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PubMed1987

Different patterns of postprandial lipoprotein metabolism in normal, type IIa, type III, and type IV hyperlipoproteinemic individuals. Effects of treatment with cholestyramine and gemfibrozil.

To study exogenous fat metabolism, we used the vitamin A-fat loading test, which specifically labels intestinally derived lipoproteins with retinyl palmitate (RP). Postprandial RP concentrations were followed in total plasma, and chylomicron (Sf greater than 1,000) and nonchylomicron (Sf less than 1,000) fractions. In normal subjects postprandial lipoproteins were present for more than 14 h, and chylomicron levels correlated inversely with lipoprotein lipase activity and fasting high density lipoprotein (HDL) cholesterol levels and nonchylomicron levels correlated inversely with hepatic triglyceride lipase activity. The main abnormality in type IV patients was a 5.6-fold increase in the chylomicron fraction, whereas in type III patients it was a 6.4-fold increase in nonchylomicrons. Type IIa patients had abnormally low chylomicron fractions. In type IV patients gemfibrozil decreased, whereas in type IIa patients cholestyramine increased the chylomicron fraction 66 and 88%, respectively. This study demonstrates an unexpectedly large magnitude and long duration of postprandial lipemia in normal subjects and patients. These particles are potentially atherogenic, and their role in human atherosclerosis warrants further study.

Cholestyramine Resin↗

PubMed1997

Cholestyramine therapy for quinidine-induced diarrhea. Case reports.

The effective use of quinidine as an antiarrhythmic agent is frequently curtailed by one of its most common side effects-relentless diarrhea. Seven patients are described in whom diarrhea was quickly and completely controlled by the use of cholestyramine resin. To date, this is the only therapy reported to be effective for this purpose. It has proven to be safe, well tolerated, and continuously effective in these cases.

Aged↗

PubMed1996

Drug interaction between simvastatin and cholestyramine in vitro and in vivo.

The interaction between simvastatin (SV), a prodrug lactone, HMG-CoA reductase inhibitor which converts to the active hydroxy acid form (SVH) in vivo, and cholestyramine (CT), an anionic exchange resin, was evaluated both in vitro and in vivo. In an in vitro SV-stability study, it was shown that SV degraded gradually to SVH in an aqueous solution at pH 2 and 7. To evaluate the binding ability of SV or SVH to CT, the incubation of 5 micrograms/ml of SV or SVH solution with 200 mg of CT in various pH (2.0, 5.0 and 7.0) solutions was performed at 37 degrees C for 10 min. After incubation, the concentration of SV decreased by 59.02% (pH 2), 63.90% (pH 5) and 67.36% (pH 7), respectively, and an interaction between SV and CT was suggested. The values were much larger than those expected from the stability test of SV in the absence of CT. SVH was found to bind more strongly to CT. The binding ability of SVH to CT was 66.71% (pH 2), 87.44% (pH 5) and 92.11% (pH 7), respectively. Judging from these results, SV was considered to interact with CT by the following procedure: SV underwent hydrolysis to SVH in aqueous solution, then CT activated the hydrolysis by binding the formed SVH, resulting in a significant reduction in concentration of SV. On the other hand, an in vivo animal experiment also demonstrated a significant reduction (about 50% with AUC) in the concentration of SVH in plasma following the coadministration of SV (500 mg/kg p.o.) and CT (600 mg/kg p.o.), compared with the administration of SV alone. This phenomenon suggested that a combination therapy using SV and CT might result in a smaller cholesterol-lowering effect of SV.

Animals↗

PubMed1979

The effect of cholestyramine on bile acid kinetics in healthy controls.

Serum lipids and the kinetics of the two primary bile acids, cholic acid (C) and chenodeoxycholic acid (CD), were studied in six normolipidaemic subjects before and during treatment with cholestyramine (12 g/day). After therapy, total serum and low-density lipoprotein cholesterol decreased by about 15%. These changes were accompanied by significant increases in the pool size, synthesis, and fractional turnover rate (FTR) of C and in the synthesis and FTR of CD. In spite of the enhanced formation of CD, the CD pool size decreased in all subjects, on average by more than 50%. The combined pool size of C and CD remained constant, but the mean total bile acid formation increased by a factor of 2.9. It is suggested that the different responses of C and CD, with an augmented contribution of C to the total amounts of bile acid produced, reflect an enhanced hepatic cholesterogenesis and, possibly, that C and CD to some extent originate from different cholesterol precursor pools.

Adult↗

PubMed1980

Studies on the use of activated charcoal and cholestyramine for reducing the body burden of polybrominated biphenyls.

Weanling male rats were exposed to a polybrominated biphenyl (PBB) mixture (Firemaster FF-1) in their diet so that they received 1 mg/kg/day for 6 months. They were then fed a normal diet for 4 months. Following this they were placed on diets containing either activated charcoal (AC) or cholestyramine (CSA) for 6 months to evaluate the usefulness of these compounds in reducing the body burdens of the retained PBBs. Periods of restricted caloric intake were also used in an effort to mobilize PBBs stored in fat. Neither compound nor restricted caloric intake was found to be effective in reducing tissue bromine levels but CSA proved useful in preventing the progression of chronic progressive nephropathy, a spontaneous lesion of aging rats.

Animals↗

PubMed1999

Cholestyramine protection against ochratoxin A toxicity: role of ochratoxin A sorption by the resin and bile acid enterohepatic circulation.

We have shown that the addition of cholestyramine (CHA, a resin known to bind bile salts in the gastrointestinal tract) to ochratoxin A (OTA)-contaminated rat diets reduced plasma levels of the toxin and prevented OTA-induced nephrotoxicity. To elucidate the mechanism of action of CHA, we carried out in vitro experiments to determine whether the resin may bind the toxin. For comparative purposes, binding of bile salts to the resin was also examined. Results showed that CHA binds both OTA and bile salts (taurodeoxycholate [TDC] and taurocholate [TCA]). Also, CHA showed greater affinity for OTA and TDC than for TCA. At 1 mM concentration, 96% of OTA and 80% of TDC were bound to the resin, while for TCA binding was only 50%. However, saturation of the resin was reached at higher levels with bile acids compared to OTA (3.67 mmol/g resin for TCA and 3.71 mmol/g resin for TDC versus 2.85 mmol/g resin for OTA). To characterize the nature of the binding of the toxin to CHA, NaCl (0 to 200 mM) was added to a fixed amount of OTA or bile acids. As expected, TCA absorption was decreased by the addition of NaCl (<50 mM), indicating electrostatic binding. However, OTA and TDC sorption was decreased only at high concentrations of NaCl (>150 mM), suggesting a stronger binding to the resin than that shown with TCA. Sequential competitive studies demonstrated that CHA binds more OTA than TCA. The results of the in vivo study show the role of bile salts in OTA absorption. The toxin's plasma levels at 1 and 3 h after a single oral dose of OTA were significantly decreased in bile salt-depleted rats compared to the control. Thus, the alteration of the bile salt biliary pool and OTA enterohepatic circulation may be an additional mechanism of action of the resin against mycotoxin toxicity.

Animals↗

PubMed1992

[Study on the effects of the hypocholesteremic agents, cholestyramine and compactin on the induction of renal tumors in rats by N-ethyl-N-hydroxyethyl nitrosamine].

Male Wistar rats were administered with 0.1% N-ethyl-N-hydroxyethyl nitrosamine (EHEN)-containing diet for 2 weeks, and were then Rept for further 23 weeks on basal diet. At 25 weeks, the rats were divided into three groups. Group I was fed on basal diet to 40 weeks. Group II was fed on 2% cholestyramine-containing diet to 40 weeks. Group III was fed on 0.02% compactin-containing diet to 40 weeks. At 40 weeks after the start of experiment, the rats were sacrificed and examined histologically for the incidence of renal cell tumors (RCT) and dysplastic foci (DF) of the kidney. The serum levels of total cholesterol at 40 weeks were 108.9 +/- 23.4, 78.8 +/- 12.5, 95.6 +/- 43.4 mg/dl in Groups I, II and III, respectively. The levels were significantly lower in Groups II and III (p less than 0.01, 0.05, respectively, Wilcoxon test) than Group I. The average numbers of DF were 4.5 +/- 4.1, 1.3 +/- 0.3, 2.3 +/- 2.0 per cm2 of kidney slices in Groups I, II and III, respectively. DF were significantly less in Group II than Group I (p less than 0.025, Wilcoxon test), and less in Group III than Group I (not statistically significant). There was no statistical difference between Groups II and III. RCT were observed in 9 of 34 kidneys (26%), 2 of 18 (11%), 1 of 20 (5%) in Groups, I, II and III, respectively. The ratios of kidneys with RCT were lower in Group II than Group I (not statistically significant), and lower in Group III than Group I (p less than 0.05, qui-square test). There was no statistical difference between Groups II and III. RCT were classified into gross and microscopic lesions. Four gross RCT were found in 4 rats of Group I; no gross RCT was in Groups II and III. There were 5 microscopic RCT in 5 rats, 3 in 2, 1 in 1 in Groups I, II and III, respectively. In Group I, serum levels of total cholesterol were compared between the following subgroups; the rats with RCT and/or with more than 10 DF per kidney, and the rats without RCT and with less than 10 DF per kidney. The mean level was 120.8 +/- 21.8 mg/dl in the former subgroup, which was significantly higher than that (94.1 +/- 19.6 mg/dl) in the latter subgroup (p less than 0.025, Wilcoxon test). The serum cholesterol was suggested to act as a promoter in the development of DF and RCT.

Animals↗

PubMed2001

Alternate pathways of bile acid synthesis in the cholesterol 7alpha-hydroxylase knockout mouse are not upregulated by either cholesterol or cholestyramine feeding.

Bile acids are synthesized via the classic pathway initiated by cholesterol 7alpha-hydroxylase (CYP7A1), and via alternate pathways, one of which is initiated by sterol 27-hydroxylase (CYP27). These studies used mice lacking cholesterol 7alpha-hydroxylase (Cyp7a1(-/-)) to establish whether the loss of the classic pathway affected cholesterol homeostasis differently in males and females, and to determine if the rate of bile acid synthesis via alternate pathways was responsive to changes in the enterohepatic flux of cholesterol and bile acids. In both the Cyp7a1(-/-) males and females, the basal rate of bile acid synthesis was only half of that in matching Cyp7a1(+/+) animals. Although bile acid pool size contracted markedly in all the Cyp7a1(-/-) mice, the female Cyp7a1(-/-) mice maintained a larger, more cholic acid-rich pool than their male counterparts. Intestinal cholesterol absorption in the Cyp7a1(-/-) males fell from 46% to 3%, and in the matching females from 58% to 17%. Bile acid synthesis in Cyp7a1(+/+) males and females was increased 2-fold by cholesterol feeding, and 4-fold by cholestyramine treatment, but was not changed in matching Cyp7a1(-/-) mice by either of these manipulations. In the Cyp7a1(-/-) mice fed cholesterol, hepatic cholesterol concentrations increased only marginally in the males, but rose almost 3-fold in the females. CYP7A1 activity and mRNA levels were greater in females than in males, and were increased by cholesterol feeding in both sexes. CYP27 activity and mRNA levels did not vary as a function of CYP7A1 genotype, gender, or dietary cholesterol intake. We conclude that in the mouse the rate of bile acid synthesis via alternative pathways is unresponsive to changes in the enterohepatic flux of cholesterol and bile acid, and that factors governing gender-related differences in bile acid synthesis, pool size, and pool composition play an important role in determining the impact of CYP7A1 deficiency on cholesterol homeostasis in this species.

Animals↗

PubMed1991

Repeated doses of activated charcoal and cholestyramine for digitoxin overdose: pharmacokinetic data and urinary elimination.

A 48-year-old man chronically treated with digitoxin and verapamil for prevention of atrial fibrillation voluntarily ingested 2.2 mg of digitoxin. Serum digitoxin concentrations and the urinary elimination of the drug were followed over a 12-day period. Urinary data indicate that a large percentage (50%) of the drug was eliminated renally despite administration of multiple doses of activated charcoal, cholestyramine and hyperosmotic laxatives. The possible interaction with two other drugs, heparin and verapamil, is also discussed.

Charcoal↗

PubMed1991

[Therapeutic trial for promotion of fecal excretion of PCDFs and PCBs by the administration of cholestyramine in Yusho patients].

Any effective therapy for elimination of causal agents remaining in Yusho patients was not found until now. To know the profile of fecal excretion of polychlorinated dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs), the amounts of PCDFs and PCBs in the stool of six Yusho patients with the typical symptoms were determined. The stool samples of Yusho patients were collected in 1989. PCDFs, i.e., 2,3,7,8-tetrachlorodibenzofuran (TCDF), 2,3,4,7,8-pentachlorodibenzofuran (PnCDF), 1,2,3,4,7,8- and 1,2,3,6,7,8-hexachlorodibenzofurans (HxCDFs), 1,2,3,4,6,7,8-heptachlorodibenzofuran (HpCDF) and octachlorodibenzofuran (OCDF) were detected in all of the samples. PCDFs found in the stool samples were mostly PnCDF and HxCDFs. Of PCDFs detected, PnCDF and HxCDFs contributed to 42 +/- 4.7% and 43 +/- 5.5% as mean +/- SE, respectively. The fecal excretion of PnCDF and HxCDFs in Yusho patients was 720 +/- 490 pg/day and 790 +/- 620 pg/day as mean +/- SE, respectively. On the other hand, the fecal excretion of PnCDF and HxCDFs in normal controls was 32 +/- 13 pg/day and 47 +/- 5.2 pg/day as mean +/- SE, respectively. The fecal excretion of PnCDF and HxCDFs in Yusho patients was about 23 times and 17 times each higher than that in normal controls. The fecal excretion of PCBs in Yusho patients and normal controls was 400 +/- 430 ng/day and 150 +/- 39 ng/day, respectively, as mean +/- SE. In order to promote the excretion of these toxic chemicals in the stool of Yusho patients, the patients were continuously administered with cholestyramine, an anion exchange resin, at a dose of 4 g, 3 times a day, for 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Benzofurans↗

PubMed1991

[Treatment of Yusho patients with cholestyramine].

Six typical Yusho patients (3 men, 48-58 years old, and 3 women, 45-55 years old) were treated with cholestyramine, 8-12 g/day, for 24 weeks. Improvement of some symptoms, such as arthralgia and malaise, was observed in 2 men, although this effect was non-specific. None of the patients showed increment of excretion of polychlorinated biphenyl or polychlorodibenzofuran into feces.

Cholestyramine Resin↗

PubMed1991

Comparative study of a microporous cholestyramine analogue (filicol) and gemfibrozil for treatment of severe primary hypercholesterolemia. Short- and long-term results.

The hypolipidemic effect of gemfibrozil in severe hypercholesterolemia is not well established. Fifty patients with primary hypercholesterolemia (including 18 patients with familial hypercholesterolemia) and stable low-density lipoprotein cholesterol levels greater than 3.90 mmol/L (greater than 150 mg/dL) (6.10 +/- 1.30 [SD] mmol/L; 236 +/- 50 mg/dL) while on a hypolipidemic diet were assigned to treatment for 12 weeks with either 9 g/d of filicol, a microporous cholestyramine analogue, or 1.2 g/d of gemfibrozil in a randomized clinical trial. Tolerance was good with both drugs. Filicol and gemfibrozil caused similar decrements of total cholesterol (14% for both), low-density lipoprotein cholesterol (20% and 18%, respectively), and apolipoprotein B (16% and 21%, respectively). Close to 40% of the patients had decreases of greater than 25% in low-density lipoprotein cholesterol levels with both drugs. Gemfibrozil, but not filicol, significantly increased plasma high-density lipoprotein cholesterol (16%) and apolipoprotein A-I (17%) levels and reduced triglyceride levels (35%). No loss of efficacy was observed with either drug in subsets of patients who had a good 12-week response rate and had extended therapy for up to 12 months. This study demonstrates that gemfibrozil may have a beneficial effect on all aspects of the plasma lipid profile in patients with severe hypercholesterolemia, a clinical situation where it can be used with potential advantages over standard doses of anion-exchange resins.

Adult↗

PubMed1990

[Homozygous familial hypercholesterolemia. Response to combined cholestyramine and lovastatin therapy].

Homozygous familiar hypercholesterolemia (FH) is a serious inherited disease caused by a genetic defect in the cell surface receptor that controls the degradation of low density lipoprotein (LDL). These patients often have myocardial infarction in their teens or early adulthood and are usually unresponsive to drugs. Recently it has been reported promising results using combined drugs regimens in patients with residual receptor activity. We report a new additional patient with receptor-defective homozygous FH treated with a combination of lovastatin and cholestyramine. The cholesterol levels were reduced in a 67% and there were adverse events related to treatment during a 7 month period of follow-up.

Child, Preschool↗

PubMed1988

Influence of cholestyramine feeding on mevalonate-activating enzymes.

Phosphorylation and decarboxylation of mevalonic acid have been measured in different tissues of chicks fed a cholestyramine diet from hatching until 18 days of age. Hepatic and intestinal phosphorylation and decarboxylation of mevalonate were slightly although significantly increased from 15 days of treatment. Direct measurements of 5-pyrophosphomevalonate decarboxylase activity using the specific substrate of this enzyme corroborated these data. Brain enzymatic activities remained unaltered with respect to controls. These results suggest that enzymes responsible for the conversion of mevalonate to isopentenyl pyrophosphate from neonatal chick liver and intestine alter their activities in a coordinate fashion and may play an important role in the regulation of cholesterogenesis in these tissues.

Animals↗

PubMed1987

Cost-effectiveness of antihyperlipemic therapy in the prevention of coronary heart disease. The case of cholestyramine.

Using cholestyramine as a model, we considered the cost-effectiveness of antihyperlipemic therapy in the primary prevention of coronary heart disease among men between 35 and 74 years of age with elevated levels of total plasma cholesterol. Our findings indicate that the cost-effectiveness of treatment varies substantially, ranging from about $36,000 to over $1 million per year of life saved. Cost-effectiveness was highest for younger patients, for those with additional coronary risk factors (eg, smoking or hypertension), and for those whose course of therapy is of less-than-lifelong duration. Conversely, it is lowest for older patients, for those with no additional coronary risk factors, and for those who are treated for a lifetime. Our results suggest that pharmacologic therapy may not be cost-effective for all patients with elevated cholesterol levels, especially those over 65 years of age. For many younger patients, however--those with additional coronary risk factors and more severe elevations in cholesterol levels--the cost-effectiveness of therapy may be comparable with other accepted medical practices.

Adult↗

PubMed1986

Ultrastructural aspects of cynomolgus atherosclerotic carotid artery lesions on cholestyramine 'regression' treatment.

The carotid artery lesions of atherosclerotic cynomolgus monkeys treated with cholestyramine and studied with scanning electron microscopy appeared to be less bulging and largely covered by endothelial cells. With transmission electron microscopy these lesions showed an evident disappearance of cells and of extra- and intracellular lipid; a marked relative increase of fibrous material in the intercellular matrix, chiefly collagen and elastin fibers, was noted.

Animals↗

PubMed1979

[Cholestyramine and digoxin intoxication: therapeutic efficacy?].

Plasma levels of digoxin were measured in a patient after massive intoxication. Pharmacokinetic analysis of the data as compared with other cases of digoxin intoxication reveals that in these situations oral administration of cholestyramine may be of benefit to the patient.

Cholestyramine Resin↗

PubMed1979

Distribution of 3-hydroxy-3-methylglutaryl coenzyme A reductase and alkaline phosphatase activities in isolated ileal epithelial cells of fed, fasted, cholestyramine-fed, and 4-aminopyrazolo[3,4-d]pyrimidine-treated rats.

3-Hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase, E.C. 1.1.1.34), the major rate-limiting enzyme of the sterol biosynthetic pathway, was studied in ileal epithelial cells isolated in a villus-to-crypt gradient according to Weiser (Weiser, M. M. 1973. J. Biol. Chem, 248:2536-2541). Alkaline phosphatase (E.C. 3.1.3.1) served as a marker for the mature villus cells. Protease effects on activity determinations were negligible. The intracellular location of HMG-CoA reductase could not be precisely determined. The activity of ileal reductase was predominantly associated with the less differentiated lower villus and crypt cells, while the reverse gradient occurred with alkaline phosphatase. This distribution of enzymes persisted in both fed and fasted rats injected with control saline-phosphate, although fasting decreased total reductase units in the ileum by 86% in 72 hr. Treatment with cholestyramine and with 4-aminopyrazolo[3,4-d]pyrimidine (APP) enhanced reductase activity in ileal cells. The percent stimulation in both cases was higher in the upper villus cells than in the crypt cells, leading to abolition of the gradient in enzyme activity. However, APP treatment caused a 98% loss in total alkaline phosphatase units and a 55% loss in total epithelial cell protein in 72 hr. Thus, there was no increase in total reductase units. These data show that APP affects ileal cell metabolism directly. Furthermore, it appears that the regulation of sterol synthesis in the intestinal mucosa, via HMG-CoA reductase, involves a complex interplay of the effects exerted by the level of alimentation, the enterohepatic circulation of bile, and the levels of plasma lipoproteins.

Adenine↗