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PubMed2006

Influence of cholestyramine on the pharmacokinetics of rosiglitazone and its metabolite, desmethylrosiglitazone, after oral and intravenous dosing of rosiglitazone: impact on oral bioavailability, absorption, and metabolic disposition in rats.

The possible influence of the bile acid-sequestering agent cholestyramine (CSA), which is a basic co-medication in hypercholesterolemic patients, on the pharmacokinetics of rosiglitazone (RGL) and its circulating metabolite desmethylrosiglitazone (DMRGL) was investigated following a single oral and intravenous dose of RGL to Wistar rats. The pharmacokinetic parameters of RGL and DMRGL were evaluated following oral or intravenous administration of RGL to rats at 10 mg kg-1 with and without pre-treatment (0.5 h before RGL administration) of CSA at 0.057, 0.115, 0.23 and 0.34 g kg-1 doses. With an increase in CSA dose there was dose-dependent decrease in area under the curve (AUC)(0-infinity) and Cmax with no change in Tmax, Kel and t1/2 values for both RGL and DMRGL following oral administration of RGL. The oral bioavailability of RGL was reduced by 19.9, 35.6, 53.8 and 72.0% in rats following pre-treatment with CSA at 0.057, 0.115, 0.230 and 0.340 g kg-1, respectively. There was no change in the above-mentioned pharmacokinetic parameters for RGL and DMRGL in rats when RGL was given intravenously following pre-treatment with the above-mentioned oral doses of CSA. Another objective of the study was to determine the effect of staggered oral CSA dosing at 1, 2 and 4 h after oral RGL administration at 10 mg kg-1. AUC(0-infinity) of RGL and DMRGL was reduced following CSA staggered administration at 1 h, whereas 2- and 4-h staggered dose administration of CSA had no effect on the AUC(0-infinity) of RGL and DMRGL. Irrespective of CSA staggered dose administration there was no change in other pharmacokinetic parameters, namely Cmax, Tmax, Kel and t1/2. The apparent formation rate constant (Kf) of DMRGL was also calculated to show that only the absorption of RGL was affected, not the apparent formation rate of DMRGL. The authors also studied the in vitro adsorption of RGL (100, 250, 500 microg ml-1) at various pH conditions (pH 2, 4 and 7) and different concentrations of CSA (15, 30, 60 and 120 mg ml-1). The percentage binding of CSA was in the range 50-72% (at pH 2), 74-89% (at pH 4) and 97-100% (at pH 7). In conclusion, we carried out a systematic investigation demonstrating mechanistically the interaction potential of RGL when co-administered with CSA. The applicability of the metabolite data after intravenous and oral dosing and pH-based binding experiments further adds credence to the key findings.

Administration, Oral↗

PubMed1998

Dietary cholestyramine reduces ochratoxin A-induced nephrotoxicity in the rat by decreasing plasma levels and enhancing fecal excretion of the toxin.

Ochratoxin A (OTA) is a mycotoxin that may contaminate animal feed (oat, barley, and rye) and food (wheat, rice, coffee, beer, pig meat), leading to major health problems (e.g., nephropathy) in several animal species including humans. Several methods have been tested to reduce the toxicity of OTA in animals but with limited success. In rats, the effect of cholestyramine (CHA), a bile acid-binding resin, was investigated on OTA-induced nephrotoxicity and bioavailability. Animals were fed semisynthetic diets containing two levels of OTA: 1 or 3 ppm. At each level of OTA, the diets were enriched with 0.1, 1, and 5% of CHA. The results showed that CHA decreased the concentration of OTA in plasma. At 1 and 3 ppm of OTA in the diet, CHA is effective at a level of 0.1% and 5%, respectively. The excretion of OTA and its metabolites (ochratoxin alpha and hydroxylated ochratoxin A) in bile and urine was also decreased by addition of 5% CHA in the diet. This was associated with an increase of OTA excretion in feces. Enzymuria and renal morphology revealed that dietary CHA can decrease OTA-induced nephrotoxicity, probably by reducing renal exposure to the toxin. In conclusion, CHA can reduce OTA concentrations in plasma as well as reducing nephrotoxicity, which may be attributed to a decrease of bioavailability and/or enterohepatic circulation of the toxin.

Acetylglucosaminidase↗

PubMed1982

Effect of mineral oil and/or cholestyramine in the diet on biliary and intestinal elimination of 2,4,5,2',4',5'-hexabromobiphenyl in the rhesus monkey.

Addition of mineral oil to the diet (5%) of two rhesus monkeys that were dosed 29 wk earlier with 2,4,5,2',4',5'-hexabromobiphenyl (HBB) produced a 175% increase in fecal excretion of HBB. A third rhesus monkey was provided with a complete biliary bypass, which permitted the reintroduction of the monkey's own bile or the introduction of the same amount of exogenous bile, which was obtained from control donor monkeys. This experimental design made it possible to measure the portion of fecal excretion that was due to biliary elimination and the portion that was due to intestinal elimination. The effect of mineral oil and/or cholestyramine (CSA) on biliary and intestinal elimination of HBB in the rhesus monkey was then investigated. The results show that (1) fecal excretion of HBB and/or metabolites is due to both biliary and intestinal elimination; (2) during the first 2 wk after completion of dosing, mineral oil does not influence fecal excretion of HBB significantly; (3) 6-7 wk after completion of dosing, mineral oil enhances fecal excretion of HBB by 50%; (4) 8 wk after the last dose of HBB, 4% CSA in the diet increases fecal excretion of HBB and/or metabolites by about 50%; (5) mineral oil specifically stimulates intestinal elimination of HBB; and (6) combined administration of mineral oil and CSA results in an additive effect.

Animals↗

PubMed1979

The ability of cholestyramine resin and other adsorbents to bind Escherichia coli enterotoxins.

Several adsorbent materials were evaluated for their ability to bind Escherichia coli enterotoxins. Cholestyramine, a strong anion-exchange resin, bound the heat-labile and the heat-stable types of enterotoxin and reduced significantly their effects in some animal models. However, its efficacy in the treatment of diarrhoeic piglets appeared to be adversely affected by the presence of milk in the alimentary tract.

Adsorption↗

PubMed1976

Lecithin: cholesterol acyltransferase activity and cholestyramine resin therapy in man.

The effect of the bile-acid-sequestering agent cholestyramine on esterification of plasma cholesterol has been studied in vitro. No change in the activity of plasma lecithin: cholesterol acyltransferase was found by either of the two assay methods employed. Similarly the resin did not produce any significant change in the ability of plasma to act as substrate for a given lecithin:cholesterol acyltransferase source. It is concluded that the frequently reported relationship between plasma cholesterol concentration and lecithin:cholesterol acyltransferase activity does not represent cause and effect. Also other variables influenced by bile-acid-sequestering agents, such as hepatic cholesterol synthesis, are unlikely to be major determinants of plasma lecithin: cholesterol acyltransferase activity.

Acyltransferases↗

PubMed1991

Effect of cholestyramine treatment on biliary lipid secretion rates in normolipidaemic men.

This study was designed to clarify the effect of bile acid sequestrant treatment on the total biliary output rates of cholesterol, phospholipids and bile acids in man, and to correlate these changes with the alterations in plasma lipoprotein levels. For this purpose nine healthy, normolipidaemic men were treated with 16 g of cholestyramine daily over a period of 4 weeks, and the biliary secretion rates were measured by a duodenal perfusion technique. Resin therapy, which profoundly increases de novo synthesis of bile acids, resulted in a lowering of total plasma cholesterol levels, mainly due to a 35% reduction in low density lipoprotein (LDL) cholesterol, and in a 33% increase in plasma triglyceride levels, reflecting enhanced very low density lipoprotein (VLDL) triglyceride concentrations; high density lipoprotein (HDL) levels did not change. However, these lipoprotein changes did not correlate with any alterations in biliary lipid output. Total hepatic secretion rates of the biliary lipids remained generally unchanged during treatment, with a tendency towards lower cholesterol output, resulting in a lower molar percentage of cholesterol in hepatic bile, 3.4 +/- 0.4 vs. 2.9 +/- 0.2 mol %. This is probably due to an increased rate of conversion of cholesterol to bile acids in the hepatocyte. It is concluded that, in man, the liver may adapt well to changes in the enterohepatic circulation of bile acids, thereby maintaining output rates of biliary lipids at a relatively constant level.

Adult↗

PubMed1998

Comparison of atorvastatin alone versus simvastatin +/- cholestyramine in the management of severe primary hypercholesterolaemia (the six cities study).

BACKGROUND: Atorvastatin is a new member of the class of drugs which inhibit the enzyme Hydroxy-Methylglutaryl Co-A reductase, the rate limiting step in cholesterol biosynthesis. AIM: To compare the effects of atorvastatin alone versus simvastatin +/- low dose resin (i.e. versus standard care) on low density lipoprotein (LDL) cholesterol in severe primary hypercholesterolaemia. METHODS: An open, multi-centre, randomised study in patients previously stabilised on a cholesterol-lowering diet and simvastatin 40 mg daily, having LDL cholesterol > or = 5.0 mmol/L and triglycerides < 4.0 mmol/L. After five weeks washout, 92 were randomised to receive atorvastatin 10 mg and 44 to receive simvastatin 10 mg. The dose was doubled every six weeks if LDL cholesterol remained > or = 3.5 mmol/L. In accordance with manufacturers' recommendations, maximum dosage was atorvastatin 80 mg daily or simvastatin 40 mg daily (+cholestyramine 4 g daily in 84% of cases). Treatment was continued over 30 weeks. Lipids, lipoproteins, haematological and biochemical safety parameters were measured at regular intervals. Adverse events were monitored. RESULTS: Baseline LDL cholesterol was approximately 9 +/- 2 mmol/L (SD). After 30 weeks treatment serum cholesterol reduction was 42 +/- 10% on atorvastatin versus 32 +/- 13% on simvastatin +/- resin (p < 0.001), LDL cholesterol reduction 49 +/- 12% versus 38 +/- 14% (p < 0.001), and triglyceride reduction 33 +/- 20% versus 25 +/- 22% (p < 0.02). High density lipoprotein cholesterol increased by 7-10% on both treatments. The proportion of subjects achieving goal LDL cholesterol < 3.5 mmol/L was two to three times greater in those on atorvastatin compared with those on simvastatin +/- resin at each titration point. Six patients on simvastatin and one on atorvastatin were withdrawn. The drugs were generally well tolerated and the pattern of adverse events was similar with either treatment. CONCLUSIONS: Atorvastatin up to 80 mg daily appears to be an effective new treatment for the management of primary hypercholesterolaemia. It shows greater efficacy than simvastatin up to 40 mg daily +/- resin and has a similar safety profile.

Adult↗

PubMed1978

Cholestyramine: use as a new therapeutic approach for chlordecone (kepone) poisoning.

In rats, as reported in humans, chlordecone (Kepone) is excreted predominantly in the feces. Cholestyramine, an anion exchange resin, binds chlordecone in rat intestine, increases its excretion into the feces, and decreases its content in the tissues. The resin appears to offer a practical method for treating chronic poisoning with this and possibly with other lipophilic toxins.

Animals↗

PubMed1985

Comparison of the in vitro activities of teicoplanin and vancomycin against Clostridium difficile and their interactions with cholestyramine.

The in vitro activity of teicoplanin was compared with that of vancomycin against fecal isolates of Clostridium difficile. All strains were susceptible to both antibiotics, but teicoplanin was fourfold more active than vancomycin. Cholestyramine was found to bind teicoplanin almost completely, reducing its activity to nondetectable levels.

Anti-Bacterial Agents↗

PubMed1973

Reduction of absorption of paracetamol by activated charcoal and cholestyramine: a possible therapeutic measure.

The absorption of an oral 2-g dose of paracetamol was markedly reduced by the simultaneous oral administration of either activated charcoal or cholestyramine but was only slightly reduced when the adsorbents were given 60 minutes after the paracetamol. Since the absorption of a larger dose of the drug will probably be slow, the administration of adsorbents may be of value even when delayed several hours.

Acetaminophen↗

PubMed1973

Bile acids and vitamin A absorption in man: the effects of two bile acid-binding agents, cholestyramine and lignin.

In 14 healthy volunteers, the addition of 12 g cholestyramine to a vitamin A-containing test meal reduced the expected rise in serum vitamin A by 59.5% (p<0.001). By contrast, lignin had no significant effect in 12 subjects. This study confirms the importance of bile acids in vitamin A absorption and the ineffectiveness of lignin as a sequestrator of conjugated bile acids.

Adult↗

PubMed1991

Feeding diets containing 2% cheno- or urso-deoxycholic acid or cholestyramine to rats for two weeks alters intestinal morphology and bile acid absorption.

This study was undertaken to examine the effect of supplementing chow for 2 weeks with 2% cheno- (CDC) or ursodeoxycholic (UDC) acid or cholestyramine (CHOL) on the intestinal morphology and in vitro uptake of bile acids in adult rats. Food intake was higher in UDC and CHOL as compared with animals fed chow or CDC, or in animals pair-fed a chow-restricted diet (CRD). Body weight gain was lower in CDC and CRD but was unchanged by feeding UDC or CHOL. Jejunal mucosal surface area was similar in the five groups, although the ileal mucosal surface area was lower in UDC than in the other animals. Feeding UDC reduced the ileal uptake of cholic acid (C), taurocholic acid (TC), and glycocholic acid (GC). Feeding CDC had no effect on bile acid uptake except when compared with animals fed a chow-restricted diet. Feeding CHOL reduced the active ileal uptake of C, had no effect on the uptake of TC or GC or CDC, and was associated with increased uptake of stearic, linoleic, and linolenic acids. These effects were likely related to a direct effect of changes in the luminal bile acids rather than due to an indirect effect of the reduced food intake, since the ileal uptake of CDC and GC was greater in animals fed CDC than in those fed a chow-restricted diet with comparable weight gain. Thus, 2 weeks of feeding bile acids or bile acid binding agents may alter the form and function of the rat intestine, and as well may lead to changes in food intake and body weight gain.

Animals↗

PubMed1986

Intestinal interaction of bile acids, phospholipids, dietary fibers, and cholestyramine.

Binding of bile acids and phospholipids to a number of dietary fibers and cholestyramine (CH) within the small intestine was determined. The fibers used were cellulose, wheat bran, oat bran, guar gum (GG), and lignin (LG). GG, LG, and CH bound significant quantities of bile acids. However, only the CH reduced the bile acid concentration within the aqueous phase of the intestinal contents. Significant phospholipid binding was found only with CH. None of the test substances significantly reduced the quantity of solubilized lipid. Multiple regression analysis indicated that the total quantity of bile acids and phospholipids in the aqueous phase of the intestinal contents was a significant predictor of the quantity of lipid solubilized within the contents (r2 = 0.67). The failure of GG and LG to significantly decrease the amount of solubilized lipid suggests that the hypocholesterolemic effect of these fibers is due more to their bile acid binding capacity than to an effect on lipid solubilization.

Animals↗

PubMed1986

Recurrent Clostridium difficile-associated colitis responding to cholestyramine.

We describe a patient with relapses of Clostridium difficile cytotoxin-positive pseudomembranous colitis (PMC) after treatment with vancomycin, a course of metronidazole and a trial of bacitracin. She remains free of disease after a prolonged course of cholestyramine. We suggest there may be a role for anion-exchange resins in patients with PMC relapsing after vancomycin therapy.

Adult↗

PubMed1987

Feeding rats diets containing cheno- or ursodeoxycholic acid or cholestyramine modifies intestinal uptake of glucose and lipids.

We wished to test the hypothesis that variations in the luminal content of bile acid produced by feeding chenodeoxycholic acid (CDC), ursodeoxycholic acid (UDC) or cholestyramine (C) alter intestinal transport properties and morphology. Rats were fed standard chow pellets containing 0.5% CDC, 0.5% UDC or 2% C for a period of 2 weeks, and the in vitro uptake of glucose, cholesterol, bile acids and a homologous series of fatty acids was assessed. The food consumption was similar in animals fed chow, CDC, UDC and C, yet rats fed CDC or UDC gained less weight, and the weight of the jejunal and ileal mucosa was lower in animals fed CDC or C than in those fed chow or UDC. Ileal but not jejunal uptake of glucose was reduced in animals fed UDC, CDC or C. The active ileal uptake of bile acids was enhanced by UDC, CDC or C, whereas the jejunal passive permeability to bile acids was reduced by feeding C. Feeding C inhibited the jejunal and ileal uptake of cholesterol; C, UDC and CDC had a variable effect on the intestinal uptake of the fatty acids 10:0-18:0. The jejunal mucosal surface area was lower in groups fed CDC or UDC as compared with rats fed chow or C, and the ileal mucosal surface area was lower in rats fed CDC. However, the altered intestinal transport could not be explained by the altered morphology. Thus, (1) chronic variations in the intestinal luminal content of bile acids produced by the feeding of CDC, UDC or C resulted in alterations in the active and passive transport properties of the intestine, and (2) these changes differed between the jejunum and the ileum and were not explained simply by alterations in the animals' food intake or mucosal morphology. These studies suggest that chronic variations in the bile acids in the intestinal lumen may be one of the factors independently influencing the transport properties and mucosal surface area of the intestine. The long-term effect of changes in luminal bile acid content on intestinal function in man remains to be established.

Animals↗

PubMedDate not supplied

Regulation of hepatic high density lipoprotein binding proteins after administration of simvastatin and cholestyramine to rats.

We investigated the regulation of putative high density lipoprotein (HDL) receptors in rat liver after cholesterol feeding and the administration of cholesterol-lowering drugs to rats. The expression of two plasma membrane HDL binding proteins (HB1 and HB2) were compared in control and treated livers by first separating membrane proteins on sodium dodecyl sulfate-polyacrylamide gels and quantitating HB1 and HB2 levels with a specific ligand blot assay. Of the various treatments used, only simvastatin or simvastatin plus cholestyramine produced significant changes, with reductions of up to 40% and 60%, respectively, for HB1 and HB2. The effect on the binding proteins was not associated with changes in serum cholesterol concentrations, which did not change significantly after either treatment, although a marked rise in liver cholesterol concentration after cholesterol was associated with a moderate increase in HB2 expression. We show evidence for regulation of the levels of hepatic HDL binding proteins and provide another important criterion for the acceptance of HB1 and HB2 as components of a functional HDL receptor.

Animals↗

PubMed1992

Lathosterol and other noncholesterol sterols during treatment of hypercholesterolemia with lovastatin alone and with cholestyramine or guar gum.

Sixty-two patients aged 19-64 years with primary hypercholesterolemia (mean level of total cholesterol, 10.8 mmol/l) were treated with 80 mg/day lovastatin (L) alone for 18 weeks and, after randomization to either L + 20 g/day guar gum (L + GG) or L + 16 g/day cholestyramine (L + C) treatments, for an additional 18 weeks. The total cholesterol level declined from baseline by 34% during L and by 44% and 48% during L + GG and L + C, respectively. In terms of micromoles per millimole of cholesterol, serum levels of the cholesterol synthesis precursors cholestenol, desmosterol, and lathosterol were decreased and those of the plant sterols campesterol and sitosterol were increased by treatment with L. The serum contents of cholesterol precursors were increased markedly after the combination of either GG or C with L, but the increase was greater after the addition of C (e.g., the lathosterol to cholesterol ratio was 51% versus 212% for L + GG and L + C, respectively; p less than 0.001). Thus, a higher rate of removal of bile acids by C than by GG reduced more effectively the low density lipoprotein cholesterol level but simultaneously stimulated cholesterol synthesis compensatorily to a higher level even under concurrent treatment with L. The serum sitosterol to cholesterol ratio declined by 13% during L + GG but increased by 49% during L + C compared with the value under L alone, suggesting different effects of GG and C on the metabolism of plant sterols.

Adult↗

PubMed1968

Effect of cholestyramine on the fecal excretion of intravenously administered cholesterol-4-14C and its degradation products in a hypercholesterolemic patient.

The effect of cholestyramine on the fecal excretion of bile acids and neutral sterols was measured in a hypercholesterolemic patient on a low fat, high polyunsaturated fatty acid-containing diet after the intravenous injection of cholesterol-4-(14)C. A significant (16%) lowering of serum cholesterol concentration was accompanied by a 3.2-fold increase in fecal bile acid excretion but no change in neutral sterol output. The increased bile acid loss was adequate to account for the observed fall in serum cholesterol level. The implications of these findings were discussed.

Bile Acids and Salts↗