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Results for “CHOLESTYRAMINE”

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At least 253 records · Page 14Linked to original sources

PubMed1988

Lack of effect of cholestyramine on phenytoin bioavailability.

The effect of cholestyramine (4 g qid for 5 days) on the kinetics of phenytoin (400 mg orally) was investigated in normal subjects. Apart from a trend toward faster phenytoin absorption, the serum level profile of the drug during concurrent cholestyramine coadministration was similar to that observed in a control session. Areas under the serum phenytoin concentration curves were virtually identical in the two occasions. It is concluded that cholestyramine does not significantly affect the bioavailability of a single dose of phenytoin.

Adult↗

PubMed1988

Superactivated charcoal versus cholestyramine for cholesterol lowering: a randomized cross-over trial.

To evaluate the relative abilities of superactivated charcoal (20 g twice daily) and cholestyramine (8 g twice daily) to lower plasma cholesterol concentrations acutely, six hypercholesterolemic patients were studied using a randomized cross-over design. After a 1-week dietary control period, each subject received 3 weeks of each treatment regimen on separate occasions. Superactivated charcoal and cholestyramine reduced total plasma cholesterol by 21.8 +/- 3.8% and 16.2 +/- 2.4%, respectively. Side effects were mild and similar for both treatments. At the dosage regimens studied, superactivated charcoal and cholestyramine have comparable ability to lower plasma cholesterol concentrations.

Adult↗

PubMed1992

Polymeric sorbents for bile acids. I: Comparison between cholestyramine and colestipol.

Isotherms for the sorption of bile acids at 20 degrees C, in tris(hydroxymethyl)aminomethane.HCl(tris) and KH2PO4-NaOH (phosphate) buffers (pH 7.4), indicate that the binding by cholestyramine and colestipol is mainly through ionic linkages, although hydrophobic interactions are also of importance. Cholestyramine has a higher sorption capacity for bile acids, in both buffers, than colestipol. The chloride form of cholestyramine has a higher capacity for cholate in tris buffer than the iodide form. Increased ionic strength of the medium leads to decreased amounts of sorption.

Absorption↗

PubMed1992

Long-term effect of lovastatin alone and in combination with cholestyramine on lipoprotein (a) level in familial hypercholesterolemic subjects.

We have determined the effect of lovastatin alone or in combination with cholestyramine on lipoprotein (a) [Lp(a)] levels in 59 heterozygotes for familial hypercholesterolemia (FH) treated for 33.8 (+/- 6.1) months. The median pretrial Lp(a) value was 10.2 mg/100 ml, which is twice the median value in healthy people examined at the Institute of Medical Genetics, University of Oslo. The median Lp(a) level was insignificantly reduced by 10.3% during the first 20 weeks when the subjects were on a standardized medication of increasing doses of lovastatin and cholestyramine. The first 20 weeks were followed by usual care treatment period, and a further decrease in Lp(a) level to 16.2% (P = 0.0012) was observed at the end of the study. Comparison between the 20 subjects on lovastatin monotherapy and the 31 subjects on the combined therapy of lovastatin and cholestyramine, revealed that the subjects on monotherapy had a median reduction of 20.1%, and the subjects on the combined therapy had a reduction of 15.4%. Thus, it appears that the reduction in Lp(a) level could be ascribed to lovastatin alone.

Adolescent↗

PubMed1985

Effect of oral cholestyramine on the elimination of high-dose methotrexate.

The anion exchange resin cholestyramine binds methotrexate (MTX) effectively in vitro. The binding capacity exceeds that of activated charcoal by a factor of 5.4. On two patients undergoing high-dose MTX therapy it is also shown that cholestyramine binds MTX in vivo. This leads to an enhanced non-renal excretion of MTX. Therefore, cholestyramine may be of clinical value in patients who develop renal function impairment whilst undergoing MTX therapy.

Administration, Oral↗

PubMed1981

[Protective effect of cholestyramine in the hepatocarcinogenesis of the rat (author's transl)].

The influence of cholestyramine on hepatocarcinogenesis was investigated in the Wistar rat. After 14 weekly gastric instillation of 50 mg diethylnitrosamine/kg and simultaneous administration of diet supplement with 1.3% cholestyramine, half of the animals developed hepatic tumors. In contrast, nearly all the animals in the control group under similar experimental conditions, but without the cholestyramine supplement in their diet, developed hepatic tumors. The sequestration of bile acids and the reduction of the noxious lithocholic acid could be considered as an explanation for the modification of hepatic tumors induced by diethylnitrosamine in the Wistar rat.

Animals↗

PubMed1982

Studies on the in vitro binding of D-penicillamine to cholestyramine.

Adsorption of D-penicillamine to cholestyramine depends on the amount of the resin, the pH and the presence of other compounds such as bile salts. In the usual drug to resin ratio (150 mg D-penicillamine and 4-8 g cholestyramine per single dose) the percentage of D-penicillamine adsorbed to cholestyramine was about 10% of the applied dose; Bile salts (10 mmoles/l) inhibited this small adsorption by 87%.

Adsorption↗

PubMed1979

Cholesterol metabolism in the liver and intestine of the chick: effect of dietary cholesterol, taurocholic acid and cholestyramine.

The effect of feeding cholesterol, taurocholic acid, or cholestyramine to chicks on cholesterogenesis from [1-14C] acetate in liver and intestine was determined in vitro using tissue slices, and in vivo by i.v. injection of [14C] acetate. The conversion of cholesterol to bile acids in liver in vivo was measured in the same treatments after i.v. injection of [3H] cholesterol. Hepatic cholesterogenesis in vitro and in vivo was depressed by dietary cholesterol and taurocholate and enhanced by cholestyramine. Intestinal cholesterogenesis in vivo was depressed only by taurocholate whereas ileal cholesterogenesis in vitro was reduced by dietary cholesterol. Conversion of cholesterol to bile acids was enhanced by dietary cholesterol and cholestyramine and depressed by taurocholate. Hepatic cholesterol metabolism in the chick appears to be regulated by mechanisms similar to those reported for other species.

Acetates↗

PubMed1993

Cholesterol synthesis and esterification in isolated enterocytes: regulation by cholesterol and cholestyramine feeding.

The purpose of the present study was to investigate the physiological control of the main regulatory enzymes of cholesterol metabolism in isolated enterocytes obtained from chick duodenum, jejunum and ileum. Cholesterol feeding resulted in an inhibition of 3-hydroxy-3-methyl-glutaryl-CoA reductase and mevalonate 5-pyrophosphate decarboxylase, while cholestyramine feeding increased reductase activity in all the regions studied and decarboxylase activity only in duodenum. Cholesterol feeding markedly increased acyl-CoA:cholesterol acyltransferase, but the effects of cholestyramine were less clear. The effects on transferase activity cannot be due to differences in the availability of acyl-CoA as exogenous substrate as no significant differences were found in acyl-CoA hydrolase activity after any of the dietary treatments. The effects of cholesterol feeding were related to changes in the cholesterol content of epithelial cells, whereas in the case of cholestyramine this relationship was less apparent.

Animals↗

PubMedDate not supplied

Treatment of cholerheic diarrhea with cholestyramine and a hydrophilic colloid.

Eight patients with ileal-resection diarrhea who were being treated with cholestyramine took part in a trial comparing the effectiveness of cholestyramine with that of a hydrophilic colloid. Both drugs reduced overall stool frequency and improved consistency, but a larger dose of colloid was required. One patient planned to use the hydrophilic colloid instead of cholestyramine.

Adult↗

PubMedDate not supplied

Atovaquone plus cholestyramine in patients coinfected with Babesia microti and Borrelia burgdorferi refractory to other treatment.

Ten percent of US patients with Lyme disease are coinfected with Babesia microti. A double-blind, placebo-controlled, crossover trial enrolled 25 patients with confirmed Borrelia burgdorferi/B microti coinfection, abnormal visual contrast sensitivity (VCS), and persistent symptoms despite prior treatment with atovaquone and azithromycin. Patients were randomly assigned to atovaquone suspension or placebo plus cholestyramine for 3 weeks, were crossed over for 3 weeks, and then received open-label atovaquone and cholestyramine for 6 weeks. Symptoms and VCS scores were recorded at baseline and after weeks 3, 6, 9, and 12. Improvements in symptoms and VCS deficits were observed only after at least 9 weeks of treatment. At week 12, 5 patients were asymptomatic, and 16 had a notable reduction in the number of symptoms. The entire cohort demonstrated significant increases in VCS scores. Adverse effects were rare. Patients coinfected with B burgdorferi and B microti derive measurable clinical benefit from prolonged treatment with atovaquone and cholestyramine. Longer-term combination therapy may be indicated.

Adult↗

PubMed1994

Efficacy and safety of a combination fluvastatin-bezafibrate treatment for familial hypercholesterolemia: comparative analysis with a fluvastatin-cholestyramine combination.

PURPOSE: Familial hypercholesterolemia (FH) carries a markedly increased risk for coronary artery disease (CAD). Reduction of plasma low-density lipoprotein cholesterol (LDL-C) levels to the normal range may prevent premature atherosclerosis and usually requires a combination of cholesterol-lowering drugs. The major objective of this study is to compare two different drug combinations for the treatment of heterozygous FH. PATIENTS AND METHODS: The current investigation is a short-term, double-blind study comparing the efficacy and safety of fluvastatin when combined with cholestyramine (group 1) or with bezafibrate (group 2) in 38 patients with heterozygous FH. RESULTS: After 6 weeks of combination treatment, in comparison to a drug-free baseline (patients receiving single-blind placebo during the lead-in period of an earlier study, ie, before ever receiving fluvastatin), the combination of 40 mg/d of fluvastatin with 400 mg/d of bezafibrate in group 2 reduced plasma LDL-C levels by 35% as compared with 32% in group 1, and reduced the LDL-C/high-density cholesterol (HDL-C) ratio by 46%, compared to 37% in group 1 (a non-significant difference for both comparisons). When compared to an intermittent 6-week open-label administration of 40 mg fluvastatin monotherapy, the addition of cholestyramine or bezafibrate each reduced LDL-C by an additional 13% (P < 0.01 for both regimens). CONCLUSIONS: Fluvastatin-bezafibrate is superior to a fluvastatin-cholestyramine combination for lowering serum triglycerides and elevating HDL-C serum levels in patients in conjunction with a significant lowering of LDL-C/HDL-C ratios, and may be an effective synergistic therapy for heterozygous FH. No episodes of myositis were seen in this short-term study, a finding that is in agreement with most of the reported studies on statin-fibrate combinations reviewed here.

Adult↗

PubMed1978

Effect of cholestyramine and phenobarbital on pruritus and serum bile acid levels in cholestasis of pregnancy.

Serum bile acid concentrations were followed in 29 patients with cholestasis of pregnancy treated for pruritus with either phenobarbital or cholestyramine. The response of serum cholic and chenodeoxycholic acid levels to phenobarbital administered to 10 patients in a 100 to 150 mg. daily dose was variable: some decrease was found in four and some increase in three of the patients, but no clear effect on itching could be seen in any of them. In five of the other 10 patients treated with cholestyramine, 4 Gm. two or three times a day, serum cholic and chenodeoxycholic acid levels fell within 1 week of treatment, in one of these near to normal with complete relief from pruritus. It seems that patients with initially high serum bile acid levels do not respond to cholestyramine treatment. In these cases the biliary excretion and enterohepatic circulation of bile acids may be diminished to such an extent that the anion-binding resin is unable to augment fecal elimination of bile salts sufficiently to lower their serum levels.

Adult↗

PubMed1982

Effect of dietary fat saturation, cholesterol and cholestyramine on acyl-CoA: cholesterol acyltransferase activity in rabbit intestinal microsomes.

The regulation of intestinal acyl-CoA: cholesterol acyltransferase was investigated by dietary manipulation. Rabbits were fed the following diets: normal rabbit chow, 10% safflower oil, safflower oil plus 1% cholesterol, coconut oil plus 1% cholesterol, or cholestyramine. Acyl-CoA: cholesterol acyltransferase activity was increased in intestinal microsomes from animals fed safflower oil but not from animals fed coconut oil. Both diets containing cholesterol increased acyl-CoA: cholesterol acyltransferase activity; however, the safflower oil plus cholesterol diet was a more potent stimulator than coconut oil plus cholesterol. Cholestyramine decreased microsomal acyl-CoA: cholesterol acyltransferase activity. The different diets significantly modified microsomal lipid content in these groups. The two cholesterol diets resulted in equal increments in microsomal cholesterol. Microsomal cholesterol was unchanged in animals on the safflower oil diet; however, coconut oil and cholestyramine decreased the cholesterol content. Linoleic acid content increased in microsomes from animals on both the safflower oil-containing diets. Myristic acid accumulated and linoleic acid was decreased in microsomes from animals on both diets containing coconut oil. Subcellular fractionation of the intestine yielded a 4-fold enhancement of acyl-CoA: cholesterol acyltransferase activity in the rough endoplasmic reticulum. The lipid modifications and the subsequent changes in acyl-CoA: cholesterol acyltransferase activity in the rough endoplasmic reticulum from animals on normal, safflower oil, and safflower oil plus cholesterol diets paralleled that observed in the crude microsomal preparations. The changes in acyl-CoA: cholesterol acyltransferase activity observed with the different diets were not due to changes in microsomal fatty acyl-CoA pool size. It is concluded that dietary manipulation can alter microsomal lipid content. Microsomal fat saturation, independent of microsomal cholesterol content, regulates intestinal acyl-CoA: cholesterol acyltransferase and modifies the stimulatory effect of exogenous cholesterol on this enzyme.

Acyltransferases↗

PubMed1986

The activity of 3-hydroxy-3-methylglutaryl-CoA reductase and acyl-CoA: cholesterol acyltransferase in hepatic microsomes from male, female and pregnant rats. The effect of cholestyramine treatment and the relationship of enzyme activity to microsomal lipid composition.

The relationship of microsomal cholesterol and phospholipid fatty acid composition to the activities of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and acyl-CoA: cholesterol acyltransferase was investigated in male, female virgin and pregnant rats when hepatic cholesterogenesis was stimulated by cholestyramine. Cholestyramine increased HMG-CoA reductase activity in both sexes but had no effect on microsomal free cholesterol level or acyl-CoA: cholesterol acyltransferase activity. The data suggest that during cholestyramine treatment high rates of bile acid synthesis are supported by preferential channelling of cholesterol into this pathway, whilst the substrate pool and activity of acyl-CoA:cholesterol acyltransferase are maintained unaltered. The lack of a consistent relationship among enzyme activities and microsomal lipid composition infers that HMG-CoA reductase and acyl-CoA:cholesterol acyltransferase are regulated in vivo by independent mechanisms which are unlikely to involve modulation by the physical properties of the microsomal lipid.

Animals↗

PubMed1986

Regulation of squalene synthetase activity in rat liver: elevation by cholestyramine, but no diurnal variation.

Squalene synthetase activity in liver microsomes from rats sacrificed at three different times of the diurnal cycle showed no significant differences. Addition of 4% cholestyramine to the food resulted in a marked increase in activity (280% of control), independent of the time of killing. 3-Hydroxy-3-methylglutaryl coenzyme A reductase and cholesterol 7 alpha-hydroxylase activity, determined as positive controls, were also found to be elevated by cholestyramine and additionally showed a diurnal variation. On the other hand, five control enzyme activities, not directly related to cholesterol metabolism, i.e. glutamate dehydrogenase, NADPH cytochrome-c reductase, beta-hexosaminidase, catalase and acyl coenzyme A oxidase, showed neither an influence of cholestyramine feeding nor a time of sacrifice dependent variation.

Animals↗

PubMed1976

Treatment of hypercholesterolemia with Secholex. A long-term clinical trial and comparison with cholestyramine.

The efficacy of an anion-exchange gel, Secholex, as a hypocholesterolemic agent was assessed in 46 patients in 4 different studies and the effects were compared with those of cholestyramine. All patients had severe Type II-a or II-b hyperlipoproteinemia. In short-term metabolic studies Secholex (15 g/day) and cholestyramine (16 g/day) decreased serum cholesterol levels and increased total fecal sterol output and serum methyl sterol concentration to a similar extent, but cholestyramine was more effective than Secholex in increasing fecal bile acid excretion. In crossover studies, the two drugs appeared to be equally effective in lowing serum cholesterol levels but the patients mostly preferred Secholex. Twenty patients were treated with Secholex over a two-year period. The average decrease in serum cholesterol levels from the mean pretreatment value of 406 mg/100 ml was 15% during the first year, and 13% during the second year. In 5 patients the serum cholesterol was permanently lowered by more than 20% (good responders), while in 7 patients the average reduction of serum cholesterol level during Secholex administration was less than 10% (non-responders). The serum triglyceride level was slightly decreased by Secholex in Type II-b patients but was unaltered in Type II-a patients. At the end of the treatment period, serum iron and vitamin B12 levels were normal but the serum folic acid concentration was reduced in eight of 20 patients. A dose--response study indicated that a similar cholesterol-lowering effect was obtained with daily doses of 9 and 15 g of Secholex. It is concluded that Secholex is a relatively safe drug which effectively reduces serum cholesterol levels in two-thirds of patients with severe hypercholesterolemia.

Acacia↗

PubMed1979

The effects of cholestyramine on high density lipoprotein metabolism.

This study on 4 type II hyperlipoproteinaemic subjects examines the effects of pharmacologic doses (8 g twice daily) of the bile acid sequestrant cholestyramine on the plasma distribution and chemical composition of the high density lipoprotein subfractions, HDL2 and HDL3, and describes the influence of the drug on the metabolism of the major HDL aporoteins, apolipoprotein A-I and A-II. Cholestyramine lowered plasma low density lipoprotein cholesterol (32%; P less than 0.05) without affecting the level of that lipid in very low density or high density lipoproteins. However, the plasma HDL2/HDL3 ratio and apolipoprotein A-I concentration rose significantly on treatment, while apolipoprotein A-II remained unchanged. The rise in apolipoprotein A-I derived from an increase in its synthetic rate and produced a relative enrichment of the protein with respect to apolipoprotein A-II in both HDL subfractions. These results demonstrate the cholestyramine treatment affects HDL metabolism in a way which, according to current concepts, may prove beneficial to the recipient.

Apolipoproteins↗