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PubMed1988

Use of cholestyramine in the treatment of digoxin intoxication.

The bile acid-binding resin cholestyramine was administered in a dose of 4 g every six hours to a patient with digoxin intoxication. The serum digoxin concentration declined rapidly, and the digoxin half-life decreased from 75.5 hours to 19.9 hours while cholestyramine was administered. All signs and symptoms of toxic reaction subsided during the period of cholestyramine therapy, which correlated with the decline in digoxin concentrations. Cholestyramine and a related agent, colestipol, presumably interrupt the enterohepatic recycling of digoxin to enhance elimination. These agents represent potentially useful adjunctive measures in the management of non-life-threatening digitalis intoxication.

Aged↗
PubMed1988

Treatment of hypercholesterolemia by a clinical nurse using a stepped-care protocol in a nonvolunteer population.

National trials have demonstrated that the incidence of myocardial infarction and coronary death can be decreased, and progression of atherosclerosis delayed or reversed, by administration of bile acid-binding resins. A cholesterol clinic was established to determine whether a simple protocol would be effective in a nonvolunteer population referred by practicing cardiologists. The clinic was operated by a nurse who followed a stepped-care protocol, similar in concept to that used for treatment of hypertension. In the treatment of 86 patients with type II hyperlipidemia (cholesterol level, greater than 6.85 mmol/L [greater than 265 mg/dL]; triglyceride levels, normal or mildly elevated), compliance with the protocol resulted in reductions in cholesterol level of 19% in patients treated with diet, 23% for those treated with diet plus a bile sequestrant (colestipol hydrochloride or cholestyramine resin), and 25% in those treated with diet plus other cholesterol-lowering drugs. This method of treatment was effective and may serve as a model for the management of large numbers of patients with this condition.

Cholesterol, Dietary↗
PubMed1978

Acute digoxin poisonings: review of therapy.

Acute digoxin poisoning, its recognition and management, are reviewed. The uses of syrup of ipecac, gastric lavage, activated charcoal, cholestyramine, colestipol, edetate sodium and cathartics as measures to terminate the drug exposure are discussed. Measures to hasten digoxin elimination, such as the use of furosemide, hemodialysis and digoxin-specific antibodies are reviewed. Supportive management may include treatment with atropine, phenytoin, lidocaine, propranolol, glucose, insulin and sodium polystyrene sulfonate. Proper management of digoxin poisoning involves the use of standard decontamination procedures (emesis or gastric lavage). Activated charcoal is strongly recommended, followed by rapidly acting cathartics. Antiarrhythmic therapy usually involves atropine sulfate and phenytoin sodium.

Acute Disease↗
PubMed1986

Contemporary recommendations for evaluating and treating hyperlipidemia.

The biochemistry, etiology, and evaluation of hyperlipidemia and its management, including dietary and drug therapies, are discussed. Strong evidence supports the role of increased cholesterol concentrations as an independent risk factor for coronary artery disease (CAD); however, evidence that elevated triglyceride concentrations are also an independent risk factor remains questionable. The cornerstone of the laboratory diagnosis of hyperlipidemia involves repeated measurement of serum or plasma cholesterol and triglyceride concentrations. The goals of therapy should be to reduce cholesterol or triglyceride concentrations or both to below the 75th percentile, modify co-existing risk factors, individualize the treatment, and minimize any adverse effects. Specific interventions must be determined on the basis of patient age, gender, etiology of hyperlipidemia, presence of other risk factors, and degree of lipid abnormality. The majority of patients may be managed with dietary therapy alone. The three-phase diet developed by the American Heart Association emphasizes a gradual reduction in cholesterol and fats with the substitution of polyunsaturated for saturated fats. Patients at risk for CAD with sustained elevations in plasma cholesterol concentrations above the 95th percentile or a triglyceride concentration above 500 mg/dL after an adequate dietary trial should be considered for drug therapy. The effects of cholestyramine and colestipol hydrochloride, niacin, dextrothyroxine, clofibrate, neomycin sulfate, probucol, gemfibrozil, and mevinolin and compactin on lipids and lipoproteins are reviewed. Hyperlipidemia should be managed systematically using information about the association between increased lipid concentrations and CAD, patient risk factors, and limitations of both diet and drug therapy.

Clofibrate↗
PubMed1986

Cholesterol and heart disease: current concepts in pathogenesis and treatment.

One of the modifiable risk factors associated with coronary heart disease (CHD) is hypercholesterolemia. This paper reviews the major plasma lipids and how they relate to coronary heart disease. Among blacks, CHD is the leading cause of death and disability. Blacks, in general, have been found to have lower low density lipoprotein (LDL), lower very low density lipoprotein (VLDL), and higher high density lipoprotein (HDL) levels than whites, but there is some evidence to suggest that lipid and lipoprotein profiles may differ in middle and upper socioeconomic subgroups of the black population from those reported for lower socioeconomic groups.The results of the Lipid Research Clinics Coronary Primary Prevention Trial and the National Heart, Lung and Blood Institute Type II Coronary Intervention Study have shown that lowering cholesterol levels in persons with high blood cholesterol will decrease the rate of coronary heart disease events.Diet therapy is the mainstay of treatment, and may lower blood cholesterol levels by 10 to 15 percent. For those unresponsive to diet therapy alone, a number of hypolipidemic drugs are available; some drugs (cholestyramine and colestipol) work by increasing the clearance of lipoprotein and others (clofibrate, nicotinic acid, and probucol) decrease the production of lipoproteins. The combination of diet and drugs may result in a decrease in cholesterol levels of 30 percent or more. For each 1 percent that cholesterol is decreased, there is a 2 percent decrease in coronary heart disease events.

Adult↗
PubMed1983

Pharmacologic therapy for the hyperlipidemic patient.

Drug therapy should be instituted only after appropriate diet treatment has been started and adequate baseline lipid and lipoprotein values are established. Nicotinic acid is useful in treating most lipoprotein disorders and the cutaneous flushing that develops during the early part of treatment is usually alleviated by aspirin. Cholestyramine and colestipol are nonabsorbable resins whose use is limited to type II hyperlipoproteinemia. Clofibrate is primarily effective in lowering triglyceride levels, but its clinical use has considerably declined following the World Health Organization study results that reported increased morbidity and mortality rates among patients receiving this drug. Based on the finding of increased mortality among a subset of patients participating in the Coronary Drug Project, dextrothyroxine is only recommended for treating patients who do not have clinically evident atherosclerotic heart disease. Probucol lowers total and low-density lipoprotein cholesterol levels, but has the undesirable effect of simultaneously reducing high-density lipoprotein levels.

Bile Acids and Salts↗
PubMed1980

[Pharmacology of fenofibrate (author's transl)].

Fenofibrate is one of several compounds with substituted-2-phenoxy-isobutyric acids and esters. In ageing rats receiving a hyperlipidaemic diet or injections of triton, fenofibrate lowers blood lipids as much as, or more than other antilipaemic agents. It is active in man against the main types (IIa, IIb and IV) of hyperlipoproteinaemia (HLP), and this activity is sustained throughout treatment (20 months in one study). In comparative studies, the effects of fenofibrate (400 mg/day) on the lipoprotein fractions tested were superior to those of clofibrate (2 g/day) and slightly superior to those of gemfibrosil (800 mg/day) and bezafibrate (600 mg/day). The drug also enhanced the lipid-lowering effects of colestipol. In doses of 300 mg/day fenofibrate produced a significant 13-15% decrease in apoprotein B with a concomitant 19-28% increase in apoprotein A. Fenofibrate was also found to normalize platelet aggregation in patients with type IIb HLP. In animals fenofibrate is excreted in equal amounts in the urine and faeces; in man, urinary excretion predominates (85-90%). The serum half-life curve is diphasic, with a rapid (5 hours) slope and a slow (17 hours) slope. In a 10-day study conducted on 10 volunteers serum levels of fenofibric acid remained remarkably constant, indicating lack of accumulation. New data on the mode of action are needed to further differentiate fenofibrate from clofibrate.

Animals↗
PubMed1979

Use of cholestyramine resin in the treatment of digitoxin toxicity.

Two case reports describing the treatment of digitoxin toxicity with cholestyramine resin are presented. Both female patients were receiving 100 microgram/day of digitoxin when toxicity occurred. In both patients, digitoxin was discontinued and hypokalemia was corrected. In patient 1, lidocaine hydrochloride and phenytoin sodium also were administered. Serum digitoxin levels were decreased from 43 ng/ml to 21.8 ng/ml and from 42 ng/ml to 29 ng/ml in patients 1 and 2, respectively, following administration of three 4-g doses of cholestyramine resin over a one-day period. Previous studies on the treatment of digitoxin intoxication with potassium chloride, phenytoin sodium, lidocaine hydrochloride, digitoxin-specific antibodies, colestipol hydrochloride and cholestyramine resin are discussed. Ion-exchange resins may be valuable adjuncts in the treatment of digitoxin intoxication but further studies of their utility are needed.

Aged↗
PubMed1993

Pharmacist management of a hyperlipidemia clinic.

A hyperlipidemia clinic in which a pharmacist provides primary care is described. The clinic was established at a Veterans Affairs medical center in January 1990. A pharmacist performs limited physical assessments, refers patients to other clinics as necessary, orders laboratory and diagnostic tests, and selects and monitors the use of lipid-lowering medications. Interventions are performed according to the pharmacist's clinical judgment; there is no set protocol. Recommendations for patient management are approved by an attending physician, who prescribes the antilipemic drugs. The pharmacist teaches patients about hyperlipidemia, the impact of diet and life-style, and the mechanism of action, administration, and adverse effects of the antilipemics prescribed. The pharmacist also monitors compliance, laboratory test values, and the response to treatment. Treatment is modeled after the recommendations of the National Cholesterol Education Program. If a patient has not achieved the targeted cholesterol concentration after receiving dietary therapy for three months, further education about diet and lifestyle is provided. If, after three more months, the cholesterol level remains high, drug therapy is begun. Four antilipemic drugs--colestipol, gemfibrozil, lovastatin, and niacin--are used in the clinic. Since it began operating, the clinic has enrolled 284 patients. Compliance with the lipid-lowering agents has ranged from 43% to 100%. Adverse effects have accounted for the majority of cases of noncompliance. A pharmacist provides primary care for patients with hyperlipidemia in an ambulatory-care clinic.

Chicago↗
PubMed1998

[Hyperlipidemia in children and adolescents: diagnosis and therapy].

Severe hyperlipidemias should be diagnosed and treated even in childhood and adolescence, because vascular lipid deposition in the form of fatty streaks and progressive atherosclerotic lesions start to develop early in life. The heterozygous form of familial hypercholesterolemia found in about 1 of 500 newborn infants, and polygenic forms of hypercholesterolemia, are the most frequent forms of primary genetic hypercholesterolemia found in children. Secondary hyperlipidemias, e.g. in diabetes mellitus, hypothyroidism and renal disease, are relatively frequent in children and adolescents and need to be searched for in the diagnostic evaluation, because they can be influenced by treatment of the underlying disorder. Children and adolescents with severe forms of hyperlipidemias should be diagnosed and treated early in life. Dietary modification is the basis of treatment of affected children and can lower LDL cholesterol by about 15-20%. In patients with severe hypercholesterolemia, dietary cholesterol intake should not exceed 150 mg/day in children or 250-300 mg/day in adolescents. Even more important is a reduction of the intake of saturated fats and trans fatty acids and their replacement by polyunsaturated and particularly monounsaturated fats. Some additional lowering of LDL cholesterol may be achieved by the preferential use of vegetable over animal proteins and of complex carbohydrates over sugars. Repeated motivation, counseling and intensive practical training of the patient and family, supported by appropriate teaching materials, are essential for effective dietary treatment. Additional drug treatment is considered in children from the age of 8-9 years of age onwards if, in spite of adequate dietary modification, LDL cholesterol remains above 190 mg/dl (4.9 mmol/l), or above 160 mg/dl (3.9 mmol/l) in the presence of additional risk factors. The drugs of first choice are anion exchange resins (colestyramine or colestipol) because of their well documented efficacy and safety. More convenient to take but often somewhat less effective is beta-sitosterol. If efficacy or compliance with resins or sitosterin is unsatisfactory, fibrates (e.g. bezafibrate, fenofibrate) may be considered as a drug of second choice. Cholesterol synthesis inhibitors are not recommended for general use in children at this time.

Adolescent↗
PubMedDate not supplied

[Clostridium difficile infections. Current aspects].

Clostridium difficile is a gram-positive anaerobe that forms subterminal spores. It is now one of major nosocomial pathogens, mainly in older patients, because of its ability to persist in the environment and to become established in the gastrointestinal tract once the natural microflora has been modified by antibiotic therapy. Toxigenic strains of C. difficile produce toxin A (enterotoxin) or toxin B (cytotoxin) or both with cause the cytotoxic effect "rounding". C. difficile can spread from patient to patient and, probably, the primary way by which the organism is spread is by health care workers. C. difficile causes intestinal diseases ranging by mild diarrhea (antibiotic associated diarrhea) to fatal pseudomembranous colitis (PMC). The current therapy is based on oral administration of metronidazole or vancomycin . In patients non responders or that continue to relapse can be used other forms of therapy: antibiotic (teicoplanine, bacitracine, rifamixine); anion exchange resin (colestipol, colestiramine); probiotic therapy (S. boulardii, lactobacilli and fecal enemas). New and improved studies will lead to new and better ways of treating patients and better understanding of this unusual pathogen and how it causes diseases.

Anti-Bacterial Agents↗
PubMed1998

Treating to meet NCEP-recommended LDL cholesterol concentrations with atorvastatin, fluvastatin, lovastatin, or simvastatin in patients with risk factors for coronary heart disease.

BACKGROUND: Our study compared use of atorvastatin, fluvastatin, lovastatin, and simvastatin for lowering low-density lipoprotein (LDL) cholesterol concentration in patients at risk for coronary heart disease (CHD). The goal was to reach the LDL cholesterol levels recommended by the National Cholesterol Education Program (NCEP). METHODS: A combined total of 344 men and women took part in this 54-week, multicenter, open-label, randomized, parallel-group, active-controlled, treat-to-target study. Patients were selected on the basis of their LDL cholesterol concentration and their risk for CHD. During treatment, doses were titrated at 12-week intervals to a maximum of 80 mg per day of atorvastatin and lovastatin, or 40 mg per day of fluvastatin and simvastatin, with colestipol added if necessary to attain the NCEP-recommended LDL cholesterol concentration. RESULTS: At the starting dose, atorvastatin decreased plasma LDL cholesterol significantly (P < .05) compared with the other reductase inhibitors, and the percentage of patients reaching target LDL cholesterol concentration at the starting dose was significantly greater in the atorvastatin group (P < .05). Overall, a significantly (P < .05) greater percentage (95%) of atorvastatin-treated patients achieved target LDL cholesterol concentration. The safety profile was similar among all reductase inhibitors tested. CONCLUSIONS: At the starting dose, a significantly (P < .05) greater percentage of atorvastatin-treated patients at risk for CHD reached the target LDL cholesterol concentration than patients with treated with other reductase inhibitors.

Adult↗
PubMed2002

Low- and high-density lipoprotein cholesterol and ischemic cerebrovascular disease: the bezafibrate infarction prevention registry.

BACKGROUND: Despite increasing evidence that beta-hydroxy-beta-methyglutaryl coenzyme A reductase inhibitors reduce the incidence of stroke in patients with coronary heart disease (CHD), the associations between blood lipid levels and cerebrovascular disease (CVD) are not clear. OBJECTIVE: To evaluate whether blood cholesterol level and its fractions are risk factors for stroke in a large group of patients with CHD. METHODS: We followed up 11 177 patients with documented CHD who were screened for but not included in the Bezafibrate Infarction Prevention study, a secondary prevention randomized clinical trial of lipid modification, and had no history of stroke for subsequent CVD. During a 6- to 8-year follow-up period, 941 patients were identified as having nonhemorrhagic CVD, of whom 487 had verified ischemic stroke or transient ischemic attack (TIA). RESULTS: Increases in age-adjusted rates of both nonhemorrhagic CVD and verified ischemic stroke or TIA were identified with increasing cholesterol and low-density lipoprotein cholesterol levels, decreasing high-density lipoprotein cholesterol levels, and decreasing percentage of total serum cholesterol contained in the HDL moiety. In logistic regression models, adjusting for clinical covariates, the following odds ratios (95% confidence intervals) were identified for lipid values in the upper vs lower tertile for the end point of nonhemorrhagic CVD: total cholesterol, 1.43 (1.20-1.70); low-density lipoprotein cholesterol, 1.52 (1.27-1.81), high-density lipoprotein cholesterol, 0.84 (0.70-1.00); and percentage of serum cholesterol contained in HDL, 0.69 (0.58-0.83). Similar trends appeared for the end point of verified ischemic stroke or TIA. CONCLUSION: These findings clearly support the role of total cholesterol and its fractions in prediction of ischemic CVD among patients with established CHD.

Adult↗
PubMed2003

Differential effects of lipid-lowering therapies on stroke prevention: a meta-analysis of randomized trials.

BACKGROUND: Previous overviews suggested that hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins), but not other lipid-lowering therapy (LLT), may reduce stroke incidence in coronary patients. OBJECTIVE: To investigate the amplitude and sources of heterogeneity of LLT effects on stroke prevention. METHODS: We searched the literature from 1966 to 2001 and then conducted a meta-analysis including randomized trials of primary and secondary coronary heart disease prevention, testing statins, nonstatin drugs, diet, or other interventions and providing data on stroke incidence. RESULTS: The meta-analysis (38 trials, 83 161 patients, mean follow-up of 4.7 years) showed a significant relative risk reduction (RRR) of strokes by LLT of 17% (P<.001), without significant heterogeneity between trials and between subgroups according to either the type of prevention (primary or secondary) or the type of LLT. The most substantial effects were obtained, however, with statins (RRR, 26%). Effect model analysis showed that treatment benefit appeared constant whatever the risk of stroke, suggesting that LLT may be effective in a population with a higher risk of stroke. Weighted regression showed a significant correlation between RRR of stroke and total cholesterol levels (baseline, final, and change). Only final cholesterol allowed clear separation between benefit (RRR>0) and no effect (RRR<0) of LLT on stroke incidence, with a cutoff for benefit of 232 mg/dL (6.0 mmol/L). CONCLUSION: Lipid-lowering therapy reduces stroke incidence in coronary patients, especially when total cholesterol level is lowered to less than 232 mg/dL (6.0 mmol/L), which explains the best results being obtained with statins.

Anticholesteremic Agents↗
PubMed1995

Update on the treatment of hypercholesterolemia, with a focus on HMG-CoA reductase inhibitors and combination regimens.

Numerous studies involving patients with hypercholesterolemia have demonstrated that reduction of lipid levels markedly reduces morbidity and mortality from cardiovascular disease. Diet alone may enable patients without established disease to attain target lipid levels, but pharmacotherapy generally is necessary for those with coronary artery disease. Choice of a suitable agent for monotherapy--a bile acid resin, niacin, or an HMG-CoA reductase inhibitor--may be determined by patient phenotype. For resistant cases, therapy combining an HMG-CoA reductase inhibitor with another agent generally is effective and well tolerated.

Cholestyramine Resin↗