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PubMed1990

Comparison of hypocholesterolemic activities of the bile acid sequestrants cholestyramine and colestipol hydrochloride in cholesterol fed SEA quail.

The pharmacopolymer bile acid sequestrants cholestyramine and colestipol hydrochloride were mixed with a diet supplemented with 0.5% cholesterol at levels of 0.25%, 0.5%, and 1.0% for cholestyramine and 0.5% and 1.0% for colestipol and fed to young, male, SEA (Susceptible to Experimental Atherosclerosis) Japanese quail (Coturnix coturnix japonica) for a period of seven days. After treatment blood was obtained by venipuncture from non-fasted animals and analyzed for serum total cholesterol concentration. Cholestyramine significantly reduced total cholesterol concentrations at all doses in a dose dependent manner. Colestipol significantly reduced total cholesterol only at the 1.0% dose. Based on these observations, cholestyramine is significantly more potent for reducing serum cholesterol in hypercholesterolemic male SEA quail than is colestipol hydrochloride.

Animals↗

PubMed1990

Effects of simvastatin and cholestyramine in familial and nonfamilial hypercholesterolemia. Multicenter Group I.

Simvastatin, a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, was compared with cholestyramine resin in a randomized open-label 12-week multicenter study of 251 high-risk patients with familial or nonfamilial hypercholesterolemia. Simvastatin, 20 mg and 40 mg daily, produced mean reductions in total cholesterol of 26% and 33%, respectively, and reductions in low-density lipoprotein cholesterol level of 32% and 40%. Cholestyramine resin, 4 to 12 g twice daily, reduced total cholesterol and low-density lipoprotein cholesterol levels 15% and 21%, respectively. High-density lipoprotein cholesterol levels were increased 8% to 10% by all treatments. Plasma triglyceride levels were moderately decreased by simvastatin treatment, while triglyceride levels increased with cholestyramine treatment. Simvastatin was better tolerated than cholestyramine, which had numerous gastrointestinal tract side effects. No patient had a serious drug-related adverse event.

Adult↗

PubMed1988

Localization of 3-hydroxy-3-methylglutaryl CoA reductase and 3-hydroxy-3-methylglutaryl CoA synthase in the rat liver and intestine is affected by cholestyramine and mevinolin.

In the normal fed rat, both 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) synthase and HMG-CoA reductase are found in high concentrations in hepatocytes that are localized periportally. The majority of the liver cells show little or no evidence of either enzyme. Addition of cholestyramine and mevinolin to the diet resulted in all liver cells showing strong positive staining for both HMG-CoA reductase and HMG-CoA synthase. These two drugs increased the hepatic HMG-CoA reductase and HMG-CoA synthase activities 92- and 6-fold, respectively, and also increased the HMG-CoA reductase activity in intestine, heart, and kidney 3- to 15-fold. We used immunofluorescence and avidin-biotin labeled antibody to localize HMG-CoA reductase in the rat intestine. In rats fed a normal diet, the most HMG-CoA reductase-positive cells were the villi of the ileum greater than jejunum greater than duodenum. Crypt cells showed no evidence of HMG-CoA reductase. Addition of cholestyramine and mevinolin to the diet led to a dramatic increase in the concentration of HMG-CoA reductase in the apical region of the villi of the ileum and jejunum and in the crypt cells of the duodenum. Hence these two drugs affected both the relative concentration and distribution of intestinal HMG-CoA reductase. Cholestyramine and mevinolin feeding induced in the liver, but not intestine, whorls of smooth endoplasmic reticulum that were proximal to the nucleus and contained high concentrations of HMG-CoA reductase. Administration of mevalonolactone led to the rapid dissolution of the hepatic whorls within 15 min, at a time when there is little or no change in the mass of HMG-CoA reductase. We conclude that the whorls are present in the livers of rats fed cholestyramine and mevinolin because the cells are deprived of a cellular product normally synthesized from mevalonate.

Animals↗

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↗

PubMed1986

Effect of cholestyramine on acute diarrhoea in children receiving rapid oral rehydration and full feedings.

Cholestyramine 2 g twice daily for 3 days was compared to an equivalent placebo in a randomized double-blind study of infants hospitalized for acute diarrhoea. All the patients received oral rehydration with the WHO solution, and full feedings were reintroduced after 6-10 hours' rehydration. Cholestyramine therapy, initiated at the time of feedings, significantly shortened the duration of watery diarrhoea (0.8 +/- 0.6 vs. 2.3 +/- 1.6 days, p less than 0.005), although it did not significantly reduce the total stool volume. No adverse effects were associated with cholestyramine treatment. It is concluded that diarrhoea patients treated according to the present WHO guidelines may benefit from short adjunct therapy with cholestyramine.

Acute Disease↗

PubMed1986

The effect of cholestyramine on apolipoproteins in cholesterol-fed rabbits.

The changes in apolipoproteins on cholestyramine therapy associated with cholesterol feeding were compared to those observed in cholesterol-fed rabbits. Only one molecular species of apo B, identified as apo B-100, was present whatever the dietary or pharmacological treatment indicating the hepatic origin of apo B-containing lipoproteins in these conditions. Cholestyramine has a clear preventive effect on the rise of apo B and apo E which appear following cholesterol feeding. These changes are highly correlated with those of the plasma cholesterol level. In addition, cholestyramine induced a 50% increase in apo AI compared with normal rabbits. These data strongly confirm the beneficial effects of cholestyramine in the treatment of hypercholesterolemia.

Animals↗

PubMed1986

Use of oral gentamicin, metronidazole, and cholestyramine in the treatment of severe persistent diarrhea in infants.

Oral gentamicin, metronidazole, and cholestyramine were given either as single agents or in various combinations to infants who still required treatment after seven days in the hospital for persistent diarrhea. The effect of these drugs and the interactions between them were assessed by comparing daily stool output during treatment with that in the pretreatment period. The effect of the drugs on apparent nitrogen and fat absorption was also studied. On the first day of treatment the presence of cholestyramine was associated with a significantly greater decrease in stool output. This effect appeared to be largely due to an interaction with gentamicin. Thereafter, only gentamicin produced a significantly greater decrease in stool weight. At no stage was metronidazole of benefit. Gentamicin and cholestyramine also indirectly improved apparent nitrogen and fat absorption by reducing stool output. The combination of oral gentamicin and cholestyramine is recommended as a safe and effective way of treating infants with severe persistent diarrhea following acute gastroenteritis.

Cholestyramine Resin↗

PubMed1985

Cholestyramine-induced changes in low density lipoprotein composition and metabolism. I. Studies in the guinea pig.

In previous animal studies, bile acid sequestrant resins have been shown to increase the fractional catabolic rate (FCR) of a low density lipoprotein (LDL) tracer isolated from a normal donor animal and to increase hepatic LDL-receptor activity. In addition, in man, these resins are known to alter LDL composition such that low density lipoproteins are smaller, more dense, and have a decreased cholesterol:protein ratio. To determine whether metabolic consequences resulted from these changes in LDL composition, we fed cholestyramine chow (2% resin by weight) to guinea pigs, which lowered LDL cholesterol levels by 55%. LDL was isolated from control donors (C-LDL) and from cholestyramine-treated donors (CH-LDL). Compared to the C-LDL, the CH-LDL were smaller in size, depleted of cholesteryl ester and phospholipid, and had a marked decrease in their cholesterol:protein ratio. To determine whether the clearance of the altered CH-LDL was different from that of C-LDL, we labeled the two LDL preparations with 125I or 131I and simultaneously injected them into control and cholestyramine-treated guinea pigs. In 27/29 animals studied, the FCR of the CH-LDL was slower than that of C-LDL, demonstrating that the compositional changes alter the metabolism of CH-LDL. When C-LDL was used as the sole tracer in both control and treated animals, cholestyramine treatment increased the FCR by 41%; when CH-LDL was used as sole tracer, the increase in FCR on treatment was only 26%. This suggested that C-LDL was cleared more rapidly by the LDL-receptor pathway than was CH-LDL. Further support for this idea came from observations that C-LDL was degraded more readily by cultured fibroblasts and that nonenzymatic glucosylation abolished the difference in FCR between C-LDL and CH-LDL. These studies show that the effects of bile sequestration are complex and that the compositional changes produced have profound metabolic consequences. The implications of these observations for interpretation of LDL turnover studies are discussed.

Animals↗

PubMed1984

Use of cholestyramine in three patients with beta-acetyldigoxin, beta-methyldigoxin and digitoxin intoxication.

The effect of cholestyramine (8 g every 6 h by oral administration) on glycoside plasma concentrations of three patients with suicidal and accidental digitalis intoxications were studied. During treatment with cholestyramine the plasma concentrations of beta-acetyldigoxin and beta-methyldigoxin declined with half-lives of 20.4 or 30.0 h. These values are significantly shorter than the therapeutic half-lives reported in the literature. The digitoxin plasma concentration decreased with a half-life of 74.5 h during the first 2 days. When the digitoxin plasma level dropped under 40 ng/ml, the half-life increased, similar to the half-life without cholestyramine administration. From these case reports cholestyramine seems to be helpful in managing intoxications with digoxin derivates as well as with digitoxin.

Acetyldigoxins↗

PubMedDate not supplied

Paracetamol hepatic necrosis and its prevention by cholestyramine.

The aim of this study was to test the effect of cholestyramine on the hepatotoxic reactions due to paracetamol overdose. Wistar rats receiving a 5% aqueous solution of paracetamol at a dose of 750 mg/kg intraperitoneally showed a extensive necrosis within 24 hrs, whereas the addition of 4% cholestyramine to the diet inhibited the hepatic aggression. The protective mechanisms of cholestyramine against paracetamol overdose were admitted to be identical to those observed in the inhibition of liver cirrhosis induced by CCl4. The authors' hypothesis is that the paracetamol aggression and cholestyramine protection are both bile salts related.

Acetaminophen↗

PubMed1982

Cholestyramine treatment reduces postprandial but not fasting serum bile acid levels in humans.

Fasting serum concentrations of cholic acid, chenodeoxycholic acid, and deoxycholic acid were determined in healthy subjects and in patients with familial hypercholesterolemia before and during treatment with cholestyramine. The bile acids were analyzed by a specific isotope-dilution technique by using gas chromatography-mass spectrometry. Cholestyramine treatment did not change the fasting concentration of total bile acids, but the contribution of cholic acid was increased; those of chenodeoxycholic acid and deoxycholic acid were decreased. No decrease of fasting bile-acid concentrations in portal venous serum was seen in 2 cholestyramine-treated gallstone patients. The postprandial total bile-acid concentration was about 40% lower during cholestyramine treatment in healthy subjects, reflecting a reduced postprandial inflow of bile acids to the liver. This degree of interruption of the postprandial enterohepatic circulation may be sufficient to produce a near maximal bile-acid biosynthesis rate and to promote lowering of plasma cholesterol also in the fasting state. It is concluded that the postprandial bile-acid inflow to the liver may be more important as a regulator of bile-acid biosynthesis than is the fasting level of bile acids.

Bile Acids and Salts↗

PubMedDate not supplied

[Effect of cholestyramine on lipoprotein metabolism in rat blood].

The effect of cholestyramine on lipoprotein metabolism in the rat blood has been explored. Administration of cholestyramine changed both the concentration and the ratio of lipid components in all the classes of lipoproteins. Despite the fact that the activity of postheparin lipoprotein lipase was unchanged upon cholestyramine action, almost double rise in the activity of LChAT and an increase in the specific radioactivity of LDL attests to the intensification of VLDL metabolism. Therefore, the increased biosynthesis of VLDL by the liver is the main reason for the development of hypertriglyceridemia upon the action of cholestyramine.

Animals↗

PubMed1980

[Effect of cholestyramine and chenodesoxycholic acid on liver cirrhosis. An experimental study in rats].

The influence of cholestyramine and chenodeoxycholic acid on the induction of cirrhosis of the liver of the male Wistar strain rats was studied. The simultaneous dietary exposure of 1 g cholestyramine in 100 g diet prevented the development of cirrhosis induced by carbon tetrachloride. Whereas all the animals in the control group (CCl4-Exposure plus normal diet) developed cirrhosis, histologic examination showed cirrhosis in only 2 of 9 rats fed with diet containing cholestyramine. On the contrary, the exposure to chenodeoxycholic acid at a concentration of 1 g in 300 g diet potentiated the induction of cirrhosis. The experimental results support the clinical findings in which the administration of cholestyramine caused an improvement of liver function tests by cirrhosis.

Animals↗

PubMed1980

Comparison of the effects of cholestyramine and aluminium hydroxide on the biliary bile acid excretion in rats. An experimental model for the depletion of bile acids in bile.

Bile flow and biliary excretion of dihydroxy- and trihydroxy-bile acids have been determined in control, cholestyramine (250--2000 mg/kg p.os)- and aluminium hydroxide (250--2000 mg/kg p.os)-pretreated rats. Cholestyramine proved to be a more potent bile acid depleting agent than aluminium hydroxide. The depressing effect of cholestyramine on bile flow was also more significant than that of aluminium hydroxide. Cholestyramine-pretreatment seemed to be a suitable experimental model for the depletion of bile acids in rat bile.

Aluminum Hydroxide↗

PubMed1996

Effect of cholestyramine resin on single dose valproate pharmacokinetics.

Cholestyramine, a nonabsorbable anion exchange resin, has been reported to bind concomitantly administered drugs and decrease their bioavailability. The objective of the study was to determine the effect of cholestyramine on the plasma concentrations of valproic acid (VPA) following concurrent and staggered (VPA 3 hours before cholestyramine) dosing. Six healthy volunteers participated in an open-label, 3-way crossover study. In each phase fasting subjects received 250 mg of VPA followed by serial blood sampling for VPA plasma concentrations over a 37-hour period. In the concurrent and staggered phase the subjects received 4 g of cholestyramine (CHOL) twice daily 24 hours prior to and following the VPA dose. During the concurrent phase the coadministration of CHOL resulted in a decrease (p < 0.05) in the area under the curve (AUC) for VPA compared to VPA alone (415.2 +/- 113.2 mg*hr/l vs 489.2 +/- 153.0 mg*hr/l, respectively). When the same dose of each drug was administered 3 hours apart, the AUC for VPA (454.8 +/- 123.1 mg*hr/l) was not significantly decreased when compared to VPA alone (489.2 +/- 153.0 mg*hr/l). Also, the bioavailability relative to VPA alone was 86.2% +/- 7.1 for the concurrent phase and 95.3% +/- 13.6 for the staggered phase. Based on the AUC of VPA concurrent administration of CHOL significantly decreases VPA absorption and separating the doses of the 2 drugs by 3 hours may lessen the interaction.

Adolescent↗

PubMed2000

Bile Salt Anion Sorption by Polymeric Resins: Comparison of a Functionalized Polyacrylamide Resin with Cholestyramine.

Cholestyramine and a cross-linked polyacrylamide resin with lateral alkyl quaternary ammonium groups (QPDA12) were used to study their ability to bind several bile salt anions (including the cholate, glycocholate, taurocholate, and chenodeoxycholate), individually and competitively, from phosphate buffer solutions at room temperature. The latter resin showed high affinities for all the bile salt anions examined, while cholestyramine exhibited a high affinity only for the more hydrophobic chenodeoxycholate. However, for the binding with cholestyramine, cooperative effects were more pronounced, leading to the enhancement of sorption at higher concentrations. The Langmuir equation and its modified versions were used in the interpretation of both individual and competitive binding of bile salts. The data from competitive binding studies indicated that the presence of the tightly bound chenodeoxycholate did not significantly diminish the ability of QPDA12 resin to bind cholate. However, for cholestyramine, the sorption of chenodeoxycholate increased the relative binding affinity for the more hydrophilic cholate, revealing a novel "cooperative" effect involving different bile salt anions. The latter results suggest that the observed higher affinity of QPDA12 is brought about predominantly through the hydrophobic interactions with the pendant alkyl groups rather than with the resin backbone. Copyright 2000 Academic Press.

Journal Article↗

PubMed2002

Fatal drug interaction between cholestyramine and phenprocoumon.

We describe a patient with a prosthetic aortic valve who developed fatal valve thrombosis due to an interaction between phenprocoumon and cholestyramine. The general practitioner who had prescribed cholestyramine was aware of a potential interaction between these two drugs and the patient ingested cholestyramine exactly according to the rules of the manufacturer (>1 h before phenprocoumon). However, due to enterohepatic cycling and the long half-life of phenprocoumon, an interaction between these two drugs could not be avoided. We therefore recommend that cholestyramine not be administered to patients treated with drugs undergoing enterohepatic cycling, such as oral anticoagulants.

Journal Article↗

PubMedDate not supplied

Interaction of naproxen with cholestyramine.

'In vitro' and 'in vivo' studies were used to determine the interaction of naproxen, an anti-inflammatory agent, and cholestyramine, a hypocholesterolemic substance. Cholestyramine shows a marked affinity for naproxen and the intensity of this is governed by the pH values. The maximum amount of naproxen adsorbed by the resin is close to 2.2 mM g-1. The pharmacokinetics of naproxen was studied in eight healthy volunteers after concurrent oral administration in a single dose of 250 mg of naproxen and 4 g of cholestyramine. The resin causes an important delay in the incorporation of naproxen into the systemic circulation, though no significant modifications are seen to take place in any other pharmacokinetic parameters of the drug.

Adsorption↗