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PubMed1984

Cholestyramine-enhanced fecal elimination of carbon-14 in rats after administration of ammonium [14C]perfluorooctanoate or potassium [14C]perfluorooctanesulfonate.

After a single intravenous dose of ammonium [14C]perfluorooctanoate [( 14C]PFO, 13.3 mg/kg) or of potassium [14C]perfluorooctanesulfonate [( 14C]PFOS, 3.4 mg/kg) to rats, cholestyramine fed daily as a 4% mixture in feed was shown to increase the total carbon-14 eliminated via feces and to decrease liver concentration of carbon-14. Rats were fed cholestyramine in feed for 14 days after administration of [14C]PFO and for 21 days after administration of [14C]PFOS. Control rats were administered radiolabeled fluorochemical but were not treated with cholestyramine. Cholestyramine treatment increased mean cumulative carbon-14 elimination in feces by 9.8-fold for rats administered [14C]PFO and by 9.5-fold for rats administered [14C]PFOS. After [14C]PFO, a mean of 4% of the dose of carbon-14 was in liver of cholestyramine-treated rats at 14 days versus 7.6% in control rats; after [14C]PFOS, 11.3% of the dose was in liver at 21 days versus 40.3% in control rats. After administration of either radiolabeled compound, plasma and red blood cell carbon-14 concentrations, which were relatively lower than liver concentrations, were also significantly reduced by cholestyramine treatment.

Animals↗

PubMed1984

A clinical trial evaluating cholestyramine to prevent diarrhea in patients maintained on low-fat diets during pelvic radiation therapy.

A prospective randomized trial to determine the value of a low fat diet with or without cholestyramine in the treatment of acute intestinal complications of pelvic irradiation is presented. A total of 35 patients receiving pelvic irradiation were entered in the study and all patients had received a 40 gm fat diet. The group was then randomized to receive either placebo (17 patients) or cholestyramine (18 patients). Diarrhea occurred in six out of 16 evaluable patients in the control group and only one of the 17 evaluable patients in the cholestyramine group. The frequency of diarrhea and the diarrhea scale remained high in the placebo group in the entire observation period. Statistical analysis had revealed better diarrhea control in the cholestyramine group (p = less than 0.05). In this report mechanism by which diarrhea occurs following pelvic irradiation is discussed. The adverse effects associated with the use of cholestyramine have been presented. It was concluded that cholestyramine is effective in preventing acute diarrhea induced by pelvic irradiation in patients receiving a low fat diet but is associated with side effects.

Aged↗

PubMed2006

Roles of nuclear receptors in the up-regulation of hepatic cholesterol 7alpha-hydroxylase by cholestyramine in rats.

Nuclear receptors are involved in regulating the expression of cholesterol 7alpha-hydroxylase (CYP7A1), however, their roles in the up-regulation of CYP7A1 by cholestyramine (CSR) are still unclear. In the present study, male Wistar rats were divided into four groups and fed [high sucrose + 10% lard diet] (H), [H + 3% CSR diet] (H + CSR), [H + 0.5% cholesterol + 0.25% sodium cholate diet] (C), or [C + 3% CSR diet] (C + CSR) for 2 weeks. Cholestyramine decreased serum and liver cholesterol levels significantly in rats fed C-based diets, but had no effect on these parameters in rats fed H-based diets. Cholestyramine raised hepatic levels of CYP7A1 mRNA and activity in both groups. The gene expression of hepatic ATP-binding cassettes A1 and G5, regulated by liver X receptor (LXR), were unchanged and down-regulated by cholestyramine, respectively. The mRNA levels of the hepatic ATP-binding cassette B11 and short heterodimer partner (SHP), regulated by farnesoid X receptor (FXR), were not changed by cholestyramine. C-based diets, which contained cholesterol and cholic acid, increased SHP mRNA levels compared to H-based diets. Consequently, in rats fed the C+CSR diet, hepatic FXR was activated by dietary bile acids, but the hepatic CYP7A1 mRNA level was increased 16-fold compared to that in rats fed an H diet. These results suggest that cholestyramine up-regulates the expression of CYP7A1 independently via LXR- or FXR-mediated pathways in rats.

Animals↗

PubMed1995

Changes in plasma apolipoprotein B-containing lipoparticle levels following therapy with fluvastatin and cholestyramine. European Fluvastatin Study Group.

Epidemiologic studies have demonstrated that apolipoprotein (apo) B-containing lipoparticles (LpE:B, LpC-III:B) are associated with the risk of coronary artery disease whereas apo A-1-containing lipoparticles (LpA-I) are protective against coronary artery disease. The effect on lipoparticle levels of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin, in combination with cholestyramine, was assessed in a double-blind randomized study. A total of 144 patients with primary hypercholesterolemia were recruited, who had successfully completed an original study comparing the effects of fluvastatin and cholestyramine on plasma lipoparticle levels. All subjects fulfilled the following inclusion criteria: plasma low density lipoprotein cholesterol (LDL-C) levels > 160 mg/dL, with premature coronary artery disease and 2 associated risk factors; or LDL-C > 190 mg/dL, no coronary artery disease, and triglycerides < 300 mg/dL, after a lipid-lowering diet. Patients were randomized to 1 of 3 combination therapy groups: fluvastatin 20 mg/day plus cholestyramine 4 g/day; fluvastatin 20 mg/day plus cholestyramine 8 g/day; and fluvastatin 20 mg/day plus cholestyramine 16 g/day. The study length was 6 weeks and patients were examined at 3-week intervals. Fluvastatin plus cholestyramine produced a significant (p < 0.001), dose-dependent reduction in levels of cholesterol (range, -29 to -34%), LDL-C (range, -30 to -44%), apo B (range, -23 to -34%), and apo E (range, -33 to -43%). LpE:B levels were also reduced (range, -19 to -26%), but not significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Anticholesteremic Agents↗

PubMed1977

Effect of cholestyramine on digoxin absorption and excretion in man.

Six subjects receiving digoxin therapy for heart disease were studied on two occasions with a single oral dose of 0.5 mg of tritiated digoxin. In every study, all stools and urine were saved for 1 week. Before the second study, treatment with cholestyramine, 4 g every 6 hours, was begun and continued throughout. In three patients, a third study was performed after cholestyramine treatment had been continued for 1 month. Results showed that after cholestyramine administration serum levels, stool output and urinary output of tritiated digoxin varied over a wider range, but cholestyramine had no net short-term effect of any of these variables. After 1 month of cholestyramine administration, there was a small statistically significant increase in stool output of tritiated digoxin and metabolites. In vitro studies suggested that cholestyramine is likely to be a weak digoxin binder in the gut and that changes induced by this resin in digoxin metabolism are not likely to be due to drug binding.

Administration, Oral↗

PubMed1996

Sitosterolemia: opposing effects of cholestyramine and lovastatin on plasma sterol levels in a homozygous girl and her heterozygous father.

Sitosterolemia is a genetic disorder characterized by sitosterol accumulation in plasma and clinically accelerated atherosclerosis. Under a condition of metabolic control with a 30% fat, low-sitosterol diet, we compared the effects of monotherapy and dual-drug treatment with lovastatin and cholestyramine on plasma sterol parameters and endogenous cholesterol synthesis in a homozygous sitosterolemic patient with concomitant heterozygous familial hypercholesterolemia (FH), her obligate heterozygous father, and hyperlipidemic control subjects. We found that for both the sitosterolemic homozygote and heterozygote, cholestyramine plus lovastatin dual therapy proved not to be superior to either drug treatment alone. In the homozygous patient, cholestyramine accounted for the decrease of plasma sterol (ie, lovastatin was ineffective), whereas in the heterozygote, lovastatin represented the margin of difference (ie, low-dose cholestyramine was relatively ineffective). Thus, the best treatment option for this homozygote child and her heterozygote father appears to be monotherapy with cholestyramine and lovastatin, respectively. Stimulation by bile acid malabsorption produced a dramatic decrease of plasma sterols in the homozygote, without increasing endogenous cholesterol synthesis, but this therapy was ineffective in the heterozygote. Decreasing endogenous cholesterol synthesis with lovastatin was effective in the heterozygote, but ineffective in the homozygote. In suspected sitosterolemia, a poor sterol response to lovastatin and a dramatic response to cholestyramine may differentiate homozygous from heterozygous and other familial forms of hyperlipidemia.

Adult↗

PubMed2001

In vitro assessment of the mucoadhesion of cholestyramine to porcine and human gastric mucosa.

Previous in vivo studies have suggested that the extended gastric residence and uniform intragastric distribution of cholestyramine may be due to mucoadherent properties. This series of in vitro investigations explored the possibility of the anion exchange resin exhibiting bioadhesive behaviour, and investigated the characteristics, such as particle size and surface charge, that may affect it. Tensile strength measurements were carried out to determine the mucoadhesion of cholestyramine and other test materials (resin particulates, polymers and hydrogels) with varying adhesive properties, to isolated porcine and human gastric mucosa. Optimal instrumental parameters for the system were determined initially and used; all procedures were carried out at room temperature (22 degrees C). The particle size of cholestyramine did not affect mucoadhesion to either porcine or human gastric mucosa (P=0.673, porcine; P=0.969, human), whilst anionic exchangers were found to provide better mucoadhesion than cationic exchangers (P=0.0002, porcine; P=0.0009, human). In some instances, it was found that the detachment forces recorded were lower with human gastric mucosa than with porcine gastric mucosa, although this was not consistently statistically significant. A rank order of mucoadhesion was constructed from a comparison of cholestyramine with eight other test materials. Cholestyramine produced the second highest degree of mucoadhesion, with Carbopol producing the greatest adhesion. Dextran and polyethylene glycol did not display good mucoadhesion under these conditions. From the findings presented here, we have found that cholestyramine demonstrates good mucoadhesion to both porcine and human gastric mucosa when compared to other known bioadhesives. It is suggested that particle size does not contribute to this mucoadherent behaviour but the surface charge of the resin has a significant part to play.

Adhesiveness↗

PubMed2005

Cholestyramine feeding lowers number of colonic apoptotic cells in rat.

Secondary bile acids that are formed in the colon by bacterial action have the potential property of eliciting pathological conditions. Apoptosis of mucosal epithelial cells is recognized as an adaptation that may counteract such pathologies. Cholestyramine, an anion exchange resin that sequesters bile salts in the gut, could decrease levels of secondary bile salt stress and thus conserve the potency of the protective action. Two groups of rats were studied: those fed 4% cholestyramine and those fed regular rat food. Rats were fed cholestyramine for 7, 14, 21, or 28 d. All animals were evaluated for cell death (apoptosis) using in situ TUNEL staining, and confirmed with single-stranded DNA (ssDNA). The effect of cholestyramine on the proliferating cell nuclear antigen (PCNA) in colonic crypt cells was also examined. Our data shows that animals fed cholestyramine for 28 d show evidence of a significant decrease in the levels of apoptotic cells in their large intestines, particularly goblet cells, when compared with the control animals and no change in cell proliferation. Thus, cholestyramine may serve as an alternative in attenuating apoptosis associated with inflammatory disorders that can result in significant enterocyte and goblet-cell death.

Administration, Oral↗

PubMed1992

Promoting effects of both dietary cholesterol and cholestyramine on pancreatic carcinogenesis initiated by N-nitrosobis(2-oxopropyl)amine in Syrian golden hamsters.

The effects of dietary cholesterol and cholestyramine on pancreatic carcinogenesis initiated with N-nitrosobis(2-oxopropyl)amine (BOP) were investigated in 120 female Syrian golden hamsters. BOP (70 mg/kg body weight) was injected s.c. once at the beginning of the experiment. Starting 2 weeks later, the animals were then maintained on basal diet or diets containing either 0.5% cholesterol or 1% cholestyramine for a further 16 weeks. All surviving hamsters were killed at week 18, and the pancreas tissues examined histologically. The incidences of pancreatic carcinomas in hamsters fed cholesterol and the cholestyramine supplement were 40.0 and 30.0% respectively; in both cases significantly higher than the 6.9% incidence in the basal diet group. Cholesterol contents of the serum, pancreas and liver were significantly increased by cholesterol feeding and significantly decreased by the cholestyramine diet. The cholesterol diet also significantly increased pancreatic protein and DNA contents, and the concentration of total bile acids and the level of lithocholic acid in gallbladder bile. The cholestyramine diet significantly increased total pancreatic DNA and protein contents, and pancreatic weight. The results thus indicated that both dietary cholesterol and cholestyramine can enhance BOP-initiated pancreatic carcinogenesis in hamsters.

Adenocarcinoma↗

PubMed1993

Adjunctive cholestyramine therapy for thyrotoxicosis.

OBJECTIVE: Initial therapy of thyrotoxicosis usually includes beta-blockade for symptom relief and thionamides to block new thyroid hormone synthesis. In view of the increased enterohepatic circulation of thyroxine (T4) and triiodothyronine (T3) in thyrotoxicosis, we proposed that cholestyramine, an anion exchange resin which binds iodothyronines, when used adjunctively with thionamides and a beta-blocker, would lower serum iodothyronine levels faster than would standard therapy alone. DESIGN: A double blind placebo-controlled cross-over design was used with patients randomly assigned to either the treatment or control groups. They received their initial treatment for two weeks (Phase 1) followed by a one-week washout period, and then crossed to the opposite treatment for two weeks (Phase 2). Standard therapy included atenolol 50 mg daily, individualized dosages of methimazole and either 4 g of cholestyramine or 4 g of placebo powder four times per day. PATIENTS: Fifteen patients with thyrotoxicosis (14 Graves' disease, 1 toxic adenoma) participated in this study. MEASUREMENTS: Total and free thyroxine and triiodothyronine, as well as thyroid-stimulating immunoglobulin and thyrotrophin-binding inhibitory immunoglobulin, were measured weekly. RESULTS: Seven patients received cholestyramine and eight patients received placebo during Phase 1. A more rapid decline in all thyroid hormone levels was seen in the cholestyramine-treated group (F = 4-7, P < 0.01) than in the placebo group (F = 2-3.1, P = 0.05). In Phase 2, the eight patients who received cholestyramine showed an additional decline in free thyroxine from weeks one to two, but the overall rate of decline in hormone levels was not different between the groups. Immunoglobulin levels remained unaffected regardless of group, treatment, or time. CONCLUSIONS: We conclude that cholestyramine is a safe and effective adjunctive agent in the treatment of thyrotoxicosis and that its greatest efficacy may be during the first few weeks of treatment.

Adult↗

PubMed1994

The effect of colestipol and cholestyramine on the systemic clearance of intravenous ibuprofen in rabbits.

The effect of oral administration of the non-absorbable anion-exchange resins cholestyramine and colestipol on the systemic clearance and other pharmacokinetic parameters of intravenously administered ibuprofen (25 mg kg-1) was studied in rabbits. Single doses of colestipol hydrochloride (0.4 g kg-1) or cholestyramine (0.17 g kg-1) were given 30 min before ibuprofen administration. In cholestyramine-treated rabbits a significant reduction in ibuprofen plasma concentration was observed compared with both control (water only) and colestipol-treated rabbits. Cholestyramine treatment resulted in a significant decrease in the terminal elimination half-life and the mean residence time. Furthermore, a 31% increase in the systemic clearance and 23% decrease in the area under the plasma concentration-time curve were also observed in cholestyramine-treated rabbits. Colestipol treatment did not change these parameters. The volume of distribution parameters (Vdss and Vd(area)) did not change following either treatment. The changes in the pharmacokinetic parameters are compatible with an acceleration of ibuprofen elimination induced by oral administration of cholestyramine and not by colestipol. This effect is thought to be due to augmentation of net biliary excretion through enteric binding.

Administration, Oral↗

PubMed1995

Calorimetric evaluation of hydration of cholestyramine.

We have investigated the mechanism of hydration of cholestyramine, a water-insoluble resin used pharmaceutically. Two types of water of hydration (freezing and non-freezing) and the amounts of heat evolved or absorbed during the hydration of cholestyramine were determined. From differential scanning calorimetry, 0.57 g water was observed to be tightly bound per gram of resin (non-freezing water). The hydration of dry cholestyramine was found to be exothermic. The heats of hydration of cholestyramine with chloride or nitrate counter-anions were found to be -6.05 and -3.46 cal g-1, respectively. Some of the partially hydrated cholestyramine samples showed absorption of heat during hydration. The data generated in the study were utilized to better understand the mechanism of hydration and swelling of cholestyramine.

Calorimetry, Differential Scanning↗

PubMed1984

Selectivity of cholestyramine treatment on hepatic mixed function oxidase activity.

The possibility that oral cholestyramine treatment might indirectly increase hepatic drug oxidations was investigated in rats using pentobarbital, antipyrine, zoxazolamine, and aminopyrine as probes of the hepatic mixed function oxidase system and in humans using amobarbital and antipyrine as probes. Cholestyramine pretreatment of rats for 5 days (87.5 mg/kg twice daily by stomach tube) shortened pentobarbital sleep times, decreased antipyrine-induced hypothermia, but did not influence either zoxazolamine paralysis times or the in vitro N-demethylation of aminopyrine. Neither pentobarbital nor antipyrine pharmacokinetics in rats were affected by the cholestyramine pretreatment. Similarly, in two-way crossover studies with human subjects, a 5-day oral cholestyramine pretreatment (4 g 3 times daily) had no demonstrable effect on the pharmacokinetics of single doses of amobarbital (200 mg i.v.) or antipyrine (500 mg per os). After cholestyramine pretreatment, a trend toward diminished CNS depression produced by amobarbital was observed, but the effect was not statistically significant. The results suggest that hepatic mixed function oxidases in rats for which aminopyrine, antipyrine, pentobarbital, and zoxazolamine are substrates and that hepatic mixed function oxidases in humans for which amobarbital and antipyrine are substrates are not significantly affected by cholestyramine pretreatment.

Adult↗

PubMed1971

Interruption of the enterohepatic circulation of digitoxin by cholestyramine. II. Effect on metabolic disposition of tritium-labeled digitoxin and cardiac systolic intervals in man.

Previous studies of digitalis glycoside metabolism and excretion have indicated that these compounds undergo a significant enterohepatic cycle in some species. It has been suggested that the existence of such a cycle in man contributes to the prolonged action of certain cardiac glycosides. Previous studies have demonstrated that cholestyramine binds digitoxin and digoxin in vitro and accelerates the metabolic disposition of digitoxin in rats and guinea pigs, presumably by interrupting the enterohepatic circulation. In order to assess the role of the enterohepatic circulation in the metabolism of digitalis glycosides in humans, maintenance doses of cholestyramine were administered to 7 of 15 normal human subjects beginning 8 hr after digitalization with 1.2 mg of digitoxin-(3)H. All subjects had frequent measurements of serum radioactivity, left ventricular ejection time (LVET), and electromechanical systole (QS(2)), the latter recorded as the interval from onset of Q wave to first major component of second heart sound. Measurement of the LVET and QS(2) intervals affords a sensitive index of the cardiac response to digitalis. In addition, chloroform extraction of serum was performed to separate unchanged digitoxin and active metabolites from cardioinactive metabolites of digitoxin. Cholestyramine treatment resulted in reduction in half-life to total serum radioactivity from 11.5 to 6.6 days, and in chloroform-extractable radioactivity from 6.0 to 4.5 days, as compared to controls. In addition, cholestyramine treatment was accompanied by more rapid return to base line values of digitoxin-induced changes in the LVET and QS(2) intervals. A significant positive correlation was found between QS(2) values and chloroform-extractable radioactivity, the latter reflecting unchanged digitoxin-H(3) (r=0.64; P=<0.01). The results indicate that administration of cholestyramine to digitalized human subjects accelerates the metabolic disposition of digitoxin and abbreviates the physiologic response to the glycoside. This effect is presumably mediated by interruption of the enterohepatic circulation of digitoxin by cholestyramine.

Administration, Oral↗

PubMed1982

[Carcinogenicity study of cholestyramine in mice].

Carcinogenicity study of cholestyramine, an anti-hypercholesterolemic agent, was carried out by feeding B6C3F1 mice of both sexes with the pellet diet in which cholestyramine was admixed at the rates of 1.25, 2.5 and 5%. The animals were fed on the drug-admixed diet for 18 months and on a normal diet for subsequent 3 months. After 32 weeks the mortality of male mice began to increase in the 5% cholestyramine group and the number of dead or moribund mice increased markedly after 60 weeks. Hemorrhage recognized in pleural cavity, heart and other organs, was suggested to be the main cause of death. Some kinds of tumors occurred in each group, but the tumor-incidences seen in mice of 1.25 and 2.5% cholestyramine groups were similar to those in mice of the control group and the occurrence of the specific tumor or an acceleration of tumor-development by feeding cholestyramine were not observed. Furthermore, the tumor-incidence in mice fed on the 5% cholestyramine diet was less than that in mice of the other three groups.

Animals↗

PubMed1993

Cholestyramine and bile diversion lower the aminopeptidase activity in the intestinal brush border membrane of rats.

To examine the effect of bile acids on the activity of intestinal aminopeptidase in vivo, we measured the activity of aminopeptidase in the intestinal mucosa from rats fed the diet containing cholestyramine which sequesters luminal bile acids (experiment 1) and from bile diverted rats (experiment 2). After 32 h fasting, rats were refed for 16 h either of a standard diet (25% casein diets), the same diet containing cholestyramine, or the fat-free diet in experiment 1. In the intestinal washing, the content of total bile acids was markedly decreased with feeding cholestyramine and activities of trypsin and chymotrypsin were also lowered with cholestyramine. Cholestyramine feeding decreased the specific activity of aminopeptidase in the homogenate of intestinal mucosa but increased the specific activities of sucrase and alkaline phosphatase. All these parameters were not modified by the fat-free diet. In experiment 2, bile diverted and sham operated rats were refed the standard diet for 16 h with prior 32 h fasting. Bile diversion, like cholestyramine feeding, lowered the content of total bile acids, the activities of pancreatic hydrolases in the intestinal washings, and the specific activity of aminopeptidase in the intestinal mucosa. The specific activity of sucrase in the intestinal mucosa was higher in bile diverted rats but the activity of alkaline phosphatase was not changed. These data indicate that the decreased abundance of intraluminal bile acid affects the activity of intestinal aminopeptidase not through the decreased absorption of dietary lipid.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗

PubMed1975

Effect of cholestyramine on tissue pools of cholesterol a preliminary report.

Four Type II Hyperlipoproteinemic subjects were investigated before and after treatment with cholestyramine. Plasma cholesterol was significantly reduced (365 plus or minus 23 vs 273 plus or minus 34 mg/100 ml) and triglycerides significantly increased (149 plus or minus 55 vs 181 plus or minus 59 mg/100 ml) on cholestyramine treatment. The daily turnover of cholesterol, as determined by the method of Goodman and Nobel, was nearly doubled by the treatment (0.813 plus or minus 0.11 vs 1.595 plus or minus 0.176 g). Although previous workers have already suggested that cholestyramine does not decrease tissue cholesterol pools, we observed a significant increase in tissue pools in each of the three subjects given cholestyramine alone (10.1 plus or minus 1.4 vs 16.2 plus or minus 6.9 g) for Pool A - EXCLUDING PLASMA; AND 27.2 PLUS OR MINUS 4.6 VS 43.7 PLUS OR MINUS 6.4 G FOR Pool B). Treatment for the fourth subject consisted of a combination of cholestyramine and clofibrate. This combination appeared to prevent increases in the size of Pool B and in the size and production rate of Pool A. These preliminary observations suggest that the hypocholesterolemic effect of cholestyramine may be enhanced and its effects on tissue cholesterol prevented by giving it in combination with other agents such as clofibrate.

Adult↗

PubMed2000

Effects of cholestyramine on vitamin E levels in patients treated with statins.

The aim of this study was to investigate the effects of cholestyramine in combination with statins on vitamin E levels and their concentration related to LDL-cholesterol (LDL-C) in patients with hyperlipidemia. In an open-label, randomized study of 25 patients with elevated LDL-C, 12 received cholestyramine (12 g/d) in addition to chronic statin therapy, which had been started at least 8 weeks prior to the study in all patients. At the start and end of the 12-week study period, vitamin E concentrations were measured by high-performance liquid chromatography and cholesterol and triglycerides enzymatically in all patients. Vitamin E levels remained virtually unchanged within normal range before (11.90 +/- 0.71 mg/l) and after 12 weeks (11.69 +/- 0.82 mg/l) of concomitant therapy with cholestyramine. However, the ratio of vitamin E/LDL-C increased from 7.48 +/- 0.56 to 8.58 +/- 0.75 (x 10(-2)) (p < 0.09) in the cholestyramine group but not in the control group. LDL-C concentrations decreased from 162.00 +/- 5.98 to 144.33 +/- 12.48 mg/dl. The authors conclude that cholestyramine 12 g/d given for 12 weeks in addition to chronic statin therapy did not lower vitamin E levels in hyperlipemic patients. However, antioxidant status (vitamin E/LDL-C ratio) seems to be improved by a cholestyramine-associated LDL-C decrease.

Adult↗