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PubMed1992

Effects of cholestyramine on lipoprotein levels and metabolism in Syrian hamsters.

Oral administration of cholestyramine to adult male hamsters not only induced a marked decrease in plasma concentrations of cholesterol and LDL but had a similar lowering effect on plasma triacyglycerol and VLDL concentrations. The hypotriglyceridaemic effects of resin administration were not due to an increase in lipoprotein lipase, as post-heparin plasma lipoprotein lipase activities were unchanged, but rather to a 35% decrease in VLDL synthesis. Measurement of the disappearance rate of apolipoprotein B from VLDL after i.v. injection of 125I-labelled hamster or human VLDL into control and cholestyramine-fed recipient animals showed a 2-times lower T1/2 in the drug-treated animals. The fraction of VLDL apolipoprotein B, recovered at any time after injection in the LDL, was equal or higher in cholestyramine-fed animals as compared to controls. These data indicate that the lowering in plasma LDL by cholestyramine in male hamsters is due not only to LDL receptor up-regulation but also to a lower rate of VLDL synthesis. No indications were found for a decreased efficiency of VLDL to LDL conversion in cholestyramine-fed animals.

Animals↗

PubMed1995

Fermentable carbohydrates exert a more potent cholesterol-lowering effect than cholestyramine.

The purpose of this work was to assess the respective role of bile acid excretion and of the end-products of cecal fermentations in the cholesterol-lowering effect of complex carbohydrates. The effects of two different fermentable carbohydrates (guar gum, beta-cyclodextrin), and sequestrant resin (cholestyramine) have been investigated in male Wistar rats. Guar gum and beta-cyclodextrin are broken down in the large bowel, with fermentation rich in propionic acid (37% against 26% for control), whereas cholestyramine did not enhance cecal fermentation. beta-Cyclodextrin and guar gum were less potent than cholestyramine to enhance bile acids and sterol excretion. Nevertheless, fermentable carbohydrates exerted a more potent cholesterol-lowering effect than cholestyramine. beta-Cyclodextrin also depressed triacylglycerol-rich lipoprotein (TGRLP). Fermentable carbohydrates lowered cholesterol of LDL and HDL1 fractions. The induction of hepatic HMG-CoA reductase was practically proportional to rate of fecal steroid excretion. Moreover, with beta-cyclodextrin, hepatic HMG-CoA reductase induction was concomitant to a decrease in fatty acid synthase (FAS) activity. Thus, the cholesterol-lowering effect of fermentable carbohydrates could be related to a depressed lipogenesis, as well as to an accelerated removal of HDL1, in relation to an elevated hepatic demand of cholesterol. In conclusion, fermentable carbohydrates could favour cholesterol elimination and have a general lipid-lowering effect by exerting more complex physiological effects than cholestyramine.

Animals↗

PubMedDate not supplied

Cholestyramine in type IIa hyperlipoproteinemia. Is low-dose treatment feasible?

The present study was undertaken to evaluate the possible lipid-lowering effects of low-dose cholestyramine medication in type IIa hyperlipoproteinemia. A total of 16 patients, 8 with heterozygous familial hypercholesterolemia and 8 with polygenic hypercholesterolemia, were investigated. After an initial 3-month period of dietary treatment, 8 of the patients were randomly selected for medication with 4 g of cholestyramine twice daily, and the other 8 received a dose of 8 g twice daily for 2 months. The regimens were then exchanged, and the patients followed for a further 2 months. Plasma lipids and lipoprotein cholesterol were determined at intervals of 4 weeks. Total plasma cholesterol was reduced by 17% during treatment with 8 g and somewhat more (26%) during treatment with 16 g of cholestyramine daily. The decrease in plasma LDL cholesterol did not differ during treatment with 8 g (27%) and 16 g (31%); no changes in plasma triglycerides, VLDL- or HDL-cholesterol were seen. Although plasma LDL-cholesterol was higher in patients with familial hypercholesterolemia, there was no obvious influence of the genetic origin of hypercholesterolemia on the response. It is concluded that low-dose treatment with cholestyramine lowers, and sometimes normalizes, LDL-cholesterol in hypercholesterolemia. Furthermore, the LDL-cholesterol level obtained during the 16-g dose could be predicted from the response seen during treatment with 8 g of cholestyramine daily.

Adult↗

PubMed1982

Cholestyramine plus pectin in treatment of patients with familial hypercholesterolemia.

The effects of a combined therapy, composed of a cholesterol-lowering diet, cholestyramine (16 g/day) and apple pectin (12 g/day), were studied on serum lipoproteins in 6 men with familial hypercholesterolemia. All subjects were treated with diet alone, diet plus cholestyramine and diet plus cholestyramine and pectin for at least 8 weeks on each regimen. In these severely hypercholesterolemic subjects the combined treatment with diet plus cholestyramine and pectin lowered serum cholesterol by 31% and LDL-cholesterol by 35% corresponding to a 19% and 22% further decrease respectively relative to diet plus cholestyramine. We conclude that the addition of the well-tolerated natural cholesterol-lowering product is valuable in the treatment of familial hypercholesterolemia.

Adult↗

PubMed1984

A comparison of cholestyramine and probucol in the treatment of familial hypercholesterolaemia.

Twelve patients with familial hypercholesterolaemia (FH) who had not achieved satisfactory cholesterol levels on dietary advice alone were treated with cholestyramine for 6 months and probucol for 6 months in a randomised cross-over study to compare the relative effectiveness of the two drugs. Over the 6-month period, mean total cholesterol fell by 16.4% on cholestyramine and 12.7% on probucol. Cholestyramine produced a 17.4% fall in low density lipoprotein (LDL) cholesterol, no significant changes in very low density lipoprotein (VLDL) cholesterol or high density lipoprotein (HDL) cholesterol, a 21.4% increase in HDL cholesterol subfraction HDL2 and a 24.1% increase in the HDL/LDL cholesterol ratio. Triglyceride levels rose by 29.6% but remained within the normal range. Probucol produced a 11.7% fall in LDL cholesterol, a 9.9% fall in VLDL cholesterol, a 10% fall in total HDL cholesterol, a 37% fall in HDL cholesterol subfraction HDL2 and no change in the HDL/LDL cholesterol ratio. Triglyceride levels fell by 14%. The mean corrected QT interval increased from 0.418 to 0.434 s (P less than 0.01) on probucol but did not change significantly on cholestyramine (from 0.405 to 0.41 s). The two drugs have different metabolic effects on FH. Cholestyramine has a more marked effect on LDL cholesterol, favourably influences the HDL/LDL cholesterol ratio and is therefore considered to be the drug of choice.

Cholesterol↗

PubMed1993

SK&F 97426-A a more potent bile acid sequestrant and hypocholesterolaemic agent than cholestyramine in the hamster.

SK&F 97426-A is a novel bile acid sequestrant which was selected for comparison with cholestyramine in vivo because of its superior in vitro bile acid binding properties. The effects of the two sequestrants on faecal bile acid excretion, plasma total cholesterol, VLDL + LDL and HDL cholesterol and triglyceride concentrations and on liver enzymes involved in the synthesis and metabolism of cholesterol were investigated in normocholesterolaemic hamsters. Four studies were conducted to determine the relative potencies of the two resins using a range of doses of the sequestrants over treatment periods of up to 2 weeks. Curves fitted to the resulting data allowed common maximum responses and separate ED50s to be calculated for each sequestrant. The maximum response of both sequestrants was to increase bile acid excretion by 352% and lower plasma total cholesterol by 37-58%. LDL + VLDL and HDL cholesterol were reduced by 56-75% and 25-41%, respectively. SK&F 97426-A was 3 times more potent than cholestyramine at increasing the excretion of bile acids in the faeces and 2.1-3.4-fold and 2.3-3.2-fold more potent at lowering total plasma cholesterol and LDL plus VLDL cholesterol, respectively. In some of the experiments SK&F 97426-A was also more potent than cholestyramine at lowering HDL cholesterol. Plasma triglycerides were also lowered by both sequestrants by up to 31% after 1 week but the relative potency could not be determined. These HDL cholesterol and total triglyceride lowering effects of bile acid sequestrants in the hamster are known not to occur in people treated with cholestyramine. There were minimal differences between hamsters treated for 1 or 2 weeks in the relative potencies or ED50s calculated for the total plasma cholesterol, LDL + VLDL and HDL cholesterol. Both sequestrants may have been slightly more efficacious on these parameters after 2 weeks of treatment. Liver weights were reduced by about 15% by both sequestrants at 2% (w/w) in the diet for 1 week. The activities of the liver HMG-CoA reductase and cholesterol 7 alpha-hydroxylase were increased as expected, whilst the activity of the acyl-CoA:cholesterol acyltransferase was reduced by both sequestrants at this dose. SK&F 97426-A was, therefore, 2-3-fold more potent as a bile acid sequestrant and hypocholesterolaemic agent than cholestyramine when tested in the hamster.

Animals↗

PubMed1989

Regulation of low density lipoprotein apoprotein B metabolism by lovastatin and cholestyramine in miniature pigs: effects on LDL composition and synthesis of LDL subfractions.

A major factor in the regulation of low density lipoprotein (LDL) apoprotein B (apo B) concentrations in miniature pigs is the direct synthesis of LDL apo B. LDL apo B derived from plasma very low density lipoproteins (VLDL) accounts for only 20% to 30% of total LDL synthesis. Treatment with lovastatin and cholestyramine can inhibit the direct synthesis pathway in this species, thereby lowering LDL apo B concentrations. The present study was carried out to determine if lovastatin alone was as effective as in combination with cholestyramine. The possibility that the direct synthesis pathway was confined to a specific subclass of LDL and the effect of lovastatin and cholestyramine on the metabolism of LDL subfractions were also investigated. Homologous 125I-VLDL and 131I-LDL were injected into miniature pigs during a control period and again following 18 days of treatment with lovastatin (1.2 mg/kg/d, n = 4) or in combination with cholestyramine (1.0 g/kg/d, n = 4). Kinetic analysis of apo B specific activity curves following lovastatin treatment indicated that LDL apo B pool size was decreased by 25% (P less than .025), which was due entirely to a 70% (P less than .025) decrease in the direct synthesis of LDL apo B, since VLDL-derived apo B, and LDL fractional catabolic rate (FCR) were not affected. Parameters of VLDL apo B metabolism were not affected. Lovastatin in combination with cholestyramine was more effective than lovastatin alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Effects of short-term cholestyramine feeding on cholesterol metabolism in differently aged rats.

The effects of short-term (7 days) feeding of a diet containing cholestyramine (5%) on the cholesterol metabolism were studied in male Sprague-Dawley rats at ages of 5 weeks (young) and 9-10 months (adult). Cholestyramine significantly enhanced the activities of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase and cholesterol 7 alpha-hydroxylase both in young and adult rats; however, the absolute values were significantly higher in the former. The time-courses of changes in the activities of these enzymes after cessation of cholestyramine were comparable in both groups of rats. The rate of incorporation of mevalonate into sterol was also higher in young than in adult rats, while the stimulating effect of cholestyramine was markedly greater in adult rats. Hepatic acyl-CoA:cholesterol acyltransferase activity was comparable, but cholestyramine significantly decreased it only in adult rats. In adult rats hepatic cholesterol was decreased significantly by the resin while it remained uninfluenced in young rats. The serum cholesterol level tended to be higher in adult rats regardless of the dietary manipulation. The results indicate an appreciable age-dependent change in the hepatic cholesterol metabolism in response to the interruption of enterohepatic circulation of bile acids.

Aging↗

PubMed1993

Use of cholestyramine in the treatment of children with familial combined hyperlipidemia.

We studied the effectiveness of and compliance with the use of cholestyramine in children with heterozygous familial hypercholesterolemia (FH) and familial combined hyperlipidemia (FCHL). During a 10-year period, 673 children (aged 10.5 +/- 4.0 years) were referred for evaluation of hyperlipidemia, of whom 87 (36 with FH; 51 with FCHL) were treated with cholestyramine (8 to 24 gm/day). In both groups, total cholesterol, low-density lipoprotein (LDL)-cholesterol, and apolipoprotein B levels were significantly reduced after cholestyramine use. In those with FH, plasma LDL-cholesterol levels decreased from 258 +/- 35 mg/dl (6.67 +/- 0.90 mmol/L) to 190 +/- 31 mg/dl (4.91 +/- 0.80 mmol/L); in those with FCHL, LDL-cholesterol levels dropped from 207 +/- 40 mg/dl (5.35 +/- 1.03 mmol/L) to 141 +/- 35 mg/dl (3.64 +/- 0.90 mmol/L). High-density lipoprotein-cholesterol levels were not significantly changed after cholestyramine use in either group. In the FCHL group, plasma triglyceride levels increased significantly from 81 +/- 35 mg/dl (0.92 +/- 0.40 mmol/L) to 134 +/- 42 mg/dl (1.52 +/- 0.48 mmol/L). Seven patients were lost to follow-up; 18 discontinued the medication within 1 month. Of the remaining 62 children, 59 had a good response to the drug. Of the 62 patients, 52 discontinued the medication after 21.9 +/- 10 months. Adverse effects included foul taste (73%), nausea with bloating (18%), and constipation. Cholestyramine is effective in reducing LDL-cholesterol levels in children with inherited hyperlipidemia, but the majority of children will not comply with its long-term use.

Adolescent↗

PubMed1988

Effects of simvastatin and cholestyramine on lipoprotein profile in hyperlipidaemia of nephrotic syndrome.

The efficacy, safety, and tolerability of simvastatin (20 mg twice a day) in the treatment of hyperlipidaemia due to unremitting nephrotic syndrome was compared with that of cholestyramine (8 g twice a day) in a crossover trial in ten patients. Two patients were taken off the protocol, one because he could not tolerate cholestyramine and one because of non-compliance with the cholestyramine regimen. No clinical or laboratory adverse experiences were noticed during the study in the other eight patients. Simvastatin was significantly more effective than cholestyramine in reducing the hyperlipidaemia--it produced a 36% decrease in total cholesterol and a 39% decrease in low density (LDL)-cholesterol, whereas cholestyramine reduced total cholesterol by 8% and LDL-cholesterol by 19%. With simvastatin the apolipoprotein B level decreased by 30%, whereas the apolipoprotein A level increased by 10%.

Adult↗

PubMed1991

Effect of competing anions on binding of bile salts by cholestyramine.

The binding of bile salts by cholestyramine may be influenced by other anions, as the Langmuir adsorption coefficients for three bile salts tested were similar to the model anion, citrate. However, the selectivity coefficient indicated preferential binding of cholate anion in comparison to citrate anion. Binding experiments confirmed cholestyramine's preference for bile salts as the presence of other anions reduced but did not prevent the binding of cholate anion. Binding of cholate anion was reduced in direct relationship to the citrate anion concentration. Prior exposure of cholestyramine to citrate anion caused the binding of cholate anion to decrease slightly. Sequential exposure of cholestyramine to simulated gastric fluid and simulated intestinal fluid containing cholate anion resulted in a decrease in cholate binding which was attributed to competition with anions present in the gastrointestinal fluids. Components of tomato juice and orange juice, fluids, commonly used to enhance ingestion of cholestyramine, also reduced the binding of cholate anion.

Adsorption↗

PubMed2005

The effect of cholesterol reduction with cholestyramine on renal function.

BACKGROUND: Epidemiological studies suggest that dyslipidemia is an independent risk factor for the development of renal insufficiency in otherwise healthy individuals. Yet, data on the effect of cholesterol reduction are lacking in this population. We performed a secondary analysis of a large existing cohort to determine whether treatment with cholestyramine improved renal function compared with placebo. METHODS: A total of 3,603 middle-aged men from the Lipid Research Clinics Coronary Primary Prevention Trial comprised the study group: 1,806 men were randomly assigned to treatment with cholestyramine, and 1,797 men, placebo. The primary outcome is difference in glomerular filtration rates between the 2 groups. RESULTS: A total of 1,806 men were randomly assigned to treatment with cholestyramine, and 1,797 men, placebo. For the entire group, the estimated mean difference in glomerular filtration rates between the cholestyramine and placebo groups was 0.39 mL/min/1.73 m2 (0.007 mL/s/1.73 m2; P = 0.28) during a follow-up period of more than 8 years. CONCLUSION: Cholesterol reduction with cholestyramine treatment did not meaningfully affect renal function compared with placebo in the present analysis. Prospective intervention trials are needed to determine whether decreasing serum cholesterol levels benefits kidney function in otherwise healthy individuals.

Adult↗

PubMed2006

Intestinal cholesterol absorption inhibitor ezetimibe added to cholestyramine for sitosterolemia and xanthomatosis.

Sitosterolemia is a rare, recessively inherited disorder characterized by increased absorption and delayed removal of noncholesterol sterols, which is associated with accelerated atherosclerosis, premature coronary artery disease, hemolysis, and xanthomatosis. Treatments include low-sterol diet and bile salt-binding resins; however, these often do not reduce the xanthomatosis. We examined the effects of the intestinal cholesterol/phytosterol transporter inhibitor ezetimibe added to cholestyramine in a young female patient with sitosterolemia and associated xanthomatosis. The patient was an 11-year-old female with sitosterolemia presenting with prominent xanthomas in the subcutaneous tissue of both elbows who was receiving treatment with cholestyramine 2 g once daily. Bilateral carotid bruits were audible, and a grade II/VI systolic murmur was detected at the left upper sternal border. She also had a low platelet count of 111,000/microL. Ezetimibe 10 mg once daily was added to the patient's ongoing cholestyramine regimen, and she was evaluated for 1 year. The patient followed an unrestricted diet during the 1-year treatment period. After 1 year of treatment with ezetimibe added to ongoing cholestyramine therapy, the patient's plasma sitosterol and campesterol levels decreased by approximately 50%. Her carotid bruits completely resolved, her systolic murmur diminished, and her platelet count rose to 268,000/microL. More remarkably, the tuberous xanthomas on her elbows had completely regressed. Ezetimibe added to ongoing low-dose cholestyramine therapy led to a marked improvement in plasma sterol concentrations, complete regression of xanthomatosis, resolution of carotid bruits, and improvement in cardiac murmur in a young female patient with sitosterolemia.

Anticholesteremic Agents↗

PubMed1982

Effect of feeding beta-sitosterol alone or in combination with cholestyramine during early life on subsequent response to cholesterol challenge in adult life in guinea-pigs.

The effect of feeding 20 g beta-sitosterol/kg alone or in combination with cholestyramine (20 g/kg) during neonatal life of guinea-pigs on their subsequent response to a dietary cholesterol challenge in adult life was examined. 2. beta-Sitosterol pretreated animals showed higher plasma cholesterol values following 2 weeks on a cholesterol challenge (2-5 g/kg) diet, but did not differ significantly from control values for the remainder of the cholesterol challenge period. 3. Guinea-pigs pretreated with beta-sitosterol plus cholestyramine, on the other hand, showed a marked increase in plasma cholesterol levels over those of controls during the cholesterol challenge period, and this "hyper-responder" behaviour was maintained throughout the study period. 4. Despite the increase in plasma cholesterol, beta-sitosterol plus cholestyramine pretreated animals excreted significantly (P less than 0.05) greater amounts of bile acids and total sterols. 5. These findings demonstrate that neonatal pretreatment with beta-sitosterol plus cholestyramine has detrimental effects on the handling of a cholesterol challenge in adult life, and does not achieve the beneficial effect previously noted with pretreatment with cholestyramine alone.

Animals↗

PubMed1983

Comparative effects of chitosan and cholestyramine on lymphatic absorption of lipids in the rat.

The effects of chitosan and cholestyramine on intestinal absorption of oleic acid and cholesterol were assessed in adult male rats with cannulae in the thoracic duct lymphatic channel. In acute studies, 50 mg of either cholestyramine or chitosan were included in the test emulsion for intragastric administration. Over a 24-h lymph collection period, cholestyramine caused a 47% depression of cholesterol absorption and a 32% interference with oleic acid absorption. Chitosan had a similar effect on the absorption of both lipids under these conditions (51 and 41% depression, respectively). Studies were also conducted in animals fed for 4 wk on defined diets containing 1 and 5% levels of the test materials. Absorption of lipids from the standard aqueous emulsion was tested in lymph duct cannulated rats which had been fasted overnight. In these animals, prefeeding either cholestyramine or chitosan at the 1% level caused an 18 to 28% reduction in absorption of both lipids with greater variability in the chitosan-fed group. When either test material was fed at the 5% level, absorption of cholesterol was reduced by 63 to 69% and absorption of oleic acid by 58 to 62%. Although these agents may act by different mechanisms, the data suggest that chitosan is as effective as cholestyramine in its acute effects on lipid absorption and that, with chronic feeding, both materials cause equivalent adaptive changes in intestinal transport of administered fatty acid and cholesterol.

Animals↗

PubMed1995

Pretreatment with enteral cholestyramine prevents suppression of the cellular immune system after partial hepatectomy.

OBJECTIVE: The authors tested the hypothesis that the beneficial effects of the endotoxin-binding agent cholestyramine on the postoperative course in rats that had undergone a partial hepatectomy was the result of improvement of cellular immune functions. SUMMARY BACKGROUND DATA: Major liver resection is associated with severe postoperative complications and a high incidence of systemic infections. Gut-derived endotoxins previously were shown to be involved in the pathogenic processes after partial hepatectomy in rats. In addition, enteral cholestyramine improved postoperative survival, but how its beneficial effects are mediated is not clear. METHODS: Rats that were force-fed for 7 days with either cholestyramine (150 mg/day) or 0.9% saline (equal volume) were randomized to undergo a partial hepatectomy or a sham operation. After 24 hours, the rats were killed and splenic mononuclear cells were tested in vitro for mitogenic responses and cytokine production. RESULTS: Proliferative responses of splenic B and T lymphocytes and lipopolysaccharide-stimulated production of tumor necrosis factor and interleukin-1 by splenocytes were lower in rats after partial hepatectomy than in sham-operated animals. An increased concanavalin A-stimulated production of interleukin-2 also was found after partial hepatectomy compared with sham levels. Pretreatment with enteral cholestyramine preserved cellular proliferative responsiveness of both B and T cells, and restored cytokine production by splenocytes to sham levels. CONCLUSION: Prophylactic treatment with enteral cholestyramine preserved cellular immune functions after partial hepatectomy in the rat, which may explain its beneficial effects on the postoperative course. Furthermore, the authors' results are consistent with the hypothesis that endotoxemia is involved in the pathogenesis of the cellular immune derangements after partial hepatectomy.

Administration, Oral↗

PubMed1985

Oral rehydration, rapid feeding, and cholestyramine for treatment of acute diarrhea.

Different combinations of fluid therapy, feeding regimen, and cholestyramine were compared in search for optimal treatment of infants hospitalized for acute diarrhea. The infants (n = 81) received either rapid oral rehydration using the oral rehydration solution-World Health Organization formula (sodium 90 mmol/L, ORS-WHO) or traditional oral fluid replacement using a commercial glucose-electrolyte solution (sodium 35 mmol/L). One-half of the infants in both groups received full feedings at 24 h of hospitalization; in the remaining infants, feedings were gradually introduced over a period of 5 days. In addition, all the children were randomized to receive either cholestyramine 2 g four times daily or an equivalent amount of placebo. Rehydration with ORS-WHO, but not traditional fluid replacement therapy, led to correction of initial metabolic acidosis after 6-10 h; no cases of hypernatremia were observed with the use of ORS-WHO. Rapid return to full feedings appropriate for age, including milk products, was associated with better weight gain and significantly shorter duration of diarrhea compared with gradual introduction of feedings. Cholestyramine treatment further shortened the duration of diarrhea without adverse effects in those children who had received ORS-WHO and thus were properly rehydrated. In contrast, in children with poor initial hydration, cholestyramine treatment was associated with prolonged metabolic acidosis. We conclude that treatment of acute diarrhea by rehydration with ORS-WHO and rapid introduction of full feedings is effective and safe, and this combination forms a therapy of choice for typical hospitalized cases of acute infantile diarrhea in Finland. Cholestyramine may be of value as an adjunct therapy after adequate rehydration.

Acute Disease↗

PubMed1992

Interaction of tricyclic antidepressants with cholestyramine in vitro.

The adsorption of amitriptyline, desipramine, doxepin, imipramine, and nortriptyline onto cholestyramine was demonstrated in vitro with use of 1.2 mol/L HCl at 37 degrees C to simulate gastric fluid. Binding to cholestyramine was approximately 80% for each of the tricyclic antidepressants, and this was about the same degree of binding noted with a nonpharmaceutical, non-ionic resin widely used in the diagnostic toxicology laboratory (Amberlite XAD-2). In contrast, five other non-antidepressants (acetaminophen, chlordiazepoxide, procainamide, quinidine, and theophylline) showed only minimal binding to cholestyramine under these conditions. Activated charcoal completely bound all drugs studied. These findings suggest that cholestyramine should be used with caution in patients receiving tricyclic antidepressants. They also suggest that cholestyramine may be a potentially useful adjunctive therapy in treatment of overdose with the tricyclic antidepressants.

Adsorption↗