lipoproteins play an important role in the progression of atherosclerosis. The combined niacin-colestipol treatment resulted in a 40-50% decrease in the levels of cholesterol-rich lipoprotein B but had no effect on triglyceride-rich lipoproteins. Patients who had increased levels of latter lipoproteins, as demonstrated by decreased levels of apolipoprotein C-III in heparin-Mn++ supernates, showed progression of atherosclerotic lesions. On the other hand, in the Helsinki Heart Study, despite minimal reduction in the levels of LDL-cholesterol, patients with phenotypes IIB and IV had higher reduction rates in coronary end points than patients with phenotype IIA.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins↗

PubMed1990

Comparison of cholesterol-lowering regimens.

Drug therapy should be reserved for patients with marked total cholesterol elevation not amenable to dietary measures. While current guidelines suggest that bile acid sequestrants, such as cholestyramine and colestipol, are first-line drugs for the treatment of hypercholesterolemia, recent studies suggest that lovastatin is a safe, more potent alternative. Gemfibrozil reduces the serum triglyceride level and raises the high-density lipoprotein (HDL) cholesterol level, but has only a moderate effect on the serum cholesterol level. Nicotinic acid lowers serum low-density lipoprotein (LDL) cholesterol and triglyceride levels and raises serum HDL levels, but its use is limited because of troublesome side effects, notably a flushing reaction. Probucol lowers both serum LDL and HDL levels and is a second-line agent for the treatment of hypercholesterolemia.

Anticholesteremic Agents↗

PubMed1990

Management of hyperlipidemia: goals for the prevention of atherosclerosis.

The goals of treatment for patients with hyperlipoproteinemia are to reduce plasma concentrations of known atherogenic lipoproteins, thereby exerting a favorable effect upon lipid deposition in the arterial wall and, less commonly, to prevent the adverse sequelae of hyperchylomicronemia in patients with severe hypertriglyceridemia. Diet is the cornerstone of the therapy after the exclusion of secondary factors; the decision to begin drug therapy should be made only after an adequate trial of diet has failed to achieve satisfactory concentrations of plasma lipids and lipoproteins. For patients without evidence of atherosclerosis the goals is to reduce the plasma concentrations of low density lipoproteins to below 160 mg/dl (4.2 mM/L); for those individuals with atherosclerosis or the concurrent presence of two risk factors, a lower level of LDL is desirable (less than 130 mg/dl; 3.4 mM/L). For regression to occur the LDL level may need to be below 100 mg/dl (2.6 mM/L). The bile acid sequestrants (cholestyramine and colestipol), nicotinic acid, fenofibrate, and inhibitors of HMG CoA reductase (e.g., lovastatin or simvastatin) are the most effective drugs for use in patients with primary hypercholesterolemia and these agents reduce plasma concentrations of total and LDL cholesterol by 15-45%. For those patients with concurrent hypertriglyceridemia, nicotinic acid, lovastatin or simvastatin, or fenofibrate are the preferred drugs for initial use. Fibric acid derivatives (e.g., clofibrate, gemfibrozil, bezafibrate, or fenofibrate) are all effective in the therapy of patients with type III hyperlipoproteinemia, as is nicotinic acid or lovastatin.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriosclerosis↗

PubMed1990

Promotion of extended-release niacin tablets at a Veterans Affairs medical center.

A program to modify the prescribing of antilipemic agents by promoting the use of extended-release niacin tablets is described. Between December 1987 and August 1988, pharmacists at a 1188-bed Veterans Affairs medical center observed a large increase in the number of outpatient prescriptions for antilipemic agents. In an attempt to control costs, a program to promote the use of extended-release niacin tablets for treating hyperlipemia was conducted during August and September 1988. Various educational materials on niacin were distributed to physicians. A display on therapy of hyperlipemia was featured at the monthly drug fair, and articles on niacin were presented during a journal club meeting of ambulatory-care clinicians. Pharmacists succeeded in having extended-release niacin tablets placed on the formulary in September. Data on the number of prescriptions filled for antilipemic agents were collected before and after the niacin promotional program. The number of prescriptions filled for extended-release niacin 500-mg tablets increased steadily during a six-month study period after the program ended; the number of prescriptions filled for regular niacin decreased by 50%. As prescribing of extended-release niacin increased, prescribing of colestipol, gemfibrozil, and probucol declined. The promotional program was well received by most of the medical staff. A program of education and formulary management successfully changed physician prescribing habits for antilipemic agents.

Cost Control↗

PubMed1988

Drug therapy of hypercholesterolemia.

The rationale for drug treatment of patients with hypercholesterolemia is that sustained reductions in the plasma concentrations of atherogenic lipoproteins will retard the development of atherosclerosis. Drug therapy should be initiated only after the exclusion of secondary factors and after an adequate trial of dietary therapy has failed to lower plasma cholesterol to a satisfactory level. The bile-acid sequestrants (cholestyramine and colestipol), nicotinic acid, and lovastatin are the most effective drugs for use in patients with primary hypercholesterolemia; these agents reduce total and LDL cholesterol concentrations by 15-35%. For patients with high concentrations of LDL cholesterol who concurrently have hypertriglyceridemia, nicotinic acid is the drug of choice, and bile-acid sequestrants are contraindicated. Combined therapy with drugs that have different mechanisms of action can be effectively utilized in the treatment of patients with severe hypercholesterolemia; combinations involving lovastatin, nicotinic acid, and bile-acid sequestrants are the most effective.

Bile Acids and Salts↗

PubMed1988

Drug and nutrient interactions in the elderly diabetic.

Elderly diabetics take more drugs than other groups of elderly patients. Their multiple drug use is largely explained by the drugs that they take for complications of their primary disease; these include cardiovascular drugs for macrovascular disease and antibiotics for secondary infections. They also take more drugs for control of other conditions that are etiologically associated with the development and progression of their diabetes, including antihypertensive agents, antilipemic agents and steroids, and nonsteroidal antiinflammatory drugs (NSAIDs), which are taken for relief of joint pain that is intensified by arthritic joints bearing excess weight. Drugs taken by elderly diabetics that contribute to the high prevalence of drug-nutrient interactions include those taken as antidiabetic agents, including both insulin and sulfonylureas as well as calcium channel blockers; they also include thiazides, loop diuretics, sulfa drugs, cephalosporin antibiotics, tetracyclines, antifungal agents, cholestyramine and colestipol, niacin, prednisone and other corticosteroids, and NSAIDs. These drugs and drug combinations contribute to the risk of hyperglycemia, which can cause nonketotic hyperglycemia in the elderly; to the risk of hypoglycemia, which in the elderly carries the risk of inducing pseudo-stroke; to the risk of drug-induced nutritional deficiencies from antilipemics and cephalosporins, which can induce vitamin K deficiency; to the risk of acute incompatibility reactions, including flush reactions from chlorpropamide, niacin, and calcium channel blockers; and to the risk of edema, anemia, and hyperkalemia from NSAIDs.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗