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At least 397 records · Page 22Linked to original sources
PubMed1991

[Cost-effectiveness of lowering of blood cholesterol using simvastatin and cholestyramine].

With use of a model of the costs and effects of cholesterol lowering therapy in the primary prevention of coronary heart disease, the cost-effectiveness of simvastatin and cholestyramine in the Netherlands have been estimated. Costs per year of life saved by cholestyramine therapy are several times greater than those of simvastatin therapy and compared unfavorably with those of generally accepted health care programs in the Netherlands. Cholesterol-lowering with simvastatin in men can be cost-effective when therapy is initiated at an early age. At cholesterol levels between 6.5 and 8 mmol/l, however, therapy should be restricted to men with at least one, preferably two additional risk factors such as hypertension or diabetes mellitus. Among women, cholesterol lowering can only be cost-effective when therapy is limited to women with diabetes mellitus or severely elevated serum cholesterol levels.

Adult↗
PubMed1990

[Cholestyramine in the treatment of hypercholesterolemia. Our experience in 11 cases].

Bile acid sequestrant resins are considered agents of choice in the therapy of hypercholesterolemia non responsive to diet treatment. We evaluated the effects of cholestyramine, 12 g per day during 4 weeks, in 11 adult patients with severe hypercholesterolemia. Total cholesterol decreased from 414 +/- 112 to 302 +/- 140 mg/dl (28%), LDL cholesterol from 330 +/- 122 to 226 +/- 143 (33%) and Apo B lipoprotein from 141 +/- 31 to 115 +/- 34 mg/dl (18%), p < 0.01. HDL cholesterol including fractions HDL2 and HDL3, Apo A1 and Triglyceride levels were not modified. No significant side effects on gastrointestinal function were observed. Thus, we confirm that cholestyramine is an effective therapy for severe hypercholesterolemia.

Adolescent↗
PubMed1975

Cholestyramine, clofibrate and nicotinic acid as single or combined treatment of type IIa and IIb hyperlipoproteinaemia.

1. In type IIa and IIb hyperlipoproteinaemia, treatment with 16 g cholestyramine daily reduced the cholesterol concentration 23%. By adding clofibrate this effect was enhanced to a 29% reduction and at the same time clofibrate reduced the triglyceride (TG) concentration 33%. 2. The optimal cholesterol reduction with clofibrate in type II was 17% and was found after treatment with 1.5 g clofibrate/day. The optimal TG reduction appeared to be achieved with a daily dose of 2 g.3. Nicotinic acid in the form of niceritrol had another type of dose-response in type II with doses from 3 to 6 g/day. It appeared as if the optimal dose probably was above 6 g daily. The 6 g dose produced a cholesterol reduction of 22% and in type IIb there was at the same time a 50% reduction of the TG concentration. 4. By combining 3 g niceritrol with 2 g clofibrate almost the same effect on serum lipids was obtained as with 6 g niceritrol. When choosing a drug for treatment of hyperlipoproteinaemia it is necessary to consider not only the lipid lowering effect but also the side effects which are not discussed here. By combining clofibrate with either cholestyramine or niceritrol it was possible to improve the lipid lowering effect. There were no side effects which were not seen when the drugs were used alone. A more frequent use of combinations to improve the treatment of hyperlipoproteinaemia is recommended.

Cholestyramine Resin↗
PubMedDate not supplied

[Cholestyramine adsorbs Escherichia coli and Vibrio cholerae toxins by way of ion exchange mechanism].

The use of cholestyramine in the treatment of enterocolitis is justified by its ability to fix the LT toxin of Vibrio cholerae and ETEC, the ST toxin of ETEC and the verotoxin of EHEC at the pH of intestinal fluid. To elucidate the nature of the ion-exchange mechanism in the binding of the toxins on the resin, we try to eluate the toxins with 0.1 M to 0.9 M NaCl solution at pH 7. Irrespective of their presence or absence in the different fractions, the biological activity of the toxins was assessed in cell culture and in the new-born mouse test. Desorption of the LT toxin from Vibrio cholerae is obtained with 0.6 M to 0.8 M of NaCl, with 0.3 M to 0.5 M of NaCl for the LT, 0.4 M to 0.5 M for the VT and 0.6 M for the TS toxins. The eluated toxins are biologically active; these facts demonstrate that the adsorption of toxin on cholestyramine result of a ion-exchange mechanism.

Animals↗
PubMed1990

Metabolic variables of cholesterol during squalene feeding in humans: comparison with cholestyramine treatment.

Squalene, a key intermediate of cholesterol synthesis, is present especially in olive oil. Regulation of cholesterol metabolism by dietary squalene in man is unknown, even though olive oil users in Mediterranean areas have low serum cholesterol levels. We have investigated absorption and serum levels of squalene and cholesterol and cholesterol synthesis with the sterol balance technique and serum levels of cholesterol precursors in humans during squalene feeding (900 mg/d for 7-30 days). The results were compared with those during cholestyramine treatment. Fecal analysis suggested that about 60% of dietary squalene was absorbed. Serum squalene levels were increased 17 times, but serum triglyceride and cholesterol contents were unchanged. The squalene feeding significantly (P less than 0.05) increased serum levels of free (1.7-2.3 times) and esterified (1.9-2.4 times) methyl sterol contents, while elevations of free and esterified delta 8-cholesterol and lathosterol levels were inconsistent. Cholestyramine treatment modestly augmented free methyl sterol levels (1.3-1.7 times), less consistently than those of esterified ones, while, in contrast to the squalene feeding, serum contents of free and esterified delta 8-cholesterol and lathosterol were dramatically increased (3.3-8 times). Neither of the treatments significantly affected serum plant sterol and cholestanol levels. The squalene feeding had no consistent effect on absorption efficiency of cholesterol, but significantly increased (paired t-test, P less than 0.05) the fecal excretions of cholesterol and its nonpolar derivatives coprostanol, epicoprostanol, and coprostanone (655 +/- 83 SE to 856 +/- 146 mg/d) and bile acids (212 +/- 24 to 255 +/- 24 mg/d), indicating an increase of cholesterol synthesis by about 50%. We suggest that a substantial amount of dietary squalene is absorbed and converted to cholesterol in humans, but this squalene-induced increase in synthesis is not associated with consistent increases of serum cholesterol levels. The clearly increased serum contents of esterified methyl sterols may reflect stimulated tissue acyl CoA: cholesterol acyltransferase (ACAT, EC 2.3.1.26) activity during squalene feeding as these sterols are not esterified in serum.

Cholestanol↗
PubMed1990

Response to diet and cholestyramine in a patient with sitosterolemia.

In this report, an 11-year-old boy with diffuse tendinous and tuberous xanthomatosis and a plasma sterol concentration of 555 mg/dL, consisting primarily of cholesterol, is described. Three months after changing from an unrestricted diet to a cholesterol-lowering diet, his plasma sterol concentration decreased to 221 mg/dL. Because of the degree and rapidity of his response to diet, sitosterolemia was suspected. According to results of capillary gas-liquid chromatography of his plasma sterols, there was a sitosterol concentration of 31.3 mg/dL (normal less than 1.0 mg/dL), establishing the diagnosis of sitosterolemia. Addition of cholestyramine therapy (8 g/d) to a low sterol diet further lowered his plasma sterol concentration to 173 mg/dL and led to complete regression of all tuberous xanthomata. Tendinous xanthomata regressed at a slower rate. These findings show that the diagnosis of sitosterolemia should be suspected in severely hypercholesterolemic children (total cholesterol greater than 400 mg/dL) whose plasma cholesterol level is highly responsive to dietary manipulation. The rapid and sustained lowering of plasma cholesterol and regression of xanthomata after treatment with diet and cholestyramine suggest that sitosterolemia is a treatable cause of premature atherosclerosis.

Arteriosclerosis↗
PubMed1990

[HMG-CoA reductase inhibitors in familial hypercholesterolemia. Therapy with simvastatin alone and in combination with cholestyramine in low dosage; a report of 2 years experiences].

We have studied the effect of simvastatin, an inhibitor of the rate-limiting enzyme in cholesterol biosynthesis, alone and in combination with cholestyramine in 48 patients. Simvastatin 40 mg decreased total serum cholesterol, LDL cholesterol and apolipoprotein B by 35%, 40% and 35%, respectively, while HDL cholesterol and apolipoprotein A-I increased by 10% (p less than 0.01) and 7% (p less than 0.05), respectively. The addition of 8 g cholestyramine caused a further decrease in total cholesterol and LDL cholesterol to a total of 42% and 49%, respectively. Eighteen of the 48 patients have now been under combined treatment for 2 years. The initial high decreases in total cholesterol and LDL cholesterol were stabilized for the whole period. Some patients developed gastrointestinal complaints, which made necessary a reduction of simvastatin in two cases. Biochemical side effects (e.g. increases in CK and transaminases) were not observed.

Adult↗
PubMed1990

[Effects of low-dose cholestyramine in long-term therapy of hypercholesterolemia].

Sixty-nine patients (mean age 49 +/- 13 years), affected by primary hypercholesterolemia (65 type IIa and 4 type IIb), were treated for 2 years with 12 gr/day cholestyramine subdivided in two doses. Total serum cholesterol decreased from 353 (sd 66) mg/dl to 291 (sd 62) mg/dl (p less than 0.001) at the third month active treatment remaining thereafter constant. Overall, LDL-cholesterol reduced by 30% in cases with a familial form of the metabolic disorder, by 27% and 30% in those with polygenic or indefinite hypercholesterolemia, respectively. HDL-cholesterol remained unchanged during the study whereas serum triglycerides tended toward an increase. The frequency of reported side effects ranged between 11% and 23% of cases. Mostly they were constipation and abdominal discomfort which, however, did not cause a definitive discontinuation of the resin. The favourable side effect profile and the efficacy confirmed that low-dose cholestyramine represents the first choice drug for hypercholesterolemia.

Adolescent↗
PubMed1989

Measurement of apolipoprotein B in plasma from hyperlipidemic subjects treated with cholestyramine or placebo: differential effects of storage at -70 degrees C.

Using radial immunodiffusion, we measured apolipoprotein B (apoB) concentrations in fresh plasma from 216 hyperlipidemic male subjects and in aliquots of the same plasma stored at -70 degrees C for 22 months. At the time of sampling, 112 were being treated with cholestyramine, the rest with a placebo. ApoB concentrations in the stored samples were significantly and positively correlated with apoB concentrations in the fresh samples (r = 0.84, P less than 0.001), the mean (and SD) being 1680 (320) mg/L and 1570 (320) mg/L, respectively. This 6.5% decrease in the stored samples was statistically significant (P = 0.0005), but there was no significant correlation between the decrease in apoB values in the stored samples and plasma triglyceride concentrations measured in the fresh samples. The correlation between the two apoB analyses was greater in the cholestyramine-treated group (r = 0.90) than in subjects treated with the placebo (r = 0.75).

Apolipoproteins B↗
PubMed1989

Effects of cholestyramine feeding on tissue lipase activities and plasma fatty acids in the pregnant rat.

Rats fed a non-absorbable bile acid binding resin (cholestyramine) throughout gestation had decreased activities of adipose tissue lipoprotein lipase (LPL), hepatic triacylglycerol lipase and a heparin-releasable placental lipase distinct from LPL, when assayed at near-term gestation. The fetal plasma and liver triacylglycerol concentrations were not altered. The fetal liver total lipid and plasma triacylglycerol, however, had reduced levels of n-6 and n-3 series fatty acids, suggesting decreased availability of maternal dietary-derived essential fatty acids. These studies suggest that cholestyramine feeding may alter triacylglycerol flux and the quantity or type of maternal fatty acids available for placental transfer. The resin has application for in vivo study of the effects of maternal lipid transfer on the regulation of fetal hepatic lipid synthesis.

Animals↗
PubMed1989

Aluminium hydroxide and cholestyramine in the treatment of acute diarrhea.

A randomized, double blind control study of the treatment of acute diarrhea with aluminium hydroxide and cholestyramine in comparison with a control group demonstrated the effectiveness of cholestyramine in shortening the hospital stay, and the diarrhea course was better than that of aluminium hydroxide. However, aluminium hydroxide was superior to intravenous fluid plus early feeding.

Aluminum Hydroxide↗
PubMedDate not supplied

Enhancement of DMBA-induced mammary cancer in Wistar rats by unsaturated fat and cholestyramine.

Promotion of 7,12-dimethylbenzantracene (DMBA)-induced mammary cancer in Wistar rats, by diets containing unsaturated fat (USF) and unsaturated fat plus 4% cholestyramine (USF+ CHST) was compared to that in rats fed saturated fat (SF). The diets were fed for 100 or 200 days. Histologic examination of grossly normal mammary tissue, as well as of any tumor mass, showed a significant increase in the incidence and size of mammary tumors in USF and USF + CHST groups when compared to SF group. Moreover, in the USF + CHST group one tumor developed in one rat as early as 100 days. The serum total lipids, triglycerides and cholesterol esters decreased significantly at 200 days in USF and USF + CHST groups. These results suggest that a diet high in unsaturated fat alone, or in combination with 4% cholestyramine, promotes DMBA-induced mammary cancer in Wistar rats.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

[Ability of cholestyramine to bind Escherichia coli and Vibrio cholerae toxins].

Cholestyramine treatment of new born's infectious diarrhea has been shown to be effective. The study of in vitro binding of bacterial toxins from Vibrio Cholerae and from three strains of Escherichia coli suggest an ionic adsorption of the four toxins to this anion-exchange resin. This immediate binding is effective at the pH of intestinal fluid, therefore the protection of the enterocytes from the biological action of the toxins result of the toxins sequestering effect of the Cholestyramine.

Adsorption↗
PubMed1988

Induction of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity in foetal rats by maternal cholestyramine feeding.

Late gestation foetus from rats fed a non-absorbable bile acid binding resin (cholestyramine) have increased hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activity. This was due to increased unphosphorylated (active) as well as total reductase and was accompanied by higher fatty acid synthetase activity. No increase in foetal hepatic cystathionase or tyrosine aminotransferase activity, or changes in plasma insulin, corticosterone or thyroxine were found. The studies demonstrate that foetal hepatic cholesterol metabolism is sensitive to drug-induced perturbation of maternal lipoprotein metabolism. The data suggest induction of foetal cholesterol and fatty acid synthesis by a specific mechanism not involving generalized hormone-induction of hepatic enzyme systems. Cholestyramine appears to have application for in vivo study of the regulation of foetal cholesterologenesis and its coordination to maternal and foetal steroid requirements.

Animals↗
PubMed1978

Effects of bile acids, antacids, and cholestyramine on transmural electrical potential difference in man.

The effect of glycocholic acid (GCA) on functional changes of the gastric mucosal barrier was examined by measurement of transmural gastric potential difference (PD) in humans in the presence and absence of cholestyramine and of A1(OH)3-containing antacids possessing potent bile acid binding properties. Intagastric instillation of GCA induced reduction of PD which could be prevented by the more potent buffering Mg-A1(OH)3-containing antacid, but not by cholestyramine or the less potent A1(OH)3-containing antacid. It is concluded that for the prevention of bile acid induced damage of gastric mucosa potent antacids are superior to potent bile acid binding agents loosing the binding properties at low pH-values.

Aluminum Hydroxide↗
PubMed1979

Partial purification of a toxin found in hamsters with antibiotic-associated colitis. Reversible binding of the toxin by cholestyramine.

A toxin with cytotoxic and enterotoxic activities was isolated from cecal contents of hamsters receiving lincomycin. The toxin was partially purified by ultracentrifugation, ultrafiltration, (NH4)2SO4 precipitation, and gel filtration. Cytotoxic activity, assayed on monolayers of HeLa cells, was restricted to material that eluted in the molecular weight range of 107,000 +/- 6,000 daltons. Cytotoxicity of crude AAC toxin could be demonstrated at concentrations as low as 0.04 microgram/ml. The toxin was heat labile (55 degrees-60 degrees C for 0.5 hr) and sensitive to trypsinization, acidification at pH 3, or alkalinization at pH 9. Cytotoxic activity was inhibited by Clostridium sordellii antitoxin. Enterotoxic activity of the crude toxin and the cytotoxic fraction from gel filtration was demonstrated by fluid secretion in ligated rabbit ileal loops. Studies were done in vitro with cholestyramine resin, vancomycin, or gentamicin to determine if the toxin was bound or denatured by these drugs. It was demonstrated that cholestyramine bound the toxin, significantly reducing its cytotoxicity. Reversible binding of the cytotoxic material was demonstrated by salt gradient elution. Neither vancomycin nor gentamicin had any effect on the in vitro cytotoxic activity of the toxin.

Ammonium Sulfate↗
PubMed1986

Long-term effects of bezafibrate and of a bezafibrate and cholestyramine combination on lipids and lipoprotein lipids in type IIa hypercholesterolaemic patients.

Eighteen hypercholesterolaemic patients have been treated for four months with bezafibrate 200 mg thrice daily. After one month of therapy, total cholesterol (T-C) decreased on the average by 19%, total triglycerides (T-TG) by 28%, very low density lipoprotein-TG by 47%, LDL-C by 25% and HDL3-C increased by 16%. At the fourth month of therapy the lipoprotein pattern was unchanged as compared to the one observed at the first month. In 12 patients T-C was normalized by bezafibrate and the patients continued the treatment for one year without experiencing further changes in lipoprotein pattern. Six patients with severe hypercholesterolaemia (mean baseline T-C of 11.51 +/- 0.63 mmoles/l) failed to adequately respond to bezafibrate treatment and were put on the combined bezafibrate 600 mg/day and cholestyramine 16g/day therapy. During bezafibrate their T-C decreased on the average by 21% and LDL-C by 23% and during the combined therapy by 33% and by 37% respectively, as compared to the baseline values. Combined bezafibrate and cholestyramine treatment seems then to be more effective than bezafibrate alone in decreasing serum cholesterol and may be useful in patients with severe hypercholesterolaemia.

Adult↗