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PubMed1979

The effect of various dietary regimens and cholestyramine on aortic glycosaminoglycans during regression of atherosclerotic lesions in rhesus monkeys.

The effect of various diets on the aortic glycosaminoglycan (GAG) composition was studied in rhesus monkeys. Aortas were obtained from monkeys fed diets containing cholesterol and comparative fats including coconut oil--butter and peanut oil and with and without cholestyramine. Additional groups in each experiment were placed on regression diets of low-fat, low-cholesterol with and without cholestyramine. Further, an atherogenic diet of coconut oil--butter was alternated every 2 months with a diet enriched with corn oil. GAG isolated from intima and media--adventitia indicated slight variations in the concentration of total GAG among different dietary groups but major differences in the concentration of individual GAG. The concentrations of hyaluronic acid and heparan sulfate were generally greater in aortas of monkeys fed corn oil diets than in those fed coconut oil--butter or peanut oil diets. The concentration of dermatan suulfate generally decreased during regression of lesions induced by the saturated fat--cholesterol diet. Furthermore, the aortas of monkeys with lesions from feeding peanut oil showed higher levels of dermatan sulfate and lower levels of chondroitin 4-sulfate than the saturated fat-fed groups. The addition of cholestyramine enhanced the effects of regression. These observations show that the composition of GAG of the arterial wall can be influenced by various dietary programs and that GAG play a role in induction and regression of experimental atherosclerotic lesions.

Animals↗

PubMed1983

Some comparative effects of gemfibrozil, clofibrate, bezafibrate, cholestyramine and compactin on sterol metabolism in rats.

Liver cholesterogenesis in rats was measured by giving [l-14C]octanoate i.p.; 1 h later digitonin-precipitable sterols were isolated and counted. In rats fed normal chow and given 7 daily p.o. doses of compounds and then fasted, at 20 h after the last dose, clofibrate or bezafibrate had no effect at lower doses or inhibited incorporation at higher doses, while compactin or gemfibrozil caused increases; cholestyramine added to the diet also caused marked increases. When rats were fed chow containing 0.1% cholesterol and 5.5% peanut oil, again at 20 h following the last of 7 daily doses, gemfibrozil caused increases of incorporation which diminished at higher levels of dosage, while clofibrate caused only inhibition. A single dose of gemfibrozil caused inhibition at 3 h postdose followed by increases over control at 36 and 48 h; a single dose of compactin caused inhibition at 3 h but not subsequent increase, and a single dose of clofibrate had no effect over the entire period. In rats fed chow containing 1.5% cholesterol and 5.5% peanut oil, gemfibrozil given orally or cholestyramine in the diet prevented the diet-induced decreases of plasma HDL cholesterol and increases of liver cholesterol content, while bezafibrate treatment did not have those effects. The effects of cholestyramine rapidly disappeared when it was withdrawn from the diet, while the effects of gemfibrozil persisted after dosage was stopped. These results suggest that some of the actions of gemfibrozil on rat sterol metabolism are quantitatively different from those of the other agents tested.

Animals↗

PubMedDate not supplied

The effect of probucol and cholestyramine combination therapy in severe familial hypercholesterolaemia.

The relative effects of cholestyramine and probucol, alone and in combination, on serum total cholesterol (TC), high density lipoprotein cholesterol (HDL-C) and the ratio of TC to HDL-C (T/HDL-C) have been studied in a group of 10 subjects with severe familial hypercholesterolaemia. The combination of cholestyramine plus probucol was more potent than either agent alone in reducing TC. The use of probucol either alone or in combination reduced the HDL-C concentrations, but the ratio of T/HDL-C was not consistently affected. The effect of the combination therapy did not diminish after periods of at least 6 months and in some cases led to partial regression of long-standing xanthomata. The combination of probucol with cholestyramine did not give rise to additional side effects and it is considered to be a valuable addition to the regimens available for the treatment of severe familial hypercholesterolaemia.

Cholesterol↗

PubMedDate not supplied

Cholestyramine feeding in weaned rats. Increase in plasma corticosterone levels and bile acid synthesis following adrenalectomy.

Feeding cholestyramine to weaned rats increased the bile acid pool and activity of cholesterol 7 alpha-hydroxylase as expected. Following adrenalectomy, cholestyramine still increased the activity of cholesterol 7 alpha-hydroxylase but the magnitude of increase was lower (P less than 0.01) than noted in intact rats. Surprisingly, cholestyramine feeding to both intact and adrenalectomized rats increased plasma levels of corticosterone.

Adrenal Glands↗

PubMed1992

Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St Thomas' Atherosclerosis Regression Study (STARS)

To assess the effect of dietary reduction of plasma cholesterol concentrations on coronary atherosclerosis, we set up a randomised, controlled, end-point-blinded trial based on quantitative image analysis of coronary angiograms in patients with angina or past myocardial infarction. Another intervention group received diet and cholestyramine, to determine the effect of a greater reduction in circulating cholesterol concentrations. 90 men with coronary heart disease (CHD), who had a mean (SD) plasma cholesterol of 7.23 (0.77) mmol/l were randomised to receive usual care (U, controls), dietary intervention (D), or diet plus cholestyramine (DC), with angiography at baseline and at 39 (SD 3.5) months. Mean plasma cholesterol during the trial period was 6.93 (U), 6.17 (D), and 5.56 (DC) mmol/l. The proportion of patients who showed overall progression of coronary narrowing was significantly reduced by both interventions (U 46%, D 15%, DC 12%), whereas the proportion who showed an increase in luminal diameter rose significantly (U 4%, D 38%, DC 33%). The mean absolute width of the coronary segments (MAWS) studied decreased by 0.201 mm in controls, increased by 0.003 mm in group D, and increased by 0.103 mm in group DC (p less than 0.05), with improvement also seen in the minimum width of segments, percentage diameter stenosis, and edge-irregularity index in intervention groups. The change in MAWS was independently and significantly correlated with LDL cholesterol concentration and LDL/HDL cholesterol ratio during the trial period. Both interventions significantly reduced the frequency of total cardiovascular events. Dietary change alone retarded overall progression and increased overall regression of coronary artery disease, and diet plus cholestyramine was additionally associated with a net increase in coronary lumen diameter. These findings support the use of a lipid-lowering diet, and if necessary of appropriate drug treatment, in men with CHD who have even mildly raised serum cholesterol concentrations.

Angina Pectoris↗

PubMed1989

Cholestyramine as an antidote against paracetamol-induced hepato- and nephrotoxicity in the rat.

Besides hepatotoxicity, paracetamol may exert nephrotoxic effects in experimental animals and man. The present study in rats shows that cholestyramine given 4 and 24 h after paracetamol provided protection against both hepato- and nephrotoxicity; this was evidenced by reduced increments in plasma enzyme activities (SDH, GPT), indicating liver damage, and diminished retention of plasma and creatinine, indicating renal failure. The recovery of paracetamol and its conjugates in urine was markedly reduced by cholestyramine at 24-48 h after treatment. The protective effects of cholestyramine are explained by adsorption of paracetamol and conjugates in the intestine undergoing biliary excretion and enterohepatic circulation.

Acetaminophen↗

PubMed2004

Hydrophilic 7 beta-hydroxy bile acids, lovastatin, and cholestyramine are ineffective in the treatment of cerebrotendinous xanthomatosis.

We compared the effect of treatments with hydrophilic bile acids (ursodeoxycholic and ursocholic acids), cholestyramine, and lovastatin versus chenodeoxycholic acid in 4 patients with cerebrotendinous xanthomatosis (CTX). Bile acids and bile alcohols in plasma, bile, and urine before and after treatment were quantitated by gas-liquid chromatography. Untreated, all patients showed abnormal biliary bile acid composition: cholic acid (72.7%) and chenodeoxycholic acid (6.2%), and polyhydroxylated C(27)-bile alcohols (10.0%), and elevated plasma cholestanol levels. Treatment with hydrophobic chenodeoxycholic acid inhibited abnormal bile acid synthesis (virtual disappearance of C(27)-bile alcohols from plasma, bile, and urine and marked reduction of plasma cholestanol levels). Hydrophilic ursodeoxycholic and ursocholic acids did not inhibit abnormal bile acid synthesis, while cholestyramine increased abnormal bile acid synthesis (continued increased formation of polyhydroxylated C(27)-bile alcohols and further elevation of plasma cholestanol levels). Lovastatin did not affect abnormal bile acid synthesis or reduce plasma cholestanol levels. The results demonstrate that impaired side-chain oxidation in bile acid synthesis due to mutations of Cyp27 results in increased formation of polyhydroxylated C(27)-bile alcohols and cholestanol in CTX. Hydrophobic chenodeoxycholic acid, but not cholestyramine, lovastatin, or hydrophilic 7beta-hydroxy acids, inhibited the abnormal synthetic pathway. The role of chenodeoxycholic acid in downregulating abnormal bile acid synthesis in CTX is emphasized.

Adult↗

PubMed1989

Cost effectiveness of cholesterol-lowering therapy in The Netherlands. Simvastatin versus cholestyramine.

Using a model of coronary heart disease incidence based on multivariate logistic regression functions from the Framingham Heart Study, the cost effectiveness of simvastatin was compared with that of cholestyramine in preventing such disease. For men with initial cholesterol levels of 310 mg/dl, the cost effectiveness of cholestyramine, expressed in Dutch guilders, ranges from approximately 220,000 to 510,000 guilders per year of life saved, depending on age at initiation of therapy. For simvastatin, cost-effectiveness ratios range from 50,000 to 110,000 guilders per year of life saved among this group of men. Results are similar for women, although the cost effectiveness of both agents is considerably less. These results suggest that simvastatin is substantially more cost effective than cholestyramine; that it compares well with other generally accepted medical practices, especially if therapy is initiated at an early age; and that simvastatin should become accepted as a drug of first choice in the treatment of persons with elevated serum cholesterol levels as its long-term safety record becomes more established.

Adult↗

PubMed1997

Plasma cholesteryl ester transfer protein is lowered by treatment of hypercholesterolemia with cholestyramine.

Cholestyramine (INN, colestyramine) treatment of subjects with hypercholesterolemia reduced the plasma level of cholesteryl ester transfer protein (CETP) as measured by radioimmunoassay (CETP-RIA) and, as expected, also reduced the levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, and apolipoprotein B. The extent of CETP variation was significant only in the subjects whose LDL cholesterol levels were reduced by more than 25%. Furthermore, CETP-RIA was correlated with total cholesterol, LDL cholesterol, and apolipoprotein B concentrations. Plasma CETP was also measured by an indirect procedure that uses high-density lipoprotein (HDL) 14C-cholesteryl ester and very low-density lipoprotein cholesterol from a pool of plasma donors, and the patient's plasma as the source of CETP. The two procedures for CETP determination correlated well with each other, although the CETP-RIA was more sensitive in the detection of changes of plasma CETP ascribed to cholestyramine (INN, colestyramine) treatment. The rise of plasma HDL cholesterol levels after cholestyramine probably resulted from the reduction of CETP activity.

Anticholesteremic Agents↗

PubMed1999

Long-lasting cytoprotection after pentadecapeptide BPC 157, ranitidine, sucralfate or cholestyramine application in reflux oesophagitis in rats.

Recently, the effectiveness of pentadecapeptide BPC 157 and other anti-ulcer agents, called 'direct cytoprotection', was evidenced in totally gastrectomized rats duodenum challenged with cysteamine 24 h after surgery, and sacrificed 24 h after ulcerogen application. The further focus was on the possibility that this effect could be seen over a more prolonged period (1, 2, 4 weeks), and in other parts of the gastrointestinal tract (i.e. oesophagus). After the removal of the stomach, the oesophagus and jejunum were joined by a termino-lateral anastomosis. The animals were euthanized 7, 14 or 28 d after surgery, when oesophagitis was blindly assessed both macroscopically (percentage of ulcerations areas) and microscopically (percentage of areas of ulcers, regeneration and hyperplasia; number of inflammatory cells - polymorphonuclear and mononuclear). Starting 24 h after surgery, the medication was continuously given in the drinking water, in a volume of 12.5 mL/rat daily, until euthanasia at the end of the observation period, i.e. 7, 14, 28 d following surgery. Based on previous experiments, the doses of agents were daily calculated per kg b.w. as follows: BPC 157 125 mg or 125 ng, cholestyramine 2.5 mg, ranitidine 125 mg, sucralfate 725 mg, whereas controls received 72.5 mL x kg(-1) water. In support of these initial findings, and considering gastrectomized acid-free rats as an ideal model for long-term cytoprotective studies as well, pentadecapeptide BPC 157 markedly attenuated termino-lateral oesophagojejunal anastomosis-reflux oesophagitis also over a quite prolonged period. This efficacy was only partly shared by other anti-ulcer agents. After 1-week-old oesophagitis (microscopical assessment), but not after 2 or 4 weeks, less damaged mucosa was noted in rats drinking ranitidine or sucralfate compared to controls. Similar effectiveness was noted for cholestyramine. The obtained results were supported also by inflammatory cell assessment. Compared with control values, BPC 157-treated groups consistently presented less polymorphonuclears and less mononuclears in all assessed periods. Interestingly, the values obtained in other treated groups showed no difference compared with control values. Thus, despite limitations, a generalization supporting a direct importance of a common cytoprotective approach, could be clearly provided. A useful, long-lasting cytoprotective activity (apparently more prominent in BPC 157 rats, than in reference agents, ranitidine, sucralfate, as well as cholestyramine) may be a likely suitable therapy in otherwise resistant reflux oesophagitis conditions.

Animals↗

PubMed1980

Cholestyramine and spironolactone and their combination in digitoxin elimination.

The effects of oral cholestyramine 4 gm 8 times daily and spironolactone 300 mg daily, given independently and in combination, on the elimination rate of digitoxin were studied in 6 healthy subjects pretreated with 0.1 or 0.15 mg oral digitoxin daily for 30 days before each intervention. The mean pretreatment digitoxin concentrations for the group ranged from 21 +/- 2.9 (SD) ng/ml to 28.5 +/- 6.9 ng/ml. The mean control digitoxin half-life (t 1/2) was reduced from 141.6 to 84.4 by treatment with cholestyramine alone. Treatment with spironolactone alone prolonged the mean digitoxin t 1/2 to 192.2 hr. The mean digitoxin t 1/2 after both active drugs was intermediate at 102.9 hr. Spironolactone did not fulfill the expectation from animal studies that it would enhance the clearance of digitoxin by cholestyramine. The prolongation of digitoxin elimination after spironolactone may contraindicate this drug in digitoxin intoxication.

Canrenone↗

PubMed1998

Idiopathic bile acid malabsorption: qualitative and quantitative clinical features and response to cholestyramine.

BACKGROUND: Idiopathic bile acid malabsorption is a poorly recognized cause of chronic diarrhoea. The SeHCAT (75Selenium HomotauroCholic Acid Test) can accurately diagnose this condition. AIM: To identify patients with idiopathic bile acid malabsorption, to describe their clinical features, both qualitatively and quantitatively, and to assess the response to cholestyramine. METHOD: Idiopathic bile acid malabsorption was considered in all patients complaining of chronic diarrhoea. They were included in the study if their SeHCATs were positive (< 15% retention) and secondary causes of bile acid malabsorption were excluded. The response to therapy with cholestyramine was assessed. RESULTS: Nine patients were diagnosed with idiopathic bile acid malabsorption (median SeHCAT retention 8%, range 3-12.6). Their median daily faecal weight was 285 g (range 85-676) and median faecal fat output was 17 mmol/24 h (range 8.3-38.8). Six patients had an immediate response to cholestyramine. There was a marked reduction in stool frequency (median stool frequency pre-treatment 5/day vs. 2/day post-treatment, P = 0.03). Five patients had large volume diarrhoea (faecal weight > 200 g/day) and three had steatorrhoea. CONCLUSIONS: Idiopathic bile acid malabsorption, once suspected, especially by documenting true 'large volume' watery diarrhoea or steatorrhoea, is easily diagnosed and response to therapy is often very good. There is often a previous history of gastrointestinal infection and this condition should be considered in patients with chronic diarrhoea of undetermined origin, especially before they are labelled as having irritable bowel syndrome.

Absorption↗

PubMed1978

Treatment of chlordecone (Kepone) toxicity with cholestyramine. Results of a controlled clinical trial.

Industrial workers exposed to the organochlorine pesticide, chlordecone (Kepone), had signs of toxicity in several organs. The extent of toxicity was proportional to the levels of this chemical in the tissues. In 22 patients, chlordecone was eliminated slowly from blood (half time of 165 +/- 27 days--mean +/- S.E.M.) and fat (half time of 125 days, with a range of 97 to 177), chiefly in the stool. Output of chlordecone in bile was 10 to 20 times greater than in stool, suggesting that chlordecone is reabsorbed in the "ntestine. Cholestyramine, an anion-exchange resin that binds chlordecone, increased its fecal excretion by seven times. In a five-month trial, cholestyramine significantly accelerated elimination of chlordecone from blood, with a half life of 80 +/- 4 days (S.E.M.) (P less than 0.005) and fat (half life of 64 days, with a range of 52 to 85) (P less than 0.05). Cholestyramine offers a practical means for detoxification of persons exposed to chlordecone and possibly to other lipophilic toxins.

Adolescent↗

PubMed1980

Cholestyramine promotes receptor-mediated low-density-lipoprotein catabolism.

We studied the influence of cholestyramine (24 g per day) on receptor-mediated and receptor-independent low-density-lipoprotein catabolism in five women with heterozygous familial hypercholesterolemia. Cholestyramine lowered the level of circulating low-density-lipoprotein apoprotein by doubling (P less than 0.01) its fractional clearance via the receptor path, but fractional catabolism by the receptor-independent route remained unchanged. Moreover, although the absolute rate of catabolism of the apoprotein was not affected by treatment, the amounts handled by each pathway altered. Catabolism via the physiologically controllable receptor route increased by 71 per cent (P less than 0.05), but there was a 12 per cent drop in clearance by the nonreceptor pathway. These data demonstrate the utility of cholestyramine in promoting low-density-lipoprotein catabolism via its specific physiologic clearance pathway. They also show that heterozygotes with familial hypercholesterolemia can increase the activity of their low-density-lipoprotein receptors when presented with an appropriate stimulus.

Adult↗

PubMed1976

Effect of bran and cholestyramine on plasma lipids in monkeys.

Semipurified diets whose cholesterol content varied from 34 to 120 mg/100 kcal were given to adult female cynomolgus monkeys (Macaca fascicularis) for 9 months. The intake of dietary fiber was increased through the addition of wheat, rice, or soya bran; 5% cholestyramine was given to one group of monkeys. None of the brans reduced plasma levels of cholesterol, whereas cholestyramine produced marked hypocholesterolemic effects. Triglyceride levels increased with higher cholesterol intake, but no additional changes were induced by any of the experimental diets. Plasma phospholipids were reduced by cholestyramine.

Animals↗

PubMed1990

Cholestyramine resin ameliorates chronic aminonucleoside nephrosis.

We chose to assess the role of cholesterol reduction in chronic aminonucleoside nephrosis by pharmacologically lowering serum cholesterol with cholestyramine. Two groups of rats were made nephrotic with a single intravenous dose of puromycin aminonucleoside (PA): one group (PA/resin) received 5% (w:w in diet) cholestyramine resin and the dietary control group (PA/cell) received 5% cellulose. Cholestyramine-treated rats demonstrated significant functional and histological protection. Recurrent proteinuria was significantly lower in PA/resin animals. Whole-kidney glomerular filtration rate in the PA/resin group was preserved at a level equivalent to normal age-matched control rats whereas the PA/cell group had a significantly lower value than did the normal animals. The extent of segmental glomerulosclerosis 24 wk after PA delivery was significantly lower in the PA/resin group. These results suggest a role for hyperlipidemia as one of the mechanisms involved in the pathogenesis of progressive glomerular disease.

Animals↗

PubMed1991

Hepatic cholesterol and fatty acid synthesis in pregnant and fetal rats: effect of maternal dietary fat and cholestyramine.

Previous studies from this laboratory have demonstrated that 20% rather than 5% (wt/wt) safflower oil or addition of 5% (wt/wt) cholestyramine to the diet of pregnant rats leads to an increase in the activity of 3-hydroxy-3-methylglutaryl CoA reductase, the rate-limiting enzyme of cholesterol synthesis, in the fetal liver. Total cholesterol, however, was not altered in fetal plasma or liver. The effect of these diets on cholesterol and fatty acid synthesis in vivo was therefore studied in fetal and maternal liver. In fetuses of rats fed a reference nonpurified diet, rates of hepatic cholesterol and fatty acid synthesis decreased from gestation d 20 to 21. In contrast, total and active 3-hydroxy-3-methyl-glutaryl CoA reductase activity increased. Adding cholestyramine to the diet or modifying the quantity of safflower oil fed had no effect on fetal hepatic lipogenesis. Maternal hepatic cholesterol synthesis was greater in rats fed cholestyramine, whereas fatty acid synthesis was lower in the dams fed the diet containing 20% compared with 5% safflower oil. The results suggest near-term fetal liver 3-hydroxy-3-methylglutaryl CoA reductase activities do not reflect fetal cholesterol synthesis in vivo.

Administration, Oral↗

PubMed1995

Apolipoprotein mRNA in liver and intestine of rats is affected by dietary beet fiber or cholestyramine.

Rats were fed a cholesterol-free diet with no added fiber (fiber-free) or with 15 g/100 g beet fiber or 5 g/100 g cholestyramine for 14 d. Final plasma total cholesterol concentrations were significantly lower in rats fed beet fiber than in those fed fiber-free or cholestyramine diets. This difference was due mainly to lower HDL cholesterol concentrations. The group fed beet fiber also tended (P < 0.1) to have lower apolipoprotein A-I concentration in plasma. Northern blot analysis revealed that the relative concentrations of jejunal apolipoprotein A-I and A-IV mRNA were the same in all groups, whereas ileal apolipoprotein A-I and A-IV mRNA levels were significantly lower in rats fed beet fiber or cholestyramine than in those fed the fiber-free diet. Hepatic apolipoprotein E mRNA concentrations were the same in all groups, but apolipoprotein A-I mRNA levels were significantly lower in rats fed beet fiber than in those fed the other diets. Apolipoprotein A-IV mRNA tended (P < 0.1) to be lower in rats fed the beet fiber diet. These data suggest that the hypocholesterolemic effect of dietary beet fiber is associated with diminished expression of the hepatic apolipoprotein A-I gene.

Animals↗