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PubMed1988

Development of femoral atherosclerosis in hypercholesterolemic patients during treatment with cholestyramine and probucol/placebo: Probucol Quantitative Regression Swedish Trial (PQRST): a status report.

The Probucol Quantitative Regression Swedish Trial is being performed to investigate the effects of probucol on atherosclerosis in the femoral artery. Probucol is combined with cholestyramine and dietary management in hypercholesterolemic patients, and the effects of atheroma developing in the femoral artery will be followed by a quantitative angiographic technique. A randomly selected control group is also being managed by dietary therapy and cholestyramine, but receives placebo instead of probucol. The treatment time in this double-blind trial is 3 years, and femoral angiography is performed yearly. Detailed lipoprotein and apolipoprotein analysis are performed at monthly intervals. The basic study design is described here, and some results from the open prerandomization phase of the study are presented.

Arteriosclerosis↗

PubMed1978

Hirschsprung's enterocolitis, prostaglandins, and response to cholestyramine.

An infant with Hirschsprung's enterocolitis developed a fulminant secretory diarrhea unresponsive to all conventional therapy until cholestyramine was administered. A 12-fold decrease in prostaglandin E (PGE) levels in the colostomy fluid was documented in response to cholestyramine therapy. It is postulated that increased PGE activity, enterotoxin, and bile acid malabsorption may be involved in the enterocolitis of Hirschsprung's disease.

Cholestyramine Resin↗

PubMed1997

Acceptability and compliance with two forms of cholestyramine in the treatment of hypercholesterolemia in children: a randomized, crossover trial.

OBJECTIVE: To compare the acceptability, compliance, and effectiveness of two forms of cholestyramine resin in the treatment of hypercholesterolemia in children. STUDY DESIGN: Patients aged 10 to 18 years with familial hypercholesterolemia were enrolled in a randomized, crossover trial of two 8-week periods of either a pill or powder form of cholestyramine at a dose of 8 gm/day. RESULTS: Of 40 children enrolled, 38 completed both medication periods, with a median age of 13 years (range, 10 to 18). At the end of the study, 82% preferred the pill form, 16% the powder form and 2% neither form. Mean (+/-SD) compliance as assessed by the amount of medication taken was significantly greater for pills (61% +/- 31%) than powder (50% +/- 30%, p = 0.01). The form of the medication increased compliance by at least 25% for 16 patients (42%), 13 in favor of pills and 3 in favor of powder. Compliance was not associated with patient attitudes and perceptions of hypercholesterolemia, demographics, family history, previous experience with lipid-lowering medication, or lipid profile parameters. Significant mean reductions in low-density lipoprotein cholesterol concentrations were noted for both pills (-10% +/- 20%, p = 0.006) and powder (-15% +/- 17%, p = 0.0001), with no significant difference between forms (p = 0.16). CONCLUSIONS: A change in bile acid-binding resin formulation from powder to pills significantly increases acceptability and compliance in some children with hypercholesterolemia.

Adolescent↗

PubMed1991

Loss of dental enamel in a patient taking cholestyramine.

During treatment with cholestyramine for high concentrations of cholesterol, extensive loss of dental enamel occurred in a young boy. This outcome is thought to be attributed to mixing the cholestyramine in Kool-Aid and swirling the mixture in the mouth before swallowing.

Bone Density↗

PubMed1981

Superiority of partial ileal bypass over cholestyramine reducing cholesterol in familial hypercholesterolaemia.

Low density lipoprotein (LDL) turnover studies were conducted on three occasions in each of six patients with heterozygous familial hypercholesterolaemia (FH)-on diet, after 1 month on cholestyramine 16 g/day, and 2 months after partial ileal bypass. Partial ileal bypass lowered total and LDL cholesterol levels and increased the fractional catabolic rate of LDL to a greater extent than did cholestyramine; this difference presumably reflects the greater increase in bile acid excretion induced by the surgical procedure. Studies in two other heterozygotes showed that partial ileal bypass specifically enhanced receptor-mediated catabolism of LDL. The findings support the concept that therapeutic stimulation of bile acid synthesis increases the rate of receptor-mediated uptake and degradation of LDL by the liver.

Adult↗

PubMed2001

Analysis of the physicochemical interactions between Clostridium difficile toxins and cholestyramine using liquid chromatography with post-column derivatization.

A potential therapy for antibiotic-associated pseudomembranous colitis is to bind Clostridium difficile toxins A and B using cholestyramine, a hydrophobic anion exchange medium. Frontal analysis in isotonic phosphate buffer was studied using post-column derivatization with o-phthalaldehyde, which gave a highly sensitive (> or =30 ng) flow-through analysis. Following load (1.5-3.0 microg toxin/3.6 mg), toxin A was bound at a slightly higher capacity than B, due to slower kinetics. A salt gradient eluted roughly 20% of bound toxin A with 0.6 M NaCl and toxin B with 1.1 M NaCl, hence toxin A showed weaker electrostatic affinity. The remainder of toxin A (65%) and some of toxin B (10% out of 50%) were eluted using a subsequent gradient to 60% acetonitrile in normal saline, which measured predominantly hydrophobic binding. Low and high affinity populations of both toxins were observed. Glycocholic acid or amino acids were competitive binders, although these components had little effect on the toxin A population bound primarily through ionic interactions. Competitive protein constituents in hamster cecal contents were also profiled. These results help to explain the variable clinical response in using cholestyramine to treat colitis. Using quaternary amine-polyhydroxymethacrylate (PHM) ion exchange chromatography, a trend for increased binding at higher pH was observed, especially for toxin A. Binding to strong cation exchange resins (sulfonate-PHM) was not observed. A range of reversed phase media retained both toxins, although recovery was very poor relative to protein standards. Size exclusion chromatography with light scattering detection showed that toxin B exists in different aggregation states, while toxin A remains monomeric.

Animals↗

PubMed1996

Bile acid measurements using a cholestyramine-coated TSM acoustic wave sensor.

A novel chemical sensor for bile acids is described. A 10-MHz piezoelectric crystal operating in the thickness-shear mode (TSM) is coated on one side with cholestyramine resin and mounted in a batch-mode sensor block which exposes the coating to solution. After sample injection, the binding process is observed in real time as a drop in frequency as the bile salt binds to the coating, reaching > 90% completion within 10 min with most of the binding occurring within the first minute. Linear calibration curves are generated with sensitivity increasing in the order cholate approximately glycocholate < taurocholate < < taurodeoxycholate. Detection limits in water are in the range 0.2-9 nmol and are better than those observed in phosphate buffer. A multistep regeneration protocol allows the coating to be reused more than 400 times over a period of several months. Precision for replicate injections is approximately 10% RSD and depends on the reproducibility of the regeneration and injection steps. In terms of the binding process, hydrophobic interactions are observed to be of importance in the ability of bile salts to displace other counterions. However, anions with greater charge density also appear to compete effectively for binding sites on the resin. In particular, at equimolar concentrations of citrate and bile salt, the trivalent citrate anion reduces the amount of bile salt binding by approximately 40%. This suggests that the efficiency of cholestyramine-based bile salt sequestering drugs used in the reduction of hypercholesterolemia may be improved by eliminating citric acid as an excipient and avoiding the use of fruit juices during ingestion.

Anion Exchange Resins↗

PubMed1990

Pharmacokinetics and pharmacodynamics of pravastatin alone and with cholestyramine in hypercholesterolemia.

The pharmacokinetics, pharmacodynamics, and safety of pravastatin, a new selective 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, were evaluated during monotherapy and with subsequent concomitant cholestyramine therapy in 33 patients with primary hypercholesterolemia in this randomized study. After 4 weeks, pravastatin monotherapy (5 mg, 10 mg, and 20 mg twice daily) significantly decreased total cholesterol by 17% to 24% (p less than 0.001 versus baseline) and low-density lipoprotein cholesterol by 23% to 35% (p less than 0.001). High-density lipoprotein cholesterol increased by 8% to 9%, and triglycerides decreased by 6% to 9%. The area under the serum concentration-time curve and maximum serum concentration of pravastatin showed dose-proportionality; time to maximum serum concentration and serum elimination half-life were independent of dose. When added to pravastatin therapy, cholestyramine enhanced the lipid-lowering effects of pravastatin. After 4 weeks of combination therapy, total cholesterol was reduced by 32% to 38% (p less than 0.001 versus baseline), and low-density lipoprotein cholesterol was reduced by 47% to 56% (p less than 0.001). High-density lipoprotein cholesterol increased by 11% to 18% (p less than 0.05). Pravastatin was well tolerated; no clinical adverse events directly attributable to the drug were reported.

Adult↗

PubMed2000

Induction of bile acid synthesis by cholesterol and cholestyramine feeding is unimpaired in mice deficient in apolipoprotein AI.

High density lipoprotein (HDL) cholesterol is believed to be preferentially utilized for bile acid synthesis and biliary secretion. In mice, the deletion of apolipoprotein AI (apo AI), the major apolipoprotein in HDL, results in very low plasma HDL-cholesterol levels. This article describes bile acid metabolism in apo AI-deficient (Apo AI(-/-)) mice and their C57BL/6 (Apo AI(+/+)) controls fed either a basal rodent diet alone or containing cholesterol or cholestyramine. Basal plasma HDL-cholesterol levels in the (-/-) mice (<10 mg/dL) were less than 20% of those in their (+/+) controls, but there were no phenotypic differences in either the relative cholesterol content of gallbladder bile, bile acid pool size and composition, fecal bile acid excretion or the activity of, or mRNA level for, cholesterol 7alpha-hydroxylase. However, compared with their (+/+) controls, the (-/-) mice absorbed more cholesterol (33 vs. 24%) and manifested lower rates of hepatic sterol synthesis (534 vs. 1,019 nmol/h per g). Cholesterol feeding increased hepatic cholesterol levels in the (+/+) animals from 2.7 to 4.4 mg/g and in the (-/-) mice from 2.6 to 8.1 mg/g. Bile acid synthesis increased 70% in both genotypes. Cholestyramine feeding stimulated bile acid synthesis 3.7 fold in both (-/-) and (+/+) mice. We conclude that the virtual loss of HDL-cholesterol from the circulation in apo AI deficiency has no impact on the ability of the hepatocyte to adapt its rate of bile acid synthesis in concert with the amount of cholesterol and bile acid returning to the liver from the small intestine.

Animals↗

PubMed1982

Catabolism of low density lipoproteins by perfused rabbit livers: cholestyramine promotes receptor-dependent hepatic catabolism of low density lipoproteins.

Rabbits fed a wheat starch/casein diet develop a marked hypercholesterolemia accompanied by a decrease in the number of EDTA-sensitive binding sites on plasma membrane fractions of the liver for low density lipoproteins (LDL) and beta-migrating very low density lipoproteins [Chao, Y.-S., Yamin, T.-T. & Alberts, A. W. (1982) J. Biol. Chem., in press]. Inclusion of 1% cholestyramine resin in this diet prevents the increase in plasma cholesterol, increases the removal of LDL from plasma, and increases the number of hepatic plasma membrane LDL-binding sites. To determine the functional role of hepatic LDL-binding sites in the catabolism of LDL, we studied the catabolism of (125)I-labeled LDL ((125)I-LDL) by in situ perfused rabbit livers in a recirculating system. The rate of catabolism was measured from the increment of nonprotein-bound radioiodine in the perfusate. The receptor-dependent catabolism of LDL by the liver was calculated from the difference of hepatic catabolism of (125)I-LDL and catabolism of (125)I-labeled cyclohexanedione-modified LDL, which does not bind to LDL receptors. The data show that about 74% of LDL catabolized by perfused livers from chow-fed rabbits is through the receptor-dependent pathway and 26% is through the receptor-independent pathway. In rabbits fed a cholesterol diet, the hepatic catabolism of (125)I-LDL is reduced, and the receptor-dependent catabolism of (125)I-LDL is abolished. In rabbits fed the wheat starch/casein diet, the receptor-dependent catabolism of (125)I-LDL is reduced by 40% when compared with hepatic catabolism in chow-fed rabbits. Perfused livers from rabbits fed the wheat starch/casein diet supplemented with 1% cholestyramine show a 5,4-fold increase of receptor-dependent catabolism of (125)I-LDL when compared with that of livers from rabbits fed the wheat starch/casein diet alone. Thus, these studies demonstrate that the change in the number of rabbit hepatic membrane LDL receptors induced by dietary manipulation and drugs is correlated to the functional rate of removal of LDL by the liver.

Animals↗

PubMed1978

Adsorption of bile salts from aqueous solution by plant fibre and cholestyramine.

1. Adsorption of bile salts by dietary fibre is believed to promote their excretion and hence to reduce the serum cholesterol level in man and experimental animals. 2. We have tested a number of plant fibre fractions and other related materials for their ability to adsorb bile salts from aqueous solution. The "insoluble" plant fractions were from "dry grain" (a residue from brewing), apple, wheat bran, lucerne (Medicago sativa), soya beans, mung beans (Phaseolus mungo), chick peas (Cicer arietinum), rolled oats, spinach (Spinacia oleracea), sunflower seeds, sawdust and sheep faeces. The other materials were cholestyramine, pectin and lignins prepared from wheat bran and from sawdust. 3. Only cholestyramine and the fibre from lucerne, soya beans, mung beans, chick peas, spinach, and sunflower seeds adsorbed enough of either sodium cholate or sodium deoxycholate for adsorption to be detectable. 4. This result conflicts with a report that the lignin component of dietary fibre is responsible for adsorption of bile salts. 5. Adsorption of bile salts, when it occurs, may depend on the presence of saponins bound to the fibre.

Adsorption↗

PubMed1975

Cholesterol kinetic analysis in normal and cholesterol-fed rabbits; effects of saturated versus polyunsaturated fat and of cholestyramine.

A model for cholesterol metabolism in rabbits has been demonstrated based on kinetic analysis and total carcass analysis. As has been shown for humans and primates, the model conforms to a two-exchangeable pool model with a third pool not exchangeing during the time interval studied. Alterations in turnover rate, sizes of pools, and exchange rates were demonstrated when rabbits were fed diets containing increased amounts of cholesterol and fat. Evidence was presented that indicated that the there may be differences in tissue distribution of cholesterol, dependent on whether the fat fed with choleserol is saturated or polyunsaturated. These differences include: in rabbits fed cholesterol plus coconut oil is compared with those fed cholesterol plus corn oil, the ratio of the amount of cholesterol in plasma to the amount of cholesterol in pool B was higher, and the rate constant for transfer from pool B was higher. The serum cholesterol concentration of rabbits fed cholesterol plus coconut oil was lowered slightly by feeding cholestyramine. Cholestyramine administration at the dose fed failed to produce statistically significant alterations in pool sizes or serum cholesterol concentration in control rabbits; it did lower serum cholesterol concentration in rabbits fed cholesterol plus coconut oil.

Animals↗

PubMed1995

Cholesterol 7 alpha-hydroxylase activity is increased by dietary modification with psyllium hydrocolloid, pectin, cholesterol and cholestyramine in rats.

Sources of dietary fiber known to alter cholesterol metabolism and/or bile acid pool size were fed to rats, and activity of the rate-limiting step in bile acid synthesis, cholesterol 7 alpha-hydroxylase, was measured. In the first experiment, semipurified diets containing 5% cellulose, psyllium hydrocolloid, pectin or oat bran as dietary fiber sources or 2% cholestyramine were fed to groups of 10 male Wistar rats for 4 wk. In the second experiment, groups of six rats were fed diets containing 5% cellulose, rice bran, oat bran or psyllium with and without 0.25% cholesterol. In the first experiment, the activity of cholesterol 7 alpha-hydroxylase (pmol.min-1.mg protein-1) was highest in the cholestyramine-treated group (95.6 +/- 3.6), followed by groups fed psyllium (35.5 +/- 3.5) or pectin (36.0 +/- 4.5), which exhibited more than twice the enzyme activity of groups fed cellulose (16.9 +/- 1.9) or oat bran (12.3 +/- 2.0). In the second experiment, feeding cholesterol resulted in significantly higher enzyme activity when cellulose (65%), oat bran (118%) and rice bran (60%) were fed, but no difference in activity was observed when cholesterol was added to the psyllium-containing diet. Higher activity of cholesterol 7 alpha-hydroxylase when pectin or psyllium rather than cellulose was fed may explain the almost twofold higher bile acid pool sizes previously reported in response to feeding either of these fibers. These data support the hypothesis that the hypocholesterolemic effect of soluble fibers is modulated through increased synthesis and therefore pool size of bile acids.

Animals↗

PubMed1990

Efficacy and safety of simvastatin (alone or in association with cholestyramine). A 1-year study in 66 patients with type II hyperlipoproteinaemia.

The effects and safety of simvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, were investigated alone or in association with cholestyramine in 66 patients with hypercholesterolaemia, in a 1-year study. In type IIa hypercholesterolaemia (41 patients), the association was more effective than simvastatin used alone in lowering total cholesterol (37% vs 29%) and LDL-cholesterol (45% vs 37%). In type IIb hypercholesterolaemia (23 patients), the association simvastatin-cholestyramine did not appear more effective than simvastatin used alone. The decrease of apoprotein B was parallel to the LDL-cholesterol decrease. Apoprotein A1 did not change significantly. The long-term safety of simvastatin was good. No lens opacity was noted. The most serious side-effect in our study was myolysis which occurred in two patients with a marked increase in creatine phosphokinase.

Adult↗

PubMed1991

Combination therapy with lovastatin and guar gum versus lovastatin and cholestyramine in treatment of hypercholesterolemia.

Sixty-two patients (34 men and 28 women) aged 19-64 years, half of whom had familial hypercholesterolemia, treated initially for 18 weeks with lovastatin alone were randomly allocated either to lovastatin (L) and cholestyramine (16 g/day) or lovastatin and guar gum (L + GG 20 g/day) treatment for 18 additional weeks to compare the hypocholesterolemic effects of these two combination therapies. The patients were selected for this study from a larger study of patients (n = 120) with severe hypercholesterolemia [serum total cholesterol (serum Chol) 6.5-16.3 mM before treatment], and only those patients in whom serum Chol after lovastatin alone (dose 80 mg/day) remained greater than or equal to 5.2 mM were eligible for evaluation of combination therapies. Serum Chol decreased from 10.6 +/- 1.6 to 5.9 +/- 1.3 mM (mean +/- SD) (p less than 0.001) and low-density lipoprotein cholesterol (LDL Chol) from 8.5 +/- 1.8 to 4.1 +/- 1 mM (p less than 0.001) in patients treated with L + GG (values before the beginning of lovastatin and at the end of the combination therapy). The respective changes were from 10.9 +/- 2.2 to 5.5 +/- 1.2 mM (p less than 0.001) and from 8.7 +/- 2.3 to 3.5 +/- 1.2 mM (p less than 0.001) in patients treated with lovastatin and cholestyramine (L + C). At the end of the study, both serum Chol (p less than 0.005) and LDL Chol (p less than 0.01) were significantly lower with L + C than with L + GG.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Preventing myocardial infarction: cholestyramine (Questran) and other hypolipidemics.

For decades the association between serum cholesterol and atherosclerotic heart disease has been recognized; the higher an individual's serum cholesterol concentration, the greater the risk of myocardial infarction and other manifestations of coronary artery disease. Many of the hypolipidemics (drugs that reduce levels of lipids in the blood) have been available for more than 10 years, but only last year was one of these agents, cholestyramine (Questran), approved for use in the prevention of coronary heart disease. The purposes of this article are to describe the events that led to the approval of this indication for cholestyramine (but not for the other hypolipidemics), to explore the factors that primary health care practitioners should consider in the management of hypercholesterolemia and to anticipate future developments in hypolipidemic therapy.

Cholestyramine Resin↗

PubMed1990

Acipimox in combination with low dose cholestyramine for the treatment of type II hyperlipidaemia.

1. This study was designed to examine the effects of acipimox 250 mg three times daily and cholestyramine 4 g three times daily on plasma lipids and lipoproteins in 28 hypercholesterolaemic individuals in a prospective double-blind placebo controlled parallel group fashion. 2. Combined treatment with the two agents produced a mean reduction of 27% in plasma total cholesterol and a 32% fall in LDL cholesterol. Plasma triglyceride was reduced by 13% due to a 38% decrement in VLDL cholesterol. 3. In comparison treatment with cholestyramine alone resulted in a 12% fall in plasma cholesterol and a 15% fall in LDL cholesterol. In this group triglycerides and VLDL showed no significant change. 4. Studies of HDL subfraction mass showed that the addition of acipimox to resin therapy produced a mean increment of 45% in HDL2. 5. These results demonstrate the effectiveness of such a well tolerated low dosage combination therapy.

Cholesterol↗

PubMed1975

Lack of effect of cholestyramine on the pharmacokinetics of clofibrate in man.

The study was undertaken to determine whether cholestyramine (16 g daily) interfered with clofibrate absorption when the two drugs were given together. Fifteen patients taking 1 g of clofibrate twice daily (for 2 to 416 weeks) participated in the study. Clofibrate (as the acid, p-chlorophenoxyisobutyric acid, CPIB) was quantified by thin-layer and gas-liquid chromatography. In patients taking clofibrate only, mean plasma CPIB concentration before the morning dose of clofibrate was 123 mug/ml. Peak levels were reached 3.5 hours after drug intake, the mean peak plasma CPIB concentration being 193 mug/ml. Absorption of CPIB exceeded 99%. Ninety-eight percent of the daily CPIB-intake was excreted in the urine, 61% being conjugated. In vivo degradation of CPIB did not occur. Free and conjugated CPIB was present in bile (mean fasting level being 55 mug/ml. The decay of radioactive CPIB in plasma was not log-linear: the mean t 1/2 of the first exponential was 0.45 hours, and of the second 15.1 hours. The pool size in 3 patients 3 hours after the morning dose of clofibrate was 1054 mg. CPIB was not detectable in adipose tissue, and kinetic data gave no hint of drug accumulation in patients on long-term therapy. In 6 patients given cholestyramine together with clofibrate, there was no significant alteration in fasting plasma CPIB levels, 24-hour urinary and faecal excretion of CPIB or in the half-life and pool size of the drug. A short delay in reaching peak plasma CPIB levels was the only consistent finding.

Adolescent↗