SEARCH · PubMed Health

Results for “CHOLESTYRAMINE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

PubMed1975

Colestipol, clofibrate, cholestyramine and combination therapy in the treatment of familial hyperbetalipoproteinaemia.

Fifty-seven patients, mean age 26 years, suffering from familial hyperbetalipoproteinaemia (Fredrickson type lla and llb), were treated on a low cholesterol, modified polyunsaturated fat diet for a period of 6-12 weeks prior to the introduction of drug therapy. No significant reduction in the serum levels of total cholesterol, low density lipoprotein (LDL) cholesterol or triglyceride was found. Fifty patients were then treated with colestipol for 6 weeks; total and LDL cholesterol decreased by 23%, but triglyceride levels were unaffected. During the following 6 weeks, placebo was administered, and total and LDL cholesterol returned to pretreatment levels. The patients were then randomly allocated into two groups of 16. The first group continued with clofibrate therapy, while the second group received cholestyramine. In the clofibrate group a reduction in total and LDL cholesterol of the order of 17% was noted, similar to cholestethat achieved in this group on colestipol. Triglyceride levels were 15% lower on clofibrate therapy than on colestipol. In the cholestyramine group, there was a 25% decrease in total and LDL cholesterol, compared with pretreatment levels. This reduction was similar to that found when colestipol was administered. Triglyceride values were significantly raised during cholestyramine therapy. Thirteen patients were then subjected to a 6-week period of combination therapy, either clofibrate or colestipol, or clofibrate and cholestyramine. Total and LDL cholesterol were reduced by 32% on combination therapy compared with 18% on colestipol and 23% on either clofibrate or cholestyramine alone. Furthermore, on combined therapy, triglyceride concentrations fell by 20% when compared with the levels found when colestipol, clofibrate or cholestyramine were administered on their own.

Adolescent↗

PubMed1991

Efficacy and compliance with cholestyramine bar versus powder in the treatment of hyperlipidemia.

PURPOSE: The purpose of the study was to compare the powder and the bar forms of cholestyramine to determine efficacy and patient compliance. SUBJECTS AND METHODS: A prospective, randomized trial was conducted that included 83 healthy men and women with hyperlipidemia greater than the 90th percentile for low-density lipoprotein (LDL) or total cholesterol. Patients were randomly assigned to receive either cholestyramine powder, two packets (8 g), twice daily, or cholestyramine confectionery bar, in maple or mint flavors, two bars (8 g), twice daily. Fasting serum total cholesterol, LDL cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides were measured at baseline, after 6 to 8 weeks of following the American Heart Association Step I diet alone, and after 8 weeks of taking either the cholestyramine bar or powder. RESULTS: Total cholesterol decreased significantly (p less than 0.01) by 16% in the bar group and 17% in the powder group. LDL cholesterol decreased by 28% and 29% in the bar and powder groups, respectively (p less than 0.01). There was no significant change in HDL cholesterol. Triglycerides increased in both groups, by 29% in the bar group and by 25% in the powder group. There was no difference between bar and powder in the effect on blood lipids. The majority of the lipid-lowering effect was seen within 14 days. Mean patient endpoint compliance with the therapy was 91.8 +/- 3.6% in the bar group and 94.8 +/- 2.1% in the powder group. There was no difference between groups. CONCLUSION: The cholestyramine confectionery bar is as effective as cholestyramine powder in the treatment of hyperlipidemia. The majority of the lipid-lowering effect is seen within 14 days of therapy. Although patient compliance is comparable between the two forms, gastrointestinal side effects were slightly greater with the bar form. Therefore, although the bar offers an alternative form of therapy, there appears to be no advantage with regard to patient compliance or palatability.

Adult↗

PubMed1982

Effects of cholestyramine on low density lipoprotein binding sites on liver membranes from rabbits with endogenous hypercholesterolemia induced by a wheat starch-casein diet.

Rabbits fed a wheat starch-casein diet develop a marked hypercholesterolemia with a lipoprotein distribution similar to that of humans. Approximately 76% of the total cholesterol is carried in the low density lipoprotein (LDL) fraction (1.006 less than d less than 1.063 g/ml). Inclusion of 1% cholestyramine in the diet prevents the increase in plasma cholesterol. The cholestyramine effect is mediated through an increased fractional catabolic rate of 125I-LDL. In order to determine the potential role of hepatic LDL receptors in the removal of LDL from the plasma, binding of 125I-LDL and 125I-beta-VLDL (beta-migrating very low density lipoproteins) to hepatic membranes prepared from livers of rabbits fed the wheat starch-casein diet with or without cholestyramine supplementation was investigated. Membranes from livers of the cholestyramine-supplemented animals exhibit high levels of specific EDTA-sensitive binding of either of the 125I-labeled lipoproteins. Very little EDTA-sensitive binding occurs on liver membranes from wheat starch-casein-fed rabbits that have not been treated with cholestyramine. These results indicate that the hypercholesterolemia in rabbits associated with the wheat starch-casein diet is wholly or partially the result of a decreased number of specific hepatic LDL receptors and thus a decreased catabolism of plasma cholesterol. The response of the liver to the inclusion in the diet of the bile acid sequestrant, cholestyramine, is to maintain or increase the number of specific LDL binding sites, thus promoting catabolism of plasma cholesterol.

Animals↗

PubMed1981

Decreased acute hepatotoxicity of carbon tetrachloride and bromobenzene by cholestyramine in the rat.

Numerous factors are known to increase or decrease drug-induced liver injury. The aim of this study was to test the effect of cholestyramine. Cholestyramine, and anion exchange resin binding in the gut substances taken up and metabolized by the liver such as bile salts, vitamins, endotoxins, etc., could indirectly modify drug-induced toxicity. Two groups of animals were studied: cholestyramine-fed and pair-fed controls. Five days after feeding, carbon tetrachloride or corn oil was injected intraperitoneally. Liver function and histology were normal after corn oil injection in both groups. One day after carbon tetrachloride injection liver weight/body weight ratio was lower in the cholestyramine-fed than in the pair-fed group (4.0 +/- 0.4 mean +/- SD vs. 4.4 +/- 0.3, p less than 0.05). Alanine and aspartate aminotransferases were lower (618 +/- 782 IU and 242 +/- 147 IU vs. 8245 +/- 8189 and 1966 +/- 1524 IU, p less than 0.001), as was necrosis (p less than 0.05). Steatosis and inflammatory reaction were similar in both groups. Two and four days later there were no significant differences between the two groups, because necrosis was no longer a major feature in the pair-fed group. Similar experiments were performed with bromobenzene. Here too cholestyramine prevents necrosis but to a much lesser extent. These results confirm that steatosis and necrosis are independent toxic effects of carbon tetrachloride. Cholestyramine, a widely used drug in cholestasis, could provide a potentially clinically important hepatocellular resistance to toxicity from environmental agents.

Alanine Transaminase↗

PubMed1980

In vitro cholesterol synthesis in freshly isolated mononuclear cells of human blood: effect of in vivo administration of clofibrate and/or cholestyramine.

The rate of incorporation of [2-14C]acetate into cholesterol has been measured in freshly isolated peripheral blood mononuclear leukocytes from patients on various hypolipidemic drugs that affect whole body cholesterol synthesis. These studies have demonstrated a significant two-fold increase in mononuclear cell cholesterol synthesis rates in patients receiving cholestyramine, a response measurable after 10 days of drug treatment. Mononuclear cell cholesterol synthesis rates were also measured in four groups of patients on the following drug regimens: 1) no medication, 2) clofibrate (2 g/day), 3) cholestyramine (16 g/day) or 4) both clofibrate and cholestyramine. The results demonstrated that the rate of acetate incorporation into cholesterol was significantly greater in the mononuclear cells from patients receiving either cholestyramine (P less than 0.005) or clofibrate plus cholestyramine (P less 0.001), as compared to controls. Patients receiving clofibrate alone did not differ significantly from controls in their rates of mononuclear cell cholesterol synthesis. Factors other than plasma lipoprotein and lipid levels appeared to be responsible for the elevated sterol synthesis rates observed in all patients receiving cholestyramine.

Cell Separation↗

PubMed1994

Influence of cholestyramine resin administration on single dose sulindac 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 cholestyramine effect on the plasma concentrations of sulindac and its sulfide metabolite following concurrent and staggered (sulindac 3 hours before cholestyramine) dosing. Six healthy volunteers participated in an open-label, 3-way crossover study. Subjects received 400 mg sulindac orally followed by serial blood sampling for sulindac and sulindac sulfide plasma concentrations over a 24-hour period. During the concurrent phase, 4 g of cholestyramine was coadministered resulting in a decrease (p < 0.05) in the area under the curve (AUC) for sulindac compared to sulindac alone (7.11 +/- 3.25 micrograms-h/ml vs 31.65 +/- 7.94 micrograms-h/ml respectively). Also, the sulindac sulfide AUC decreased (p < 0.05) to 7.26 +/- 4.37 micrograms-h/ml coadministration of both drugs compared to 44.69 +/- 11.81 micrograms-h/ml when sulindac is given alone. When the same doses of each drug were given 3 hours apart, the AUC for sulindac (17.88 +/- 3.69 micrograms-h/ml) and its sulfide metabolite (20.12 +/- 7.46 micrograms-h/ml) were still significantly decreased (p < 0.05) when compared to sulindac given alone (31.65 +/- 7.94 micrograms-h/ml for sulindac and 44.69 +/- 11.81 micrograms-h/ml for sulindac sulfide). Based on the lower AUCs for sulindac and sulindac sulfide, separating sulindac and cholestyramine by 3-hour intervals did not prevent the interaction. It is likely that the enterohepatic recycling features of sulindac may not prevent the interaction with cholestyramine even when the 2 drugs are staggered.

Adult↗

PubMed1994

The effects of cholestyramine and colestipol on the absorption of diclofenac in man.

The effect of oral administration of the non-absorbable anion-exchange resins cholestyramine and colestipol hydrochloride on the absorption of diclofenac in man was studied. Adsorption studies in vitro were also performed. In a randomized crossover study consisting of three phases, single doses of water suspensions of colestipol hydrochloride (10 g), or cholestyramine (8 g), or water only were given to six healthy male volunteers immediately following ingestion of diclofenac (100 mg). After dosing, serial blood samples were collected for a period of 8 hours. Plasma harvested from blood was analyzed for diclofenac by a sensitive and accurate high-performance liquid chromatographic method. The area under the plasma concentration-time curve was moderately (33%, p < 0.05) reduced by colestipol, and greatly reduced (62%) by cholestyramine. The maximum plasma concentration was reduced (58%) by colestipol and even more (75%) by cholestyramine treatment. The in-vitro adsorption studies showed that colestipol has a weaker capacity for adsorption of diclofenac compared to cholestyramine. The in-vivo data suggest a reduction of diclofenac bioavailability when colestipol or cholestyramine is administered concomitantly.

Absorption↗

PubMed1993

Comparative efficacy and safety of pravastatin and cholestyramine alone and combined in patients with hypercholesterolemia. Pravastatin Multicenter Study Group II.

BACKGROUND: Treatment of severe hypercholesterolemia often requires high-dose therapy with a hydroxymethylglutaryl-coenzyme A reductase inhibitor alone or in combination with bile acid-binding resin. We evaluated the efficacy and safety of pravastatin, a new hydroxymethylglutaryl-coenzyme A reductase inhibitor with hydrophilic selectivity, alone and in combination with cholestyramine. METHODS: Pravastatin was studied at doses of 20 or 40 mg twice daily alone or 20 mg twice daily with cholestyramine, 12 g twice daily, vs placebo in a randomized, double-blind multicenter study of 311 patients for 8 weeks and in continued therapy through 24 weeks. RESULTS: After 8 weeks of therapy, pravastatin in a dosage of 20 mg twice daily reduced low-density lipoprotein cholesterol levels by 31%, whereas a dosage of 40 mg twice daily reduced low-density lipoprotein cholesterol levels by 38%. Cholestyramine, 24 g daily alone, reduced low-density lipoprotein cholesterol levels by 32%. Cholestyramine combined with 40 mg of pravastatin reduced the level by 51%. Pravastatin, 40 or 80 mg daily, reduced the triglyceride level by 13% to 19%, resin alone increased the triglyceride level by 21%, and no change was seen with combined therapy. High-density lipoprotein cholesterol levels increased by about 5% regardless of regimen. Similar effects were seen at 24 weeks. Symptoms reported were indistinguishable among placebo and pravastatin users and were less than with cholestyramine alone or cholestyramine in combination with pravastatin. Elevations of liver enzyme levels were small in all groups, indistinguishable between resin and pravastatin, and were highest when the two drugs were combined. Plasma creatine kinase levels did not increase in any treatment group. CONCLUSIONS: Pravastatin treatment of hypercholesterolemia is highly effective and well tolerated alone and in combination with bile acid-binding resin and shows no tendency to increase muscle enzyme levels.

Adult↗

PubMed1995

A marked and sustained reduction in LDL sterols by diet and cholestyramine in beta-sitosterolemia.

This study examines the therapeutic outcome of a low plant sterol diet and adjunctive drug therapy (cholestyramine) in the long term treatment of beta-sitosterolemia. A diet restricted in plant sterols, cholesterol and fat was implemented in a 48-year-old male beta-sitosterolemic patient. The plant sterols beta-sitosterol, campesterol and stigmasterol, and cholesterol content of the diet were quantitated by a gas chromatography method (GLC) during metabolic ward studies. Food table analysis of dietary sterols, while quantitatively similar to GLC, significantly underestimated the level of plant sterols and therefore overestimated dietary cholesterol intake. The duration of the study was 18 months. The effect of the diet over a period of 6 months on the sterol levels of plasma and individual lipoprotein fractions (VLDL, LDL, HDL) was evaluated. Apolipoproteins A-1 and B-100 levels were measured. The same parameters were assessed over the next 12 months with the adjunctive use of cholestyramine and dietary restrictions. The diet was effective in lowering total, VLDL, and LDL plant sterols by 37%, 59%, and 32% respectively. The low plant sterol diet did not change total plasma, VLDL or LDL cholesterol. With the addition of cholestyramine, total plasma and LDL cholesterol declined by 64 and 76%, respectively, while HDL-cholesterol remained unchanged. LDL plant sterols declined by 77%, while VLDL plant sterol showed no further change. The decline showed no discrimination among the individual plant sterols. One week after cholestyramine therapy, apolipoprotein B fell from 1.03 to 0.11 g/L, while apolipoprotein A rose from 1.29 to 1.79 g/L. These levels subsequently stabilized at 70% below (0.29 g/L) and 42% above (1.81 g/L) that of diet therapy alone. Xanthomas, angina pectoris, and intermittent claudication resolved during the diet and cholestyramine therapy period. Dietary restriction of plant sterols combined with cholestyramine therapy is an effective means of treating beta-sitosterolemia.

Adult↗

PubMed1997

Additive hypocholesterolemic effect of psyllium and cholestyramine in the hamster: influence on fecal sterol and bile acid profiles.

Recent findings suggest that the effects of cholestyramine and psyllium in combination could be additive for cholesterol-lowering. We therefore examined the effect of both agents, alone and in combination, on lipoprotein cholesterol and neutral and acidic steroid excretion in the hamster. Animals (n = 8/group) were fed for 21 days, either a basal chow diet supplemented with 10% palm oil and 0.2% cholesterol, or one of four treatments consisting of the basal diet plus: 5.5% cellulose; 5% psyllium with 0.5% cellulose; 0.5% cholestyramine with 5% cellulose; or 5% psyllium with 0.5% cholestyramine. Psyllium and cholestyramine both had significant hypocholesterolemic effects, but in combination produced additive reductions in lipoprotein and hepatic cholesterol. Psyllium, cholestyramine, and the combination increased total bile acid excretion by 26%, 57%, and 79%, respectively. Psyllium affected only unconjugated bile acid excretion while cholestyramine also increased the excretion of conjugated and primary bile acids. Neither agent, nor the combination, affected fecal neutral sterol excretion. We conclude that, while both agents lower cholesterol by a mechanism of increased bile acid excretion, these studies indicate that psyllium does not bind bile acids in vivo and lend further support for the concomitant use of these agents for cholesterol-lowering.

Animals↗

PubMed1994

The effect of colestipol and cholestyramine on ibuprofen bioavailability in man.

The purpose of this study was to determine whether a concomitant single oral dose of one of the anion exchange resins colestipol hydrochloride (10 g) or cholestyramine (8 g) administered with ibuprofen (400 mg) would alter the bioavailability of this non-steroidal anti-inflammatory agent. The study was performed according to a randomized three-way crossover design in six healthy male volunteers. After dosing, serial blood samples were collected for a period of 10 h. Plasma harvested from blood was analysed for ibuprofen by a sensitive high-performance liquid chromatographic method. There were no significant differences between colestipol treatment and control for peak plasma concentration (Cmax), time to peak concentration (Tmax), area under the plasma concentration-time curve (AUC), mean residence time (MRT), elimination rate constant (Kel), or elimination half-life (t1/2). Cholestyramine treatment resulted in a significant decrease in AUC (26%, p < 0.05) and Cmax (34.4%, p < 0.01) and a significant increase in Tmax (80%, p < 0.01) and MRT (20.2%, p < 0.05). Cholestyramine administration showed no significant effect on the Kel and t1/2 values. A significant correlation was obtained between the increase in MRT and the increase in Tmax. The confidence intervals (90%) of the mean values of the pharmacokinetic parameters (AUC0-infinity and Cmax) for the colestipol: control ratio were well within the acceptable range of 100 +/- 20, whereas those for the cholestyramine: control ratio were outside it. Colestipol treatment was found to be bioequivalent to the control treatment by Schuirmann's two one-sided t tests, while cholestyramine treatment was found to be bioinequivalent.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

PubMed1993

In vitro studies to investigate the reasons for the low potency of cholestyramine and colestipol.

The association rates, dissociation rates, and equilibrium binding of bile acids with cholestyramine and colestipol were measured under physiological conditions with the most abundant bile acids found in humans. Cholestyramine and colestipol equilibrated with the bile acids (5 mM) within 1 h and they bound > 58% and > 17% of the bile acid, respectively, when at equilibrium with physiological concentrations of bile acid (4.3-10.1 mM). However, the conjugated trihydroxy bile acids taurocholic acid and glycocholic acid dissociated rapidly from both cholestyramine and colestipol when the sequestrants, preloaded with the bile acid, were washed with the Krebs-Henseleit buffer. The taurine-conjugated and dihydroxy bile acids dissociated more slowly from cholestyramine and colestipol than the glycine-conjugated and trihydroxy bile acids and, therefore, would be expected to avoid reabsorption to a greater extent by the terminal ileum and colon in vivo. We predict from these results that the reasons for the low potency of cholestyramine and colestipol are that they bind a relatively small proportion of the trihydroxy bile acids in the duodenum and jejunum and that all of the bile acids dissociate to varying extents from the sequestrants in the terminal ileum where the unbound bile acids are reabsorbed by the gut.

Bile↗

PubMed1995

The effect of cholestyramine on the pharmacokinetics of meloxicam, a new non-steroidal anti-inflammatory drug (NSAID), in man.

The influence of multiple oral doses of cholestyramine on the single dose pharmacokinetics of meloxicam has been studied in 12 healthy male volunteers. Each subject received on two occasions a single IV injection of meloxicam 30 mg. The cholestyramine group received the material suspended in water 3 times a day. Compared to controls, cholestyramine accelerated the elimination of meloxicam. The mean terminal phase elimination half-life was reduced from 19.5 h to 12.7 h due to an increase in clearance of the drug (0.426 vs 0.636 l.h-1). Also, as a consequence of increased clearance in the presence of cholestyramine, the mean residence time of the drug in the body was significantly decreased (39%) P < 0.01. However, the volume of distribution for meloxicam was largely unaffected by cholestyramine which suggests that meloxicam undergoes gut recirculation. These changes are of the same magnitude as those previously reported for the structurally related piroxicam and are much smaller than those observed for tenoxicam.

Administration, Oral↗

PubMed1985

Lipid accumulation in jejunal and colonic mucosa following chronic cholestyramine (Questran) feeding.

The hypolipidemic agent, cholestyramine (Questran), when fed to rats inhibits intestinal absorption of cholesterol and triglycerides and causes significant epithelial cell damage in both small and large intestine. In this study, we report significant accumulation of lipids in the mucosal layer of both jejunum and colon in rats administered 2% cholestyramine for a four-week period, when compared to a control group maintained on regular chow. The total lipid increment with cholestyramine was 4.7-fold in the jejunum and 3.7-fold in the colon. The triglyceride fraction increased substantially in the small but not the large intestine. Relative phospholipid levels decreased in the treated jejunum but not in the colon. The biochemical data were reflected in morphological evidence of lipid-laden enterocytes obtained by light and transmission electron microscopy. Since cholestyramine has been shown to sequester 99.8% of micellar phospholipid in vitro, it is concluded that the presence of cholestyramine in the intestinal lumen may interfere with phospholipid availability for chylomicron synthesis and serosal lipid exit from the epithelium. This unusual deposition of lipid within the mucosal layer may also be correlated with the known cocarcinogenic effect of this resin in experimentally induced intestinal cancer.

Animals↗

PubMed1985

Alterations in calcium, magnesium, iron, and zinc metabolism by dietary cholestyramine.

Cholestyramine is an effective drug for the reduction of plasma cholesterol because of its ability to sequester intestinal bile acids. Since metabolic alterations, including diminished intestinal absorption of vitamin D and osteomalacia have been reported with long-term use of this resin, the influence of cholestyramine on dietary balance of four mineral elements has been investigated. Wistar-strain rats were fed either a 2% cholestyramine or control diet for one month. Dietary intakes and fecal and urinary excretions of calcium, magnesium, iron, and zinc were determined using atomic absorption spectrophotometry during three, 3-day balance periods. Cholestyramine-fed rats had a net negative balance for calcium and a lower net positive balance for magnesium, iron, and zinc than the controls. Other effects of cholestyramine were an increased urinary excretion of calcium and magnesium, a decreased urinary zinc, and an alkalinization of urine. Blood and tissue cation content was unchanged except for a reduction in serum magnesium with resin feeding. Alterations in calcium, magnesium, and zinc metabolism might be explained by inadequate vitamin D absorption from the intestine followed by an increased secretion of parathyroid hormone. A diminished iron absorption due to resin binding could account for the reported disturbance in iron balance.

Animals↗

PubMed1987

Effect of cholestyramine on bile acid metabolism in conventional rats.

Effects of cholestyramine on biliary secretion of cholesterol, phospholipids and bile acids and fecal excretion of sterols and bile acids were examined in Wistar male rats. Six rats were fed a basal diet, and the other six were fed a basal diet supplemented with 5% cholestyramine for eight days. Bile flow and biliary secretion of bile acids and phospholipids (per hour per rat) decreased with cholestyramine treatment, while biliary cholesterol secretion (per hour per rat) remained unchanged. In the biliary bile acid composition, a marked increase of chenodeoxycholic acid with a concomitant decrease of beta-muricholic acid was observed in cholestyramine-treated rats. Fecal excretion of total sterols and bile acids increased about three- and four-fold, respectively, after cholestyramine treatment. The increase of fecal bile acids derived from cholic acid was more predominant than that derived from chenodeoxycholic acid, resulting in an increase of the cholic acid group/chenodeoxycholic acid group ratio.

Animals↗

PubMed1991

Comparison of the efficacy of Questran Light, a new formulation of cholestyramine powder, to regular Questran in maintaining lowered plasma cholesterol levels.

Sixty-one men with known hypercholesterolemia (plasma cholesterol greater than 265 mg/dl), most of whom were previous participants in the Coronary Primary Prevention Trial of the U.S. Lipid Research Clinic Program, were chosen to take part in this study to test the effectiveness of a new low-calorie (Questran Light) cholestyramine formulation against the proven effectiveness of the currently marketed formulation Questran in maintaining lowered plasma cholesterol levels. The study recorded changes in fasting plasma lipids, total cholesterol, high-density lipoprotein cholesterol, triglycerides, and calculated low-density lipoprotein cholesterol. After establishing baseline lipid/lipoprotein levels in a 3-week period during which all participants received the currently marketed formulation, the men were randomized into 2 groups, 1 group (n = 31) taking the new Questran Light formulation of 4 g of cholestyramine in 5 g of powder per pack, while the other group (n = 30) continued to take the marketed Questran formulation of 4 g of cholestyramine in 9 g of powder per pack. Each group consumed a total of 24 g/day of cholestyramine in 2 divided doses. At the end of the maintenance phase of the study there were no statistically significant mean changes in percentage from baseline to end-point lipid/lipoprotein levels within either group, nor were there any significant differences between the Questran Light group or the currently marketed Questran formulation group. The new low-calorie cholestyramine formulation appears to be equally as effective in maintaining lowered plasma cholesterol levels as the currently marketed formulation.

Adult↗

PubMed1984

Altered effect of 3% dietary cholestyramine on plasma lipids and biliary bile acid output in the pregnant rat.

The effects of a diet containing 3% (w/w) cholestyramine on plasma total, free, and high-density lipoprotein cholesterol and triglycerides and on bile flow and composition were compared between pregnant rats fed the resin from before mating until the twentieth day of gestation and virgin rats fed the resin for an equivalent length of time. Pregnant and virgin rats consuming a similar diet but not receiving cholestyramine were also studied. In the nonpregnant rat the usual response to cholestyramine was observed as a significantly elevated plasma high-density lipoprotein cholesterol level and biliary bile acid secretion. Plasma cholesterol levels and bile composition were not altered by cholestyramine in the pregnant rat. The inability of resin therapy to change plasma high-density lipoprotein cholesterol and bile composition during pregnancy is likely to be causally related to a reduced efficacy of cholestyramine treatment when administered during gestation.

Animals↗