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PubMed1988

Cutting into cholesterol. Cost-effective alternatives for treating hypercholesterolemia.

We performed an analysis of the cost-effectiveness of treating individuals with significantly elevated levels of total serum cholesterol (greater than 6.85 mmol/L [greater than 265 mg/dL], comparing treatment with three alternative agents: cholestyramine resin, colestipol, and oat bran (a soluble fiber). We simulated a program for lowering cholesterol levels that was similar to that of the Coronary Primary Prevention Trial, and then used the outcomes of the trial to calculate the incremental cost per year of life saved (YOLS) from the perspective of society. Our findings suggest that the cost per YOLS ranges from $117,400 (cholestyramine resin packets) to $70,900 (colestipol packets) and $17,800 (oat bran). Using bulk drug reduces the cost per YOLS to $65,100 (cholestyramine resin) and $63,900 (colestipol). Targeting bulk colestipol treatment only to smokers has a cost per YOLS of $47,010; the incremental cost of treating nonsmokers would be $89,600 per additional YOLS. Although pharmacologic therapy has substantial costs, it may be more cost-effective when low-cost forms are applied to particular high-risk groups, such as smokers. However, a broad public health approach to lowered cholesterol levels by additional dietary modification, such as with soluble fiber, may be preferred to a medically oriented campaign that focuses on drug therapy.

Cholestyramine Resin↗

PubMed1989

Benign recurrent intrahepatic cholestasis: a long-term follow-up study of two patients.

Two brothers with benign recurrent intrahepatic cholestasis were studied over a period of 6 years. During this period, 11 episodes of cholestasis were observed, with a mean duration of 2.6 months (range: 2 weeks to 6 months). Once, both brothers developed cholestasis simultaneously. There was a prevalence for episodes of cholestasis in wintertime. The postprandial rise in serum sulfated glycolithocholic acid was increased in the patients, and the bile acid pool was enriched with secondary bile acids. In periods prior to cholestasis, the urinary 3 alpha OH-bile acid concentration was often elevated (greater than 50 mumoles per liter) without a clear correlation with the clinical prodromata. However, it could not be used as a predictor of cholestasis. In contrast, the postprandial rise in serum 3 alpha OH-bile acids was always grossly elevated in periods just before cholestasis. An increase both in fecal bile acid excretion as well as secondary bile acids in the bile acid pool indicated an increased spillover of bile acids into the large bowel. Cholestyramine administered directly after the first signs of cholestasis appeared to shorten an episode of cholestasis. On the other hand, withdrawal of cholestyramine in a cholestasis-free period may have resulted in an episode of cholestasis. Neither taurine supplementation for 3 and 7 weeks nor calcium phosphate, which binds sulfated bile acids in vitro, for 3 weeks could prevent an episode of cholestasis, although the latter normalized the bile acid pool composition. There is a rationale for a fat-restricted diet and cholestyramine therapy only as maintenance treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Bile Acids and Salts↗

PubMed1995

Disposition of lorazepam in diabetes: differences between patients treated with beef/pork and human insulins.

The pharmacokinetics of lorazepam was examined in 10 male patients with insulin-dependent diabetes mellitus before and following treatment with neomycin and cholestyramine. Neomycin and cholestyramine were given in an attempt to block the enterohepatic circulation of lorazepam and so to permit an in vivo estimate of hepatic glucuronidation. The volume of distribution and clearance of free lorazepam in diabetic patients were not significantly different from the corresponding estimates in 14 normal controls. Neomycin and cholestyramine increased the clearance of lorazepam by 63% consistent with their effect in non-diabetic controls. However, patients on beef/pork insulin exhibited a greater than normal increase on this interupting regimen (125%), and had a significantly greater neomycin/cholestyramine cycling-interrupted clearance of lorazepam than either normal controls or patients on human insulin (15.4 vs. 6.96 and 7.87 ml.min-1.kg-1). The clearance was correlated positively and significantly with HbA1c and glycated proteins (fructosamine), but only in patients on human insulin. Thus, the pharmacokinetics of lorazepam was not altered in patients with insulin-dependent diabetes mellitus. However, it is possible that there are differences in the rate and extent of hepatic glucuronidation and enterohepatic circulation of lorazepam between patients treated with beef/pork and human insulins and between diabetics treated with beef/pork insulin and non-diabetic controls.

Adolescent↗

PubMed1980

Effect of bile salt-binding resins on the morphology of rat jejunum and colon. A scanning electron microscopy study.

One mechanism suggested to account for the hypocholesteremic effect of dietary fibers is their ability to sequester bile salts. Since bile salts have been found to alter intestinal structure, the morphological effects of several commonly used, xenobiotic, bile salt-binding agents was investigated. Wistar rats were fed a purified stock diet, ad libitum, for 6 weeks containing either 2% cholestyramine, 2% colestipol, or 2% DEAE-Sephadex. The bile salt-binding capacity of these substances was tested in vitro using taurocholate and glycocholate. The effect of in vivo feeding of the resins was to evoke ultrastructural topographical deviations from control appearance in both jejunal and colonic mucosae. Colonic cell injury was more severe than that observed in the jejunum of both colestipol- and DEAE-Sephadex-fed animals while the reverse was true for the rats fed cholestyramine. The degree of distortion in each condition was positively correlated with the extent of bile salt-binding capability in vitro. The rank order of both effects in terms of increasing severity was DEAE-Sephadex less than colestipol less than cholestyramine.

Animals↗

PubMed1987

Effects of ketoconazole on cholesterol synthesis and precursor concentrations in the rat liver.

Ketoconazole, an antimycotic agent, given to rats for a week as 0.05% food addition had no effect on the hepatic concentrations of free and esterified cholesterol or on the activity of acyl coenzyme. A: cholesterol-acyltransferase (ACAT). However, the levels of free methylated cholesterol precursors, especially lanosterols, less markedly delta 8,24 and delta 8-dimethyl sterols and monomethyl sterols, were increased after only one day's treatment, while those of esterified methyl sterols were increased inconsistently, and those of free and esterified delta 8-lathosterol, lathosterol and desmosterol were not affected at all. Cholestyramine treatment had no significant effect on ACAT in spite of a decrease in the hepatic content of esterified cholesterol and caused a marked increase in the free cholesterol precursor levels, especially in those of lathosterols. Cholestyramine given to ketoconazole-treated rats increased the hepatic levels of delta 8 and delta 7-lathosterols but not desmosterol or methylated cholesterol precursors. Ketoconazole increased and cholestyramine markedly decreased plant sterols, sitosterol and campesterol in the liver. In serum, the contents of both lanosterols and lathosterol were increased but that of cholesterol tended to be decreased by ketoconazole (-19%). The results indicate that ketoconazole impairs demethylation processes at C-14 and to some extent at C-4 in the rat liver, resulting in lowered serum cholesterol level.

Animals↗

PubMed1997

Sex difference in serum 7 alpha-hydroxycholesterol levels in the rat reflect hepatic activity of 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase and cholesterol 7 alpha-hydroxylase.

Factors that affect serum levels of 7 alpha-hydroxycholesterol were studied in the rat. Serum levels of 7 alpha-hydroxycholesterol differed in male and female rats fed regular chow (male; 0.2 +/- 0.1 nmol/ml (mean +/- SD); n = 8; female; 0.4 +/- 0.1 nmol/ml; n = 8). When rats were fed with chow to which 3% cholestyramine had been added, the level increased significantly, particularly in female rats (male; 0.6 +/- 0.3 nmol/ml; n = 8; female; 2.4 +/- 1.5 nmol/ml; n = 8). The liver activity of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme for degradation of cholesterol, did not show any sex differences, irrespective of whether the animals were fed with regular chow (male; 51 +/- 15 pmol/min per mg protein; n = 8; female; 58 +/- 21 pmol/min per mg protein; n = 8), or the cholestyramine-supplemented chow (male; 162 +/- 33 pmol/min per mg protein; n = 8; female; 172 +/- 33 pmol/min per mg protein; n = 8). In contrast, the activity of 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase, which acts after cholesterol 7 alpha-hydroxylase in the catabolism of cholesterol, showed a marked difference between the sexes. In both sexes this enzyme activity was higher in cholestyramine-treated rats (male; 963 +/- 78 pmol/min per mg protein; n = 8; female; 708 +/- 106 pmol/min per mg protein, n = 8) compared to that in that rats received regular chow (male; 622 +/- 83 pmol/min per mg protein; n = 8; female; 469 +/- 41 pmol/min per mg protein; n = 8). If the serum level of 7 alpha-hydroxycholesterol depended solely on the enzyme activity of cholesterol 7 alpha-hydroxylase, it would be difficult to explain these sex differences, since there were no sex differences in levels of cholesterol 7 alpha-hydroxylase. These results clearly indicate that, in the rat, the serum level of 7 alpha-hydroxycholesterol depends not only on cholesterol 7 alpha-hydroxylase activity but also on 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase activity.

3-Hydroxysteroid Dehydrogenases↗

PubMed1985

Secondary prevention and lipid lowering: results and implications.

In a secondary prevention trial conducted by the National Heart, Lung, and Blood Institute, the effect of lipid lowering by drug intervention on the progression of existing coronary artery disease (CAD) was evaluated in type II hyperlipidemic patients. This first randomized, secondary prevention trial compared the effect of cholestyramine and diet with that of placebo and diet in 143 patients over a 5-year period. End points evaluated were progression or regression of CAD, as demonstrated by angiographic changes compared with baseline angiograms. The cholestyramine-treated group demonstrated a significant reduction in total cholesterol and in low-density lipoprotein cholesterol (LDL) levels as compared with placebo, and an 8% increase in high-density lipoprotein cholesterol (HDL). A statistically significant result supporting the use of cholestyramine treatment was found in one category of CAD progression.

Angiocardiography↗

PubMed1987

Comparison of six pharmacologic regimens for hypercholesterolemia.

Six sequential clinical trials were conducted over 5 years to evaluate the safety and efficacy of different treatment regimens for hypercholesterolemia. Of all the study participants, 11 patients were evaluated in all 6 clinical trials using the following regimens: neomycin, neomycin/niacin, cholestyramine, cholestyramine/neomycin, lovastatin and lovastatin/neomycin. All 6 regimens significantly (p less than 0.05) reduced both total and low-density lipoprotein cholesterol concentrations by 25 to 42% from baseline levels. Only neomycin/niacin, cholestyramine and lovastatin significantly increased the high-density lipoprotein (HDL) cholesterol concentration, reducing the total cholesterol/high-density lipoprotein cholesterol ratio to less than 4.7. Thus, all 6 tested regimens were effective in modifying the plasma lipoprotein concentrations in type II hyperlipoproteinemia, but neomycin/niacin, cholestyramine and lovastatin had the most favorable impact. Only lovastatin treatment was free of adverse effects.

Adult↗

PubMed1989

Down-regulation of pancreatic growth and gallbladder contractility by bile salts.

Luminal sequestration of bile salts with cholestyramine and the oral administration of bile salts represent current forms of therapy for some diseases. We have recently reported that secretion of these salts exerts negative feedback control on the release of cholecystokinin (CCK). The purpose of this study was to examine the effects of long-term alterations of luminal concentrations of bile salts on CCK target organs, the pancreas and gallbladder. The bile salt pool in adult guinea pigs was either enriched by feeding 0.5 percent sodium taurocholate or depleted by feeding 2 percent cholestyramine. Pancreatic growth, gallbladder contractility, the concentration of cholecystokinin receptors in the gallbladder muscle, and meal-stimulated plasma levels of cholecystokinin were significantly stimulated by feeding the bile salt sequestrant cholestyramine to guinea pigs. Administration of the bile salt taurocholate produced the opposite effects. Inhibition of CCK release by bile salts and up-regulation of CCK receptors by CCK may be the mechanisms responsible for the actions of bile salts on CCK target organs.

Animals↗

PubMed1975

The interaction of various control mechanisms in determining the rate of hepatic cholesterogenesis in the rat.

In these studies rats were subjected to diurnal light-cycling, stress, fasting and the feeding of cholestyramine, beta-sitosterol and cholesterol in various combinations. In control animals exposed to light cycling for 2 weeks the rate of hepatic cholesterogenesis was 3.7 fold higher in the mid-dark than in the mid-light phase of the light cycle. The magnitude of this difference varied with the duration of light cycling and the size of the animals. Similarly, enhanced rates of cholesterol synthesis were seen in the mid-dark phase relative to the mid-light phase of the light cycle in rats where the base-line level of hepatic cholesterogenesis was increased by feeding cholestyramine (1.6-fold) or beta-sitosterol (2.9-fold) or was depressed by fasting (19-fold) or cholesterol feeding (2.1-fold). Restraining animals for 48 h also increased the rate of cholesterol synthesis in the liver; in control animals, this stress enhanced the level of cholesterogenesis seen at both the mid-light and mid-dark phases of the light cycle. In addition, both the effects of stress and of diurnal light cycling could be identified in groups of animals where base-line cholesterogenic activity was varied by fasting or by feeding cholestyramine, beta-sitosterol or cholesterol. These studies illustrate the complexity of the control of hepatic cholesterol synthesis and suggest that the final rate of cholesterogenesis may be the result of several different effectors modifying by different mechanisms the activity of beta-hydroxy-beta-methylglutaryl-CoA reductase.

Animals↗

PubMed1979

Purification and properties of rat liver 3-hydroxy-3-methylglutaryl coenzyme A reductase.

3-Hydroxy-3-methylglutaryl coenzyme A reductase has been purified from rat liver microsomes with a recovery of approx. 25%. The enzyme was homogeneous on gel electrophoresis and enzyme activity comigrated with the single protein band. The molecular weight of the reductase determined by gel filtration on Sephadex G-200 was 200,000. SDS-polyacrylamide gel electrophoresis gave a subunit molecular weight of 52,000 +/- 2000, suggesting that the enzyme was a tetramer. The specific activities of the purified enzyme obtained from rats fed diets containing 0% or 5% cholestyramine were 11,303 and 19,584 nmol NADPH oxidized/min per mg protein, respectively. The reductase showed unique binding properties to Cibacron Blue Sepharose; the enzyme was bound to the Cibacron Blue via the binding sites for both substrates, NADPH and (S)-3-hydroxy-3-methylglutaryl coenzyme A. Antibodies prepared against purified reductase inactivated 100% of the soluble and at least 91% of the microsomal enzyme activity. Immunotitrations of solubilized enzyme obtained from normal and cholestyramine-fed rats indicated that cholestyramine feeding both increased the amount of enzyme protein and resulted in enzyme activation. Administration of increasing amounts of mevalonolactone to rats decreased the equivalence point obtained from immunotitration studies with solubilized enzyme. These data indicate that the antibody cross-reacts with the inactive enzyme formed after mevalonolactone treatment.

Animals↗

PubMed1986

Acetoacetyl-CoA synthetase specific activity and concentration in rat tissues.

An antibody against acetoacetyl-CoA synthetase purified from rat liver was raised in rabbits. Utilizing the binding of antibody-antigen complexes to a nitrocellulose membrane, a sensitive enzyme-linked immunosorbent assay was developed to estimate the enzyme concentration in rat tissues. The enzyme concentration (microgram immunoreactive protein/mg protein) in rat liver cytosol was increased about 3-, 1.8- and 7-fold by feeding rats diets containing 5% cholestyramine, 0.2% ML-236B (compactin), and 5% cholestyramine plus 0.2% ML-236B for 4 days, respectively, and decreased about 1.8-fold by fasting the animals or 1.3-fold by feeding them a diet containing 5% cholesterol. Changes in the enzyme activity were almost parallel to those in the enzyme concentration, suggesting the physiological role of this enzyme in cholesterol biosynthesis. Immunoblotting of the hepatic cytosol also confirmed that the increase in enzyme concentration on cholestyramine and/or ML-236B feeding was due to an increase in an enzyme protein the same as the purified enzyme and not the isozymic protein. Among various rat tissues examined, the concentrations of immunologically crossreactive enzyme were higher in lipogenic tissues, such as brain, adipose tissue and liver, than in other tissues. The enzymes in these three tissues were identical in molecular weight determined by gel filtration and immunoblotting.

Animals↗

PubMed1989

Variations of hepatic cholesterol precursors during altered flows of endogenous and exogenous squalene in the rat.

Hepatic and serum levels of cholesterol precursors were analyzed in rats under basal (control) conditions and when cholesterol synthesis was activated by feeding 1% squalene or 5% cholestyramine. Exogenous squalene stimulated the activity of acyl-coenzyme A:cholesterol acyltransferase (ACAT) but strongly inhibited the activity of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase; cholestyramine did not affect ACAT but increased HMG-CoA reductase several-fold, indicating enhanced production of endogenous squalene. Activation of cholesterol synthesis by the two methods markedly increased the hepatic and serum contents of cholesterol precursor sterols. However, the sterol profiles were clearly different. Thus, exogenous squalene raised most significantly (up to 109-fold) free and esterified methyl sterols, and less so (up to 2-fold) demethylated C27 sterols (desmosterol and cholestenols) and also esterified cholesterol. Activation of endogenous squalene production by cholestyramine was associated with a depletion of esterified cholesterol and by a marked, up to 8-fold, increase of the free demethylated sterol precursor levels, whereas the increase of methyl sterols, up to 5-fold, was less conspicuous than during the squalene feeding. The changes were mostly insignificant for esterified sterols. The altered serum sterol profiles were quite similar to those in liver. Serum cholestenols and especially their portion of total serum precursor sterols were closely correlated with the hepatic activity of HMG-CoA reductase.

Animals↗

PubMed1987

Studies of the prevalence and significance of radiolabeled bile acid malabsorption in a group of patients with idiopathic chronic diarrhea.

We studied radiolabeled fecal bile acid excretion in 11 normal subjects and 17 patients with idiopathic chronic diarrhea for three major purposes: to establish normal values for this test in the presence of increased stool volumes (induced in normal subjects by ingestion of poorly absorbable solutions); to test for bile acid malabsorption in the patients and to correlate this with an independent test of ileal function, the Schilling test; and to compare the results of the bile acid excretion test with the subsequent effect of a bile acid binding agent (cholestyramine) on stool weight. In normal subjects fecal excretion of the radiolabel was increased with increasing stool volumes. As a group, patients with idiopathic chronic diarrhea excreted radiolabeled bile acid more rapidly than normal subjects with induced diarrhea (t1/2 56 +/- 8 vs. 236 +/- 60 h, respectively, p less than 0.005). There was a statistically significant positive correlation between t1/2 of radiolabeled bile acid and Schilling test results in these patients. Although 14 of 17 patients absorbed labeled taurocholic acid less well than any of the normal subjects with comparable volumes of induced diarrhea, cholestyramine had no statistically significant effect on stool weight in the patient group, and in none of the patients was stool weight reduced to within the normal range. In summary, most patients with idiopathic chronic diarrhea have bile acid malabsorption (as measured by fecal excretion of labeled bile acid), but they do not respond to cholestyramine therapy with a significant reduction in stool weight. Although the significance of these findings was not clearly established, the most likely interpretation is that bile acid malabsorption is a manifestation of an underlying intestinal motility or absorptive defect rather than the primary cause of diarrhea.

Adult↗

PubMed1980

Lipid changes in atherosclerotic aortas of Macaca fascicularis after various regression regimens.

plasma and aortic tissue lipid changes in atherosclerotic Macaca fascicularis monkeys were studied following various regression regimens for 18 months. Atherosclerosis was induced in groups of 18 Macaca fascicularis monkeys by feeding a semipurified diet containing 43% of the calories as fat and 1.2 mg/kcal cholesterol for 6 months. Five groups of animals were continued on the same diet containing 0.34 mg/kcal cholesterol during the regression period, and were given the following hypocholesterolemic regimens: none (positive controls); D-thyroxine; pyrimidine derivative; cholestyramine; and alfalfa. Another group of animals was maintained on regular monkey chow alone during the regression period (negative control). Among the hypocholesterolemic agents, cholestyramine very effectively reduced the plasma cholesterol, and aorta free- and esterified cholesterol and phospholipids. D-Thyroxine significantly lowered the plasma cholesterol levels but, surprisingly, tissue lipid levels were the highest among the groups studied. Alfalfa, although not as effective as cholestyramine, tended to reduce the plasma and tissue lipids more than other drugs. Pyrimidine derivative actually increased the mean levels of plasma and tissue cholesterol. Plasma cholesterol correlated positively with aortic tissue cholesterol, free and esterified cholesterol. Both the plasma percentage distribution of alpha-lipoprotein and the phospholipid/cholesterol ratio were inversely related to all tissues lipids. Plasma cholesterol accounted for 43% and 30% respectively of the variability in tissue total and esterified cholesterol. Thus the effectiveness of any hypocholesterolemic regimen is probably dependent on achieving a favorable lipoprotein distribution in plasma without any adverse effect on the arterial wall metabolism.

Animals↗

PubMed1990

Abnormalities of blood rheology in familial hypercholesterolaemia: effects of treatment.

Whole blood and plasma viscosity, red cell aggregability and deformability, and plasma fibrinogen have been compared between 20 patients with heterozygous familial hypercholesterolaemia (FH), without clinical arterial disease, and 20 age- and sex-matched controls. Plasma fibrinogen was elevated in FH, associated with increased whole blood viscosity at low shear rate, plasma viscosity and red cell aggregation. At high shear rate blood viscosity was not elevated, and red cell deformability was normal. The effect of 12 weeks double blind treatment with cholestyramine 16-24 g/day, pravastatin 20 mg b.i.d. or placebo on blood rheology was studied in 17 FH patients. Mean plasma cholesterol fell significantly by 24.7% with pravastatin and 21.5% with cholestyramine, the latter also causing a significant 42% rise in triglyceride. Pravastatin, but not cholestyramine, caused a significant fall in plasma viscosity and fibrinogen, but no change was seen in whole blood rheology. This suggests that the rheological abnormalities in FH are at least partly related to the plasma lipid levels and hence reversible with treatment.

Adult↗

PubMed1995

Lipoprotein pattern and plasma lecithin cholesterol acyl transferase activity in children with Alagille syndrome.

Alagille syndrome is frequently associated with hyperlipidemia and xanthoma. The aim of the study was to assess the lipid profile (plasma lipoproteins, apolipoproteins (apo)) and lecithin cholesterol acyl transferase (LCAT) activity, with and without treatment with cholestyramine in Alagille syndrome. Five children (mean age = 6 +/- 4 years) with Alagille syndrome were studied at two different times while receiving no treatment, and while receiving cholestyramine. They were compared with 12 normal controls, who were not different from patients for age and sex. In Alagille syndrome, total serum cholesterol, triglycerides and phospholipids were elevated compared with the controls (P < 0.008). VLDL-cholesterol, LDL-cholesterol, HDL-triglycerides, LDL-triglycerides and VLDL-phospholipids were higher, whereas HDL-cholesterol was lower than controls (P < 0.03). Apo B, CIII, E and lipoprotein particles Lp AI were higher (P < 0.001), whereas Lp AI:AII was lower than controls (P < 0.03). Lipoprotein-X was present in the 5 children with Alagille syndrome and explained in part the elevation of plasma cholesterol, phospholipids, and apo CIII. LCAT activity was decreased (P < 0.01) and might cause some abnormalities of HDL with lower cholesterol, higher triglycerides, apo E and apo CIII contents than controls, and abnormalities of VLDL and LDL with higher cholesterol, triglycerides, phospholipids and apo B contents than controls. Some of the risk factors of atherosclerosis were found in Alagille syndrome, namely high levels of plasma cholesterol, LDL cholesterol, apo B, apo B/apo AI. Treatment with cholestyramine resulted in a few modifications to the lipid profile, while lipoprotein-X and the decrease of LCAT activity persisted.

Adolescent↗

PubMed1984

HMGCoA reductase and cholesterol 7 alpha-hydroxylase in human liver.

The activities of HMGCoA reductase and cholesterol 7 alpha-hydroxylase were assayed in liver biopsies of patients with or without cholestyramine treatment. The active dephosphorylated form of HMGCoA reductase and the activity of cholesterol 7 alpha-hydroxylase were under the detection limits in untreated subjects. After cholestyramine treatment activities of both enzymes were stimulated and the active form of HMGCoA reductase became detectable in four out of the five tested patients. In two subjects who received cholestyramine, the effect of exogenously added [4-14C] cholesterol on cholesterol 7 alpha-hydroxylase was tested. In the presence of Tween 80, the detergent by which [14C]cholesterol was suspended, the enzyme activity was profoundly inhibited and synthesis of 7 alpha-hydroxycholesterol was extremely low.

Adult↗