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PubMed2005

The effect of combination therapy with propylthiouracil and cholestyramine in the treatment of Graves' hyperthyroidism.

OBJECTIVE: The study aims to evaluate the efficacy of combination therapy with propylthiouracil (PTU) and cholestyramine in the treatment of Graves' hyperthyroidism. BACKGROUND: Thyroxine (T4) is metabolized mainly in the liver by conjugation to glucuronides and sulphates that enter the enterohepatic circulation. Thyrotoxic patients have an abnormal increase in thyroid hormone in their enterohepatic circulation. Previous studies on combination therapy with methimazole and cholestyramine for Graves' hyperthyroidism have shown it to be an effective adjunctive treatment. In this study, we examined the efficacy of combination therapy with PTU and cholestyramine in the treatment of Graves' hyperthyroidism. METHODS: Thirty patients with newly diagnosed Graves' hyperthyroidism were randomly divided into two groups: group I (n = 15) received PTU 100 mg twice a day, propranolol 40 mg twice a day and cholestyramine 4 g twice a day for 4 weeks; group II (n = 15) received PTU 100 mg twice a day and propranolol 40 mg twice a day for 4 weeks. The therapeutic efficacy was determined by serum total triiodothyronine (TT3), free thyroxine (FT4) and TRAb levels at baseline, and at the end of 2 and 4 weeks during the study period. RESULTS: There was no significant difference in baseline thyroid function parameters. At the end of 2 and 4 weeks of the study period, serum TT3 and FT4 levels of group I were significantly lower than those of group II. No significant differences in the TRAb level were found between the two groups. CONCLUSION: Cholestyramine contributed to a more rapid and complete decline in thyroid hormone levels in patients with Graves' hyperthyroidism. It was thus proved to be an effective and well-tolerated adjunctive therapy.

Adolescent↗

PubMed1988

Cholestyramine treatment of type IIa hypercholesterolaemia normalizes platelet reactivity against prostacyclin.

The effect of lowering total plasma and low density lipoprotein (LDL) cholesterol in heterozygous familial hypercholesterolaemia type IIa (FH) on platelet function, thromboxane (TX) formation and platelet sensitivity against iloprost, a stable prostacyclin mimetic, was studied in platelet-rich plasma ex vivo. Seven FH patients were treated with cholestyramine (12 g day 1) for 8-11 months and were compared with eight untreated FH patients and 11 healthy control subjects. In comparison with platelets from healthy controls, platelets from untreated FH patients exhibited a significantly increased aggregation response and TX formation, and a reduced reactivity against inhibition of platelet aggregation by prostacyclin. Treatment with cholestyramine for 8-11 months resulted in a 21% reduction in total serum and LDL-cholesterol. This was not accompanied by any change in platelet hyperreactivity or TX formation. However, cholestyramine treatment normalized the platelet reactivity of FH patients against iloprost, being no more different from healthy controls. It is concluded that reduction in plasma cholesterol by cholestyramine results in normalization of the reduced platelet sensitivity against prostacyclin. This might contribute to beneficial effects of cholestyramine treatment in preventing thromboembolic complications of atherosclerosis.

Blood Platelets↗

PubMed1992

Effects of cholestyramine and acipimox on subfractions of plasma low density lipoprotein. Studies in normolipidaemic and hypercholesterolaemic subjects.

Two independent studies were designed to investigate the separate and combined effects of acipimox and cholestyramine on plasma low density lipoprotein subfractions. In the first study, normolipidaemic subjects were given cholestyramine (16 g day-1, 4 weeks), followed, after an 8-week wash-out period, by acipimox (750mg day-1, 4 weeks). In the second study, moderately hypercholesterolaemic subjects were prescribed acipimox (1250mg day-1, 10 weeks), followed by acipimox in combination with low dose cholestyramine (12g day-1) for a further 10 weeks. In the normal subjects, cholestyramine decreased total LDL mass (density (d) = 1.019-1.063g ml-1) by selectively reducing the largest, least dense LDL-I (d 1.025-1.034 g ml-1, P less than 0.05) and LDL-II (d 1.034-1.044 g ml-1, P less than 0.005) subfractions. The small, dense LDL-III (d 1.044-1060 g ml-1) showed a variable response to the resin. In the same subjects acipimox produced no overall change in total LDL mass but showed a tendency to redistribute LDL towards LDL-I (+10%) and LDL-II (+10%) in a manner related to the changes in plasma triglyceride (TG) (TG vs. LDL-III r = 0.75, P less than 0.05). In the hypercholesterolaemic subjects acipimox induced a substantial redistribution of LDL subfractions (LDL-I +84% P less than 0.05; LDL-III -50%) without affecting total LDL mass. The addition of cholestyramine produced a significant decrease in total LDL mass which was again confined to the LDL-I (-28%) and LDL-II (-23%) subfractions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Clearance of chylomicron-like lipid emulsions is increased in normal rabbits but not in heterozygous Watanabe heritable hyperlipidaemic rabbits following treatment with cholestyramine or pravastatin.

1. Cholestyramine and pravastatin are two potent hypocholesterolaemic drugs which lower plasma cholesterol by increasing the clearance of low density lipoproteins by high affinity uptake mechanisms. 2. We gave heterozygous Watanabe heritable hyperlipidaemic rabbits (hz-WHHL) cholestyramine and/or pravastatin for a two week period to try and ameliorate slow clearance of chylomicron remnants, which occurs because of reduced expression of the apolipoprotein B100/E receptor. 3. In hz-WHHL rabbits the clearance of chylomicron-like lipid emulsions, traced by the decrease in plasma cholesteryl oleate radioactivity was not improved following treatment with either of the cholesterol lowering drugs. 4. In contrast, control rabbits had significantly less chylomicron-like emulsion cholesteryl-ester radioactivity remaining at each time of blood sampling. 5. Similarly, the clearance of chylomicron-like emulsion triolein was enhanced in normal rabbits receiving cholestyramine or pravastatin, whereas there was no detectable increase in clearance in hz-WHHL rabbits. 6. Combined treatment with cholestyramine and pravastatin increased the rate of receptor-mediated uptake in vivo in control rabbits but not in hz-WHHL rabbits. 7. The plasma lipid profiles of control and hz-WHHL rabbits paralleled the patterns of chylomicron-like emulsion clearance. Moderate hypertriglyceridaemia was identified in hz-WHHL rabbits compared to controls and there was no change in plasma triglyceride or cholesterol following drug therapy. In contrast, control rabbits had decreased plasma lipids following cholestyramine or pravastatin treatment. 8. It appears that therapy with lipid lowering drugs increased chylomicron remnant clearance in control rabbits by up-regulation of the apolipoprotein B100/E receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1996

Preservation of endothelium-dependent relaxation in cholesterol-fed and streptozotocin-induced diabetic mice by the chronic administration of cholestyramine.

1. Experiments were designed to investigate the effects of the low density lipoprotein (LDL)-lowering drugs cholestyramine on serum LDL levels and endothelium-dependent relaxation to acetylcholine (ACh) in cholesterol-fed or streptozotocin (STZ)-induced diabetic mice. 2. In aortic rings from control mice, ACh or A23187 caused concentration-dependent relaxation. The relaxations caused by ACh or A23187 were significantly attenuated in aortic rings from cholesterol-fed and STZ-diabetic mice. The attenuated vasodilatation in both cholesterol-fed and diabetic mice was returned to normal by chronic administration of cholestyramine. The endothelium-independent relaxations of aortic rings induced by sodium nitroprusside (SNP) were not significantly different between control, cholesterol-fed and STZ-induced diabetic mice. 3. The increased LDL levels in cholesterol-fed and diabetic mice were returned to normal by the chronic administration of cholestyramine. Chronic administration of cholestyramine had no effects on serum glucose levels. 4. These results suggest that attenuated endothelium-dependent vasodilatations in both cholesterol-fed and STZ-diabetic mice are improved by the chronic administration of cholestyramine, and these effects are, at least in part, due to lowering serum LDL levels.

Acetylcholine↗

PubMed1985

Effect of enterocoated cholestyramine on bowel habit after ileal resection: a double blind crossover study.

Ileal resection causes malabsorption of bile acid; the increased load of bile acids in the colon induces increased secretion of salt and water and hence diarrhoea. A study was carried out to test the effect of an enterocoated cholestyramine tablet designed to disintegrate in the colon and sequester the bile acids there, thereby minimising diarrhoea induced by bile acids while having no effect on malabsorption of bile acid and jejunal fat absorption. The study comprised 14 patients who had undergone ileal resection of 40-150 cm for Crohn's disease. A double blind crossover trial was performed with placebo and cholestyramine enterocoated with cellulose acetate phthalate. During treatment with cholestyramine the daily faecal output decreased, the number of defecations each week decreased, and the intestinal transit time increased. Acceptability of the tablets was high, in contrast with general clinical experience with cholestyramine powder. No change was observed in the total faecal output of bile acids or fat. Cholestyramine tablets caused a reduction in diarrhoea without noticeably interfering with the metabolism of fat or bile acid.

Adult↗

PubMed1984

The influence of changes in lipid values induced by cholestyramine and diet on progression of coronary artery disease: results of NHLBI Type II Coronary Intervention Study.

The National Heart, Lung and Blood Institute Type II Coronary Intervention Study, a double-blind, placebo-controlled trial, evaluated the efficacy of reduction in cholesterol levels induced by cholestyramine on progression of coronary artery disease (CAD). The rate of CAD progression in patients treated with cholestyramine plus diet was compared with that of patients treated with placebo plus diet. CAD progression was defined angiographically. Significant decrease in total cholesterol (TC) and low-density lipoprotein cholesterol (LDLc) and increases in high-density lipoprotein cholesterol (HDLc), as well as in HDLc/TC and HDLc/LDLc ratios, were observed with cholestyramine. HDLc change was due to increase in HDL2A and HDL2B. When the relationship between CAD progression and lipid changes was examined independent of specific treatment group, a significant inverse relationship was found between progression at 5 years and the combination of an increase in HDLc and a decrease in LDLc; changes in HDLc/TC and HDLc/LDLc were the best predictors of CAD change. While the testing of these relationships independent of treatment group was not part of the initial study design, the trends were observed in both the placebo-treated and cholestyramine-treated groups. Moreover, with multivariate analysis, the effect of cholestyramine treatment on CAD progression was eliminated by adding changes in HDLc/TC to the regression model. These findings support the hypothesis that increases in HDLc and decreases in TC (or LDLc) can prevent or delay CAD progression.

Adult↗

PubMed1996

Treatment of hyperthyroidism with a combination of methimazole and cholestyramine.

The entero-hepatic circulation of thyroid hormones is increased in thyrotoxic states. Based on this observation, the use of ionic exchange resins to bind thyroid hormones in the intestine has been tried. The present study evaluates the effectiveness of cholestyramine as an adjunctive therapy in the management of hyperthyroid Graves' disease. Thirty patients with newly diagnosed hyperthyroid Graves' disease were randomly assigned to one of the following treatment groups: methimazole, propranolol and cholestyramine for 4 weeks (group I); methimazole and propranolol for 4 weeks (group II); methimazole, propranolol, and cholestyramine for 2 weeks, followed by 2 weeks of methimazole and propranolol (group III). At the end of the study, total and free T4 as well as T3 levels had decreased more in group I compared with group II: 61%, 78%, 68% in group I compared with 43%, 65%, 50% in group II (P = 0.037 for T4, P = 0.038 for free T4, P = 0.012 for T3). Group III behaved like group I while patients were receiving cholestyramine, but once the drug was discontinued, the rate of decline of thyroid hormones slowed down. We conclude that cholestyramine represents an effective and well-tolerated adjunctive therapy in patients with hyperthyroid Graves' disease, and it produces a more rapid and complete decline in thyroid hormone levels in these patients.

Cholestyramine Resin↗

PubMed1997

Cholestyramine influences meal-stimulated pancreaticobiliary function and plasma cholecystokinin independent of gastric emptying and food digestion.

BACKGROUND: Cholestyramine enhances gallbladder emptying and plasma cholecystokinin responses to oral ingestion of a mixed meal. It is not known whether this effect occurs independently of alterations in gastric emptying or maldigestion of nutrients. METHODS: We perfused 15 g of an amino acid meal intraduodenally for 60 min in seven healthy volunteers, once with and once without cholestyramine. Intraduodenal perfusion of saline with or without cholestyramine (6 g/h) was started 60 min before the amino acid meal and continued for 2 h. RESULTS: Cholestyramine markedly enhanced the incremental plasma cholecystokinin response to the meal from 36 +/- 12 to 139 +/- 25 pmol/l x 60 min (P < 0.005), incremental amylase output from 2.4 +/- 0.7 to 5.7 +/- 0.7 kU/h (P < 0.05), and incremental integrated gallbladder contraction from 1948 +/- 235 to 2840 +/- 189% x 60 min (P < 0.05). CONCLUSION: The enhancing effect of cholestyramine on postprandial gallbladder contraction, pancreatic enzyme secretion, and plasma cholecystokinin release is not dependent on gastric emptying rates or appropriate digestion of nutrients.

Adult↗

PubMed1991

Effects of rice bran fibre and cholestyramine on the faecal excretion of Kanechlor 600 (PCB) in rats.

1. As rice bran fibre binds Kanechlor 600 (PCB), the present study was conducted to determine whether the fibre stimulates rat faecal excretion of PCB in vivo. 2. In rats fed diets containing rice bran fibre, lignin and cholestyramine, the faecal excretion of PCB was increased. Total PCB excreted in rat faeces for groups fed diets of 10% (w/w) rice bran fibre, 10% fibre plus 5% lignin, 5% cholestyramine and 10% fibre plus 5% cholestyramine were 3.4, 3.7, 2.2 and 5.4 times as much, respectively, as that of control rats. The greatest effect on the faecal excretion of PCB was thus obtained with rice bran fibre plus cholestyramine. 3. In rats fed these diets, PCB concentration of the small intestine was significantly decreased to 25-50% of that of controls. PCB of spleen in rats fed diets of 10% fibre, 10% fibre plus 5% lignin and 10% fibre plus 5% cholestyramine also decreased to 50% of that of controls. However, PCB of other tissues were not affected.

Animals↗

PubMed1990

Effect of cholestyramine in early weaning on later response to serum and fecal steroid levels and cholesterol 7 alpha-hydroxylase activity to high-cholesterol diet in ExHC rats.

Male ExHC (exogenous hypercholesterolemic) rats were either prematurely weaned at 17 days of age or allowed to nurse until 35 days of age. The prematurely weaned rats were either fed a diet containing cholestyramine or cholestyramine-free diet until 35 days of age. Cholestyramine supplementation markedly increased fecal bile acid excretion and modified the composition. After giving a stock diet for 7 weeks, all rats received a cholesterol-enriched diet for 9 weeks. The serum cholesterol level in later time was not affected by early dietary manipulation. The activity of hepatic cholesterol 7 alpha-hydroxylase and fecal bile acid excretion at the end of the cholesterol challenge decreased in the cholestyramine-pretreated group, when compared to the normally weaned group. Fecal excretion and the ratio of the secondary (deoxycholic and lithocholic acids) to the primary (cholic and chenodeoxycholic acids) bile acids significantly decreased in the early cholestyramine-treated group. These results suggest that a modification of bile acid metabolism in early life may strongly influence the hepatic and possibly colonic bile acid metabolism in later life, when challenged with a high-cholesterol diet.

Animals↗

PubMed1991

[Concentration profile of PCBs in the digestive tract of rat fed with cholestyramine and rice bran fiber diet].

The aim of this study is to examine the inhibitory effect of rice bran fiber (RBF) and cholestyramine for intestinal absorption of polychlorinated biphenyls (PCBs). Sixteen rats were orally given at the dose of 100 mg of PCBs per kg of the animal, and were divided into four groups (A-D): Rats in each group were housed with the normal diet for the first 7 days, and subsequently, were given with the same diet as control for group A, with the diet containing 10% RBF for group B, with the diet containing 5% cholestyramine for group C and with the combined diet containing 10% RBF and 5% cholestyramine for group D for the next 10 days. All rats were sacrificed on the 17th day after PCBs administration, and PCBs in contents of the digestive tracts were determined: small and large intestine resected was divided into two parts each of the same length, and the contents were chemically analyzed to determine PCBs. PCBs concentration in rats of group A decreased in order of upper portions (1.0 microgram/g) and then lower (0.6 microgram/g) of small intestine, and upper (0.5 microgram/g) and then lower (0.4 microgram/g) of large intestine. Decreasing the PCBs concentration might be due to re-absorption in the intestine. In the case of groups B-D, PCBs concentration was in order of upper and then lower of small intestine, and large intestine. It was indicated that PCBs re-absorption in intestine is inhibited by the intake of RBF, cholestyramine, and RBF and cholestyramine.

Animals↗

PubMed1991

Bioavailability of folate following ingestion of cholestyramine in the rat.

The effect of cholestyramine ingestion on the intestinal deconjugation and absorption of folic acid (PGA) and brewers yeast folate was investigated using a rat bioassay and liver folate uptake as the response parameter. Male weanling Sprague Dawley rats were depleted on a low AIN-76A formulated basal diet for 21 days. During a 14 day repletion period folic acid (PGA) and brewers yeast were added to provide 0.25, 0.5 and 1.0 mg of folate per kg of diet. Cholestyramine was administered directly as part of the diet at 1.1%. All diets were made isonitrogenous and isocaloric. Based on a parallel line assay, the relative biological value of folate for PGA + cholestyramine (79) was significantly different from the standard diet (PGA = 100), while those for brewers yeast (88) and for brewers yeast + cholestyramine (88) did not differ from the standard diet. Ingestion of cholestyramine significantly reduced the bioavailability of PGA versus brewers yeast folate in rats.

Animals↗

PubMed1990

Potentiation of azaserine by cholestyramine in the rat.

In the rat, when pancreatic growth is stimulated there is an increased incidence of spontaneous pancreatic neoplasms and marked potentiation of the pancreatic carcinogen azaserine. Since previous studies showed that cholestyramine caused pancreatic growth in this species we have now studied the effect of azaserine in rats fed soya flour diets containing cholestyramine. Two groups, each of eight rats, were fed either heated soya flour (HSF) or raw soya flour (RSF). Two further groups, each of 12 rats, received the same diets containing 2% cholestyramine (HSF + C, RSF + C). In each group, four rats received azaserine (30 mg/kg i.p.) and the remainder saline, weekly, for the first 5 weeks. Animals were killed after 24 weeks and pancreatic growth and the number and size of pancreatic neoplastic nodules was measured. RSF caused a significant increase in pancreatic weight, protein, RNA and DNA, compared with HSF and cholestyramine caused a further significant increase in pancreatic weight, protein and RNA but not DNA. Azaserine did not affect pancreatic growth. In azaserine-injected rats significantly more nodules were seen and the nodules were larger and the tumour burden greater in rats fed HSF + C than in rats fed HSF alone. However, the nodule count and other nodule parameters were not significantly different in RSF and RSF + C fed rats. It is concluded that 2% cholestyramine enhances pancreatic growth when added to soya flour diets and in rats fed HSF it potentiates the action of azaserine on the pancreas. It does not increase the potentiation of azaserine seen with RSF up to 24 weeks.

Animals↗

PubMed1988

A multicenter comparison of lovastatin and cholestyramine therapy for severe primary hypercholesterolemia. The Lovastatin Study Group III.

This study compares lovastatin and cholestyramine resin therapy in patients with severe primary hypercholesterolemia. Two hundred sixty-four patients on lipid-lowering diets were randomized equally to receive 12 g of cholestyramine resin, 20 mg of lovastatin, or 40 mg of lovastatin, each twice a day. The mean reductions among the three groups after 12 weeks' treatment in levels of total plasma cholesterol (-17%, -27%, and -34%, respectively) and low-density lipoprotein cholesterol (-23%, -32%, and -42%, respectively) and the median reductions in apolipoprotein B levels (-21%, -28%, and -33%, respectively) were all significantly different between groups. Similar mean increases in high-density lipoprotein cholesterol levels (8%, 9%, and 8%, respectively) and median increases in apolipoprotein A-1 levels (7%, 6%, and 11%, respectively) were observed in all treatment groups. Cholestyramine resin treatment had no significant effect on very low-density lipoprotein cholesterol and apolipoprotein A-II levels and produced a median 11% increase in plasma triglyceride concentration; in contrast, administration of either 20 or 40 mg of lovastatin twice a day was associated with median reductions in very low-density lipoprotein cholesterol levels (-34% and -31%, respectively) and plasma triglyceride levels (-21% and -27%, respectively) and median increases in levels of apolipoprotein A-II (8% and 13%, respectively). Adverse events in all treatment groups were preponderantly in the gastrointestinal tract; gastrointestinal tract symptoms that could be attributed to therapy with a specific drug occurred in 58% of the cholestyramine resin group, 13% of the 20-mg lovastatin group, and 14% of the 40-mg lovastatin group. The only drug-attributable serious adverse event was a reversible myopathy in a patient taking 40 mg of lovastatin twice a day. We conclude that lovastatin is both more effective and better tolerated than cholestyramine resin in the treatment of primary hypercholesterolemia.

Adult↗

PubMed1986

Acceleration of the elimination of tenoxicam by cholestyramine in the dog.

Two commonly used adsorbents, activated charcoal and cholestyramine, were evaluated in vitro for their ability to adsorb the nonsteroidal anti-inflammatory drug tenoxicam and in vivo for their use in influencing the elimination kinetics of this drug. The Langmuir binding isotherms determined in buffer solutions at pH 7.5 indicated a much greater adsorption capacity of cholestyramine (1.63 g of drug per g of resin) than of charcoal (0.18 g/g of adsorbent) for the acidic drug with a pKa of 5.3. When single i.v. tenoxicam administrations to dogs were followed by multiple p.o. cholestyramine doses the elimination rate of the drug was accelerated drastically. Due to an increased total body clearance (0.65 vs. 0.13 liters/hr), the elimination half-life was reduced from a median base-line value of 31 to 5.4 hr and the mean residence time of drug in the body was decreased from 41 to 7.9 hr. In contrast to cholestyramine, charcoal hardly increased the rate of elimination of tenoxicam over the base-line values determined in the same animals. Inasmuch as these results were similar in all three animals investigated and because the study design precluded an influence of the treatment sequence, it is concluded that cholestyramine efficiently sequesters intestinally secreted tenoxicam and can thereby accelerate drug elimination from the body.

Administration, Oral↗

PubMed1987

Acceptability of cholestyramine or colestipol combinations with six vehicles.

Preferences for cholestyramine or colestipol in combination with orange drink, orange juice, grape juice, apple juice, water, or apple sauce were evaluated in 40 healthy adults. Each subject evaluated the taste, texture, and smell of 30-mL samples of 12 drug-vehicle combinations (two drugs, six vehicles) using modified five-point wine-tasting scales. Samples were prepared to contain either cholestyramine 1.0 g or colestipol hydrochloride 1.3 g. The products were tested at room temperature and were administered in a random order. Subjects and observers were blinded to the identity of the products. Acceptability scores for taste, texture, and smell were significantly higher for cholestyramine than for colestipol. Total mean preference scores for cholestyramine-vehicle combinations ranged from 9.9 to 11.7; for colestipol, 6.3 to 8.9. Orange drink, apple juice, grape juice, and orange juice were the preferred vehicles for cholestyramine. The preferred vehicles for colestipol were orange drink, apple sauce, and apple juice.

Adult↗

PubMed1985

Hypocholesterolemic agents: a comparison of the relative effectiveness of cholestyramine and pectin in rats.

Studies were carried out to evaluate the comparative effectiveness of cholestyramine and pectin as hypocholesterolemic agents. Circulating levels of serum cholesterol and lipoprotein-associated cholesterol were measured in rats fed high cholesterol diet supplemented with either cholestyramine or pectin. When compared with controls, a significant decrease in the level of total cholesterol was observed in rats fed either cholestyramine or pectin (p less than 0.001, 43% reduction in cholesterol, and p less than 0.04, 25% reduction in cholesterol, respectively) and this was due exclusively to the lowering of low density lipoprotein. Further statistical evaluation of data revealed no significant difference between the cholesterol levels of rats fed either cholestyramine or pectin (p greater than 0.07). The data acquired in this study suggest that both cholestyramine and pectin are comparable and effective hypocholesterolemic agents and the observed hypocholesterolemic effect of these agents is mediated through lowering of cholesterol associated with the low density lipoprotein.

Animals↗