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At least 343 records · Page 19Linked to original sources

PubMed1977

'Enteral' hyperoxaluria. Effect of cholestyramine, calcium, neomycin, and bile acids on intestinal oxalate absorption in man.

The effect of oral administration of cholestyramine, neomycine, calcium, and bile acids on intestinal 14C-oxalate absorption and urinary oxalate excretion was assessed in patients with normal or increased ('enteric' hyperoxaluria) urinary oxalate excretion. Cholestyramine, neomycine and acute administration of chenodeoxycholic acid (2.75 g/24 h) did not affect significantly 14C-oxalate absorption or urinary oxalate excretion. Oral administration of calcium markedly reduced 14C-oxalate absorption (88.2%) and urinary oxalate excretion (46%). Calcium-induced reduction of intestinal oxalate absorption was more pronounced in patients with hyperabsorption of oxalate than in subjects with normal oxalate absorption or excretion. Patients on treatment with high doses of chenodeoxycholic acid (1.5-2.0 g/day) for dissolution of cholesterol gallstones had increased oxalate absorption and excretion, patients on long-term treatment with lower doses of chenodeoxycholic acid (0.75-1.0 g/day) exhibited normal absorption or urinary excretion of oxalate. The results do suggest that calcium and bile acids do play an important role in the pathogenesis of 'enteric' hyperoxaluria. It is suggested that the beneficial therapeutic effect of cholestyramine in hyperoxaluria due to ileal resection is rather caused by its bile acid binding property than by direct binding of oxalate within the intestinal lumen.

Bile Acids and Salts↗

PubMed1981

Synergistic effects of probucol and cholestyramine to lower serum cholesterol.

Ten men with hypercholesterolemia were treated sequentially with a fat-modified diet, a diet plus probucol (1 Gm/day), and a diet plus probucol plus cholestyramine (16 Gm/day). Each treatment period was 12 weeks. Diet alone reduced mean serum cholesterol by 1.0 per cent. Diet plus probucol caused a mean 7.7 per cent reduction in serum cholesterol below the baseline values (P = 0.001 compared to diet). Adding cholestyramine to probucol and diet resulted in a mean 18.2 per cent reduction in serum cholesterol below baseline values (P = 0.001 compared to probucol and diet). The treatment was well tolerated.

Adult↗

PubMed1992

Short- and long-term effects of lovastatin and pravastatin alone and in combination with cholestyramine on serum lipids, lipoproteins and apolipoproteins in primary hypercholesterolaemia.

The effects of the HMG CoA reductase inhibitors lovastatin and pravastatin on serum lipids, lipoproteins and apolipoproteins have been studied in 35 patients with primary hypercholesterolaemia. LDL cholesterol was lowered to the same extent by both agents compared on a mg basis of each drug per day. HDL cholesterol was increased by lovastatin but not by pravastatin. The reduction in serum triglycerides, VLDL triglycerides and VLDL cholesterol was more pronounced after lovastatin than pravastatin. After 1 year the effect of combined treatment with 40 mg pravastatin and 8 g cholestyramine on the reduction in LDL cholesterol (-39%) in 13 patients was comparable to that of 80 mg lovastatin plus 8 g cholestyramine (-40%) in 12 patients with identical baseline values. Differences were also found in the effects of the combination therapy with the two drugs on HDL cholesterol, serum triglycerides, VLDL triglycerides, VLDL cholesterol, and apolipoproteins.

Adolescent↗

PubMed1989

Effects of acipimox and cholestyramine on serum lipoproteins, non-cholesterol sterols and cholesterol absorption and elimination.

The hypolipidaemic and metabolic effects of cholestyramine combined with acipimox or placebo have been evaluated in a double-blind ninety-day study in 18 patients with xanthomatous familial hypercholesterolaemia. Serum LDL-cholesterol was reduced by 35% in the cholestyramine group and 39% in the acipimoxcholestyramine group. The latter treatment increased the HDL-cholesterol level. Serum VLDL-cholesterol and triglyceride concentrations were unchanged. Cholesterol absorption efficiency was significantly reduced, and bile acid synthesis and faecal cholesterol elimination in both groups were increased. The metabolic changes were similar in the two treatment groups, but the increase in faecal neutral sterol excretion was significant only when acipimox was added. The serum cholesterol precursor sterol contents were similarly increased during the two treatments, indicating enhancement of endogenous cholesterol synthesis. The decrease in cholesterol absorption and the increase in neutral sterol excretion were more pronounced in subjects with greater than 30% than in those with less than 30% reduction in LDL-cholesterol. The changes in serum total and LDL-cholesterol levels and cholesterol metabolism were not related to apoE phenotype, but the increase in HDL-cholesterol was higher in E4 then in E3 subjects.

Adult↗

PubMed1976

Bile-induced acute erosive gastritis. Its prevention by antacid, cholestyramine, and prostaglandin E2.

Intragastric administration of whole bile-produced acute erosive gastritis in rats. Concomitant intragastric administration of prostaglandin E2, Cholestyramine and an antacid (Maalox) was effective in preventing this type of acute erosive gastritis. The protective rffect of prostaglandin E - 2 in this regard was significantly more marked as compared to Cholestyramine and Maalox.

Acute Disease↗

PubMed1978

Effect of cholestyramine on bile acid kinetics in patients with portal cirrhosis of the liver. Evidence of a selective defect in the formation of cholic acid.

The kinetics of cholic acid (C) and chenodeoxycholic acid (CD) were studied in six patients with portal liver cirrhosis. The studies were conducted both before and after 5-6 weeks of treatment with cholestyramine (12 g/day). In keeping with previous observations, the pool size and formation of C showed subnormal values during the pretreatment period, while the production of CD was within normal limits. The pool sizes of C and CD did not change upon treatment with cholestyramine, but the mean total bile acid formation increased by a factor of about 2.5. The ratio between the amounts of C and CD synthesized remained essentially unchanged. Considering the therapeutic response previously observed in normal subjects and in patients with hyper-beta-lipoproteinemia, the present results suggest a selective impairment of the biosynthesis of C in patients with portal liver cirrhosis. It is suggested that the primary defect may reside in the 12alpha-hydroxylase enzyme system.

Aged↗

PubMed1981

Effects of cholestyramine and synthetic hydrotalcite on acute gastric or intestinal lesion formation in rats and dogs.

Cholestyramine, a bile-binding agent, markedly inhibited the development of gastric lesions induced by water-immersion stress in rats and of gastric and intestinal lesions induced by indomethacin in rats and dogs with an intact pylorus. However, cholestyramine had no effect on gastric lesions induced by stress in pylorus-ligated rats and on aspirin-induced gastric lesions in rats and dogs with or without pylorus ligation. Hydrotalcite, a potent antacid, significantly inhibited the gastric lesions induced by stress and aspirin in rats and dogs with or without pylorus ligation. Hydrotalcite also inhibited the gastric lesions induced by a single administration of indomethacin in rats with an intact pylorus. In contrast, the agent had no effect on gastric and intestinal lesions induced by repeated administration of indomethacin to rats and dogs with an intact pylorus. These results suggest that while bile probably plays an important role in the pathogenesis of stress-induced gastric lesions and of indomethacin-induced gastric and intestinal lesions, bile does not appear to play a role in the pathogenesis of aspirin-induced gastric lesions.

Aluminum Hydroxide↗

PubMed1986

Preparation and characterization of unilamellar vesicles from cholate-phospholipid micelle treated with cholestyramine.

Cholestyramine, a well-known bile-salt sequestrant, can be used effectively to remove cholate or deoxycholate from a solution of phosphatidylcholine-bile salt mixed micelle. Upon removal of the bile salt, unilamellar phospholipid vesicles form essentially instantaneously. Cholestyramine resin could be pelleted and removed from the vesicle solution after a low speed centrifugation. Based on phosphate analyses, the recovery of vesicles was approximately 60% of the starting material. The average diameter of these vesicles, as estimated by gel exclusion chromatography on sephacryl S-1000 beads and by trapped volume measurement using [3H]sucrose, ranged between 85 to 121 nm. Phosphatidylethanolamine, cholesterol, or n-alkane such as tetradecane can be incorporated into the vesicles without any selective loss; however, selective loss was experienced when negatively charged phospholipid species such as phosphatidylglycerol or phosphatidylserine was included in vesicle formation.

Cholestyramine Resin↗

PubMed1989

Comparison of phosphatidylethanolamine and phosphatidylcholine vesicles produced by treating cholate-phospholipid micelles with cholestyramine.

We have previously reported the preparation and characterization of unilamellar phosphatidylcholine vesicles from cholate-phospholipid micelles treated with the bile-salt sequestrant cholestyramine (Ventimiglia, J.B., Levesque, M.C., and Chang, T.Y. (1986) Anal. Biochem. 157, 323-330). We now describe a slightly modified procedure for forming unilamellar vesicles consisting of phosphatidylethanolamine, and the characterization of the resultant vesicles by gel exclusion chromatography. In contrast to phosphatidylcholine vesicles, the formation of phosphatidylethanolamine vesicles is highly pH dependent; pH 9.2 is superior to pH 8.1 or pH 7.1. Via the dialysis step, the final pH of the vesicles could be altered to be at 8.1 or at 7.1, although decreasing the pH from 9.2 resulted in the loss of approx. 20% of the total lipid as large aggregates. Residual cholate was still present in the resultant vesicles after cholestyramine treatment; the low levels of cholate, removable by dialysis, was found to stabilize the phosphatidylethanolamine vesicles formed at pH 8.1. These results suggest that the majority of the amino groups of the phosphatidylethanolamine molecules should either be in the deprotonated form, or be neutralized and/or restricted by the anionic cholate monomers in order to facilitate the vesicle formation. Phosphatidylethanolamine vesicles were found to be much more permeable to small ions than phosphatidylcholine vesicles. The incorporation of phosphatidylserine, but not phosphatidylinositol, into the phosphatidylethanolamine vesicles at 10% resulted in decreased permeability of the bilayer against the cobalt ion influx, suggesting cooperative and complementary packing of phosphatidylethanolamine and phosphatidylserine molecules within the bilayer.

Cholestyramine Resin↗

PubMed1984

Induction of peroxisomal enzymes and palmitoyl-CoA hydrolase in rats treated with cholestyramine and nicotinic acid.

Male Wistar rats were given 200 mg/kg/day nicotinic acid or 1000 mg/kg/day cholestyramine by stomach tube for ten days. Peroxisomal palmitoyl-CoA oxidation (cyanide-insensitive) and the activities of palmitoyl-CoA hydrolase and urate oxidase were significantly increased in the total liver homogenate. Subcellular fractionation showed enhanced enzyme activities after drug treatment mainly in the peroxisome-containing fractions. The increase in urate oxidase activity and its subcellular distribution suggest that the tested drugs induce core-containing peroxisomes. The findings are similar to those previously reported with low doses of peroxisome-proliferating hypolipidemic drugs and with acetylsalicylic acid, a drug which is structurally similar to nicotinic acid. Since cholestyramine is not absorbed, its influence on hepatic enzymes probably occurs indirectly as a consequence of enhanced catabolism of cholesterol.

Animals↗

PubMed1987

The effect of combined fenofibrate and cholestyramine therapy on low-density lipoprotein kinetics in familial hypercholesterolemia patients.

The effects of combined drug treatment (fenofibrate and cholestyramine) have been investigated in vivo by simultaneously determining total and receptor-independent LDL catabolism with 125I-labelled LDL and 131I-labelled LDL coupled with cyclohexanedione. Receptor-mediated catabolism of LDL determined as the difference between the turnover of 125I and 131I, was found to be reduced in heterozygotes with familial hypercholesterolemia. Treatment with combined fenofibrate and cholestyramine markedly stimulated both receptor-mediated (by more than 2-fold) and receptor-independent catabolism. LDL-Apo B and LDL-cholesterol levels were reduced by 38% and 36%, respectively. The combined treatment also reduced the absolute synthetic rate of LDL-Apo B (by 9%). The mechanisms responsible for these kinetic effects are discussed.

Adult↗

PubMed1977

The effect of cholestyramine on the faecal excretion of bile acids and neutral steroids in familial hypercholesterolaemia.

The faecal excretion of total bile acids was measured in two normal subjects and in seven patients with familial hypercholesterolaemia (four heterozygotes and three homozygotes) in the untreated state and during treatment with near-maximal doses of cholestyramine. There were no significant differences between the three groups. The increase in bile-acid excretion in response to cholestyramine was as great in the homozygotes as in the normal subjects. It is concluded that familial hypercholesterolaemia is not generally due to an inherited defect in the mechanisms for catabolizing cholesterol to bile acids.

Adolescent↗

PubMed1988

Decrease in LDL and increase in HDL concentrations in type II hyperlipoproteinaemic patients on low-dose combination therapy of cholestyramine and Complamin.

A low-dose combination of Complamin retard (1 g t.i.d.) and cholestyramine (4 g b.i.d.) was compared with each agent alone in 2 serial open trials without dietary restriction using type IIa and IIb hyperlipoproteinaemic patients. Complamin alone produced decreases in LDL and VLDL cholesterol concentrations (up to 20%) whereas cholestyramine alone produced only a modest reduction in LDL (up to 15%). The combination produced marked, progressive reductions in total cholesterol (up to 35%) and LDL (up to 40%); reductions in VLDL (up to 45%), total triglyceride (up to 60%) and free fatty acids (up to 60%) were found only in type IIb patients. The average increase in HDL-cholesterol from the 2 studies for combination therapy was 35%. No side-effects were reported or measured and compliance was excellent. The results demonstrate the potential of a method of achieving beneficial actions on lipoprotein levels with a well-tolerated therapy.

Adult↗

PubMed1991

Efficacy of cholestyramine does not vary when taken before or during meals.

Compliance to cholestyramine treatment, often unsatisfactory, may become further problematic because of the common indication that the resin should not be taken with meals. Since there is no convincing data on the validity of this therapeutic schedule, 10 type IIA hyperlipoproteinemic patients received cholestyramine either before or during the 3 major meals, according to a cross-over protocol. Plasma lipid levels were monitored after 4 and 6 weeks of each treatment schedule. The efficacy of the resin, in terms of total cholesterol (-16.5% together with food vs. -17.2% before food) and of low density lipoprotein cholesterol reduction (-22.8% with food vs. -23.1% before food) did not differ. The side effect profile was also not different between the two treatment protocols. These findings suggest that there are no significant interactions between food and the anion exchange resin and that the hypocholesterolemic effect does not depend upon a specific timing, supposedly close to the gallbladder contraction. They are particularly significant in view of the future availability of new resins in liquid form, suitable for intake during meals.

Cholesterol↗

PubMed1976

Oral cholestyramine and paregoric therapy for intractable diarrhea following surgical correction of catastrophic disease of the GI tract in neonates.

Ten surgical neonates with postoperative intractable diarrhea and secondary weight loss were treated with combination cholestyramine and paregoric therapy. Within 3-5 days all infants except two showed significant clinical improvement with a decreasing number of stools, an increase in the consistency of the stool, and gradual weight gain. The exact mechanism of action of cholestyramine is not clear. It may act by binding with bile salts and/or endotoxins in the bowel lumen or decreasing the motility of the bowel. Used in combination with paregoric, a known bowel motility depressant, the doses of each medication can be kept quite low thus avoiding undesirable side effects. Medium chain triglyceride formula is helpful in some of these infants to improve fat absorption further. Medication in all of these infants has been discontinued without any adverse effects.

Administration, Oral↗

PubMed1982

Serum bile acid levels in intrahepatic cholestasis of pregnancy during treatment with phenobarbital or cholestyramine.

Nineteen patients suffering from the intrahepatic cholestasis (IHC) of pregnancy were studied. Twelve of them were treated with phenobarbital (100 mg/day) and seven with cholestyramine (18 g/day). The overnight fasting levels of serum cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) were measured by radioimmunoassay. The activities of serum transaminases, gamma-glutamyltranspeptidase, alkaline phosphatase and total and conjugated bilirubins were also analyzed. It was found that there was no correlation between the itching symptom and the serum bile acid levels. During phenobarbital treatment serum bile acid concentrations did not change. Also, the other measured parameters as well as the CA/CDCA ratio did not change significantly. Transaminases had, however, a slight tendency to decrease. The therapy successfully relieved itching in half of the cases. There was no relationship between the relief of the itching and the change in the bile acid concentrations. Cholestyramine treatment did not decrease the CA level significantly, but that of the CDCA decreased (P less than 0.05) and the ratio of CA/CDCA increased (P less than 0.05). In the other analyzed liver function test results, an increase (P less than 0.05) occurred only in the concentrations of conjugated bilirubin. The itching was relieved in five of the seven cases during the first week of treatment, but after that the symptom tended to reappear. There was a slight correlation between the decrease in the CDCA level and in the relief of the itching. The two drugs did not cause any particular side effects.

Bile Acids and Salts↗

PubMed1979

Alteration of biliary ursodeoxycholic acid in guinea pig during early stages of cholestyramine feeding.

The effects of cholestyramine feeding on biliary ursodeoxycholic acid, fecal excretion of bile acids and neutral sterols on cholesterol 7 alpha-hydroxylase and hepatic HMG-CoA reductase were examined in the guinea pig. In the bile there was a 57% decrease in the concentration of ursodeoxycholic acid while an increase was observed in the concentration of chenodeoxycholic acid. Cholestyramine feeding for ten days resulted in a decrease in plasma cholesterol levels and an increase in both hepatic HMG-CoA reductase and cholesterol 7 alpha-hydroxylase activities. The fecal excretion of both bile acids and neutral sterols was significantly increased.

Animals↗

PubMed1995

Efficacy and safety of triple therapy (fluvastatin-bezafibrate-cholestyramine) for severe familial hypercholesterolemia.

Familial hypercholesterolemia carries a markedly increased risk of coronary artery disease. Reduction of plasma low density lipoprotein cholesterol (LDL-C) levels to the normal range may prevent premature atherosclerosis and usually requires a combination of cholesterol-lowering drugs such as 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors plus resins or fibrates. The current, 60-week, open-label investigation involved 22 patients whose plasma LDL-C had not reached the target level for prevention of coronary artery disease in 3 previous studies using fluvastatin alone and in combination with other cholesterol-lowering medications. At the beginning of the current study, patients were stabilized on fluvastatin monotherapy at 40 mg/day. After 6 weeks, the daily treatment changed to a combination of fluvastatin 40 mg/day in the evening and bezafibrate 400 mg/day in the morning. After a further 6 weeks, a lunchtime dose of cholestyramine 8 g/day was added, to form triple cholesterol-lowering therapy. Efficacy was determined by plasma lipid/lipoprotein analysis. Baseline levels were assessed after 4 weeks of placebo treatment, prior to active treatment, in the first fluvastatin study. Safety analyses included liver and renal function tests, creatine phosphokinase levels and blood counts. Compliance was determined by counting the fluvastatin capsules, bezafibrate tablets, and cholestyramine sachets returned by the patients at each visit. The triple-drug combination used in this study was more effective than the double therapy and resulted in stabilization of the LDL-C:high density lipoprotein cholesterol (HDL-C) ratio, at a reduction from baseline ranging from -40.4 to -52.5%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗