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PubMed1997

Soluble interleukin-2 receptor is a thyroid hormone-dependent early-response marker in the treatment of thyrotoxicosis.

Thyrotoxic patients exhibit increased levels of immune activation molecules (soluble interleukin-2 receptor [sIL-2R], intercellular adhesion molecule-1 [ICAM-1], and endothelial-leukocyte adhesion molecule-1 [ELAM-1]) in serum, although the clinical significance of these measurements remains unclear. In a randomized 4-week study, we have recently shown that in the treatment of hyperthyroidism, the combination of cholestyramine and methimazole (MMI) resulted in faster lowering of serum thyroid-hormone levels than did MMI alone. Stored serial serum samples from patients participating in this randomized treatment trial were analyzed for sIL-2R, soluble ICAM-1 (sICAM-1), and soluble ELAM-1 (sELAM-1). The levels of all three molecules were elevated in patients with hyperthyroidism. Although the levels of sICAM-1 and sELAM-1 remained elevated through the 4-week follow-up period in both groups of patients, the sIL-2R levels (normal levels, 1.0 to 4.2 ng/ml) decreased significantly in the 10 patients who received cholestyramine in addition to MMI (week 0, 14.2 +/- 1.5 ng/ml; week 2, 10.8 +/- 1.2 ng/ml; week 4, 8.9 +/- 1.5 ng/ml). In eight patients who received MMI alone, sIL-2R decreased less rapidly (week 0, 12.3 +/- 1.4 ng/ml; week 2, 12.3 +/- 1.3 ng/ml; week 4, 10.9 +/- 1.3 ng/ml). sICAM-1 and sELAM-1 were elevated at baseline but did not decrease during therapy. In the former group, free thyroxine and free triiodothyronine decreased faster. These data show that levels of sIL-2R in serum, but not those of sICAM-1 and sELAM-1, may be of clinical use in the early follow-up evaluation of medically treated patients.

Antithyroid Agents↗

PubMed1975

Comparison of treatments for congenital nonobstructive nonhaemolytic hyperbilirubinaemia.

A patient with Crigler-Najjar disease has survived with the help of phototherapy to the age of 2 years without neurological damage. Because long periods of phototherapy are a threat to normal development, a search was made for supplementary treatments. Cholestyramine and a high fat diet were effective, and possibly also aspartic acid. Maintenance therapy with cholestyramine allowed the amount of phototherapy given to be reduced.

Agar↗

PubMed1972

Lipid absorption, bile acids, and cholesterol metabolism in patients with chronic liver disease.

Faecal bile acids and neutral sterols of cholesterol origin were decreased in patients with chronic liver disease, while urinary bile acids were constantly, but never greatly, increased. Thus, production of cholesterol and its conversion to bile acids was decreased in these patients. Faecal fat was only slightly increased, even in cases with a very low bile salt output, but it was negatively correlated with faecal bile acids. The reduced capacity of these patients to synthesize bile acids was shown by the fact that cholestyramine treatment, although it decreased urinary bile acids, increased faecal bile acids only slightly. The resin constantly increased faecal neutral sterols, while the increase of faecal fat was insignificant. Thus, the absorption of fats, as compared with that of sterols, was less strongly reduced by interruption of the enterohepatic circulation of bile salts. In one cirrhotic patient markedly increased faecal bile acids apparently caused cholerrhoeic diarrhoea, which was easily controlled with cholestyramine. The latter consistently increased elimination of cholesterol in cirrhotic patients, but serum cholesterol was not consistently decreased, and in these patients, in contrast to the control subjects, it was difficult to detect changes in cholesterol synthesis with the acetate-mevalonate test and serum methyl sterols.

Adult↗

PubMed2002

Intraduodenal conjugated bile salts exert negative feedback control on gall bladder emptying in the fasting state without affecting cholecystokinin release or antroduodenal motility.

BACKGROUND: Intraduodenal bile salts exert negative feedback control on postprandial gall bladder emptying. AIMS: We wished to examine whether a similar control mechanism occurs in the fasting state. METHODS: Intraduodenal bile salt depletion was achieved by 12 g of cholestyramine. Thereafter, in study A (seven subjects), the effects on gall bladder volume (by ultrasound) and antroduodenal motility of intraduodenal infusions of taurocholate egg yolk-phosphatidylcholine micelles were assessed. In study B (nine subjects), the effects on gall bladder volume of infusing mixed micelles composed of taurocholate (100 mM) and low (26 mM) or high (68 mM) amounts of egg yolk-phosphatidylcholine, or low amounts of dipalmitoylphosphatidylcholine were determined. RESULTS: Cholestyramine induced strong and prolonged gall bladder contraction without cholecystokinin release. In study A, micellar infusions increased gall bladder volume without affecting migrating motor complex cycle length. In study B, intraduodenal infusion induced strong increases in gall bladder volume in the case of taurocholate micelles containing low amounts of egg yolk-phosphatidylcholine, moderate increases in micelles containing low amounts of dipalmitoylphosphatidylcholine but no change in micelles containing high amounts of egg yolk-phosphatidylcholine, in all cases without altered plasma cholecystokinin levels. Phosphatidylcholine hydrolysis was significantly higher after infusion of egg yolk-phosphatidylcholine compared with infusion of dipalmitoylphosphatidylcholine containing micelles. Intermixed micellar-vesicular bile salt concentrations (responsible for detergent effects) were higher in egg yolk-phosphatidylcholine than in dipalmitoylphosphatidylcholine containing model biles and if lyso-phosphatidylcholine was included. CONCLUSIONS: Intraduodenal bile salts exert negative feedback on fasting gall bladder volume. The modulating effects of various phospholipids may relate to their effects on intermixed micellar-vesicular bile salt concentrations.

Adult↗

PubMed1990

Reduced cholecystokinin mediates the inhibition of pancreatic growth induced by bile salts.

The effects of luminal bile salts on plasma levels of cholecystokinin (CCK) and growth of the pancreas in mice were studied. Nonfasting levels of plasma CCK in control mice were 8.1 +/- 1.5 pM. Feeding mice a 0.5% (wt/wt) sodium taurocholate-supplemented diet for 1 wk significantly lowered nonfasting levels of plasma CCK to 4.1 +/- 0.5 pM and decreased the total contents of pancreatic DNA by 22%, RNA by 25%, and protein by 24%. All of the inhibitory effects of taurocholate on pancreatic growth were completely reversed by the simultaneous administration of CCK-8 (3 micrograms/kg, 3 times daily). In contrast, intraluminal neutralization of endogenous bile salts by feeding a 4% (wt/wt) cholestyramine-supplemented diet for 1 wk significantly elevated nonfasting levels of plasma CCK to 14.7 +/- 1.5 pM and increased the total contents of pancreatic DNA by 34%, RNA by 40%, and protein by 35%. All of the stimulatory actions of cholestyramine on pancreatic growth were completely abolished by the administration of the highly potent and specific CCK-receptor antagonist L364,718 (1 mg/kg, twice daily). These findings, therefore, indicate that bile salts appear to play a physiological role in pancreatic growth by regulation of plasma levels of CCK.

Animals↗

PubMed1988

Acetyl-CoA hydrolase: relation between activity and cholesterol metabolism in rat.

To examine whether cytosolic acetyl-CoA hydrolase in rat liver is involved in regulation of cholesterol biosynthesis, we investigated the alteration of the enzyme activity under conditions of stimulation (cholestyramine treatment) and suppression [cholesterol feeding, a potent competitive inhibitor of microsomal 3-hydroxy-3-methylglutaryl-CoA reductase (CS 514) treatment, and a hypolipidemic drug [alpha-(p-chlorophenoxy)isobutyric acid, CPIB] injection) of cholesterol biosynthesis. The enzyme activity in rat liver increased significantly in the early diabetic, cholesterol-fed, CS 514-, and CPIB-treated groups, but no change in its activity was observed in chronic diabetic groups. Cholestyramine treatment to cholesterol-fed rats made the enzyme activity return to the initial level. When chronic diabetic rats were given a cholesterol diet or treated with CS 514 or CPIB, the activity increased significantly. Inhibition of cholesterol biosynthesis caused by these treatments induced increase in the enzyme activity with increase in the enzyme protein, judging from results obtained by enzyme-linked immunosorbent assay. These results suggest that this enzyme has a physiological role in maintenance of the equilibrium between the cytosolic acetyl-CoA concentration and CoA-SH pool for cholesterol metabolism.

Acetyl-CoA Hydrolase↗

PubMed1995

Probucol treatment decreases serum concentrations of diet-derived antioxidants.

The effect of probucol, which is both a cholesterol-lowering drug and an antioxidant, on the serum concentrations of diet-derived antioxidants vitamin E, beta-carotene, lycopene, and vitamin A was studied in 303 hypercholesterolemic subjects. In a 3-year, double-blind, randomized trial we investigated to determine whether combined treatment with diet, cholestyramine, and probucol could reduce the progression of femoral atherosclerosis. Serum and lipoprotein antioxidant levels were measured by reverse-phase high-performance liquid chromatography. Cholestyramine significantly lowered serum concentrations of vitamin E by 7%, beta-carotene by 40%, and lycopene by 30% (all P < .001) due to impairment of gastrointestinal absorption and to serum cholesterol lowering. Probucol reduced serum vitamin E by 14% (P < .001) secondary to cholesterol and triglyceride lowering. The carotenoids were reduced by probucol by 30% to 40% (P < .001) most probably due to reductions in lipoprotein particle size and to competition with these substances for incorporation into VLDL during its assembly in the liver. This study shows that the use of a lipid-soluble antioxidant and cholesterol-lowering drug may have unfavorable effects on blood levels of diet-derived antioxidants.

Antioxidants↗

PubMed1986

High-density lipoprotein cholesterol and coronary heart disease in hypercholesterolemic men: the Lipid Research Clinics Coronary Primary Prevention Trial.

Plasma levels of high-density lipoprotein cholesterol (HDL-C) at entry and subsequent changes from these baseline levels were inversely predictive of coronary heart disease (CHD) end points in hypercholesterolemic men followed for 7 to 10 years in the Lipid Research Clinics Coronary Primary Prevention Trial, especially in the 1907 participants receiving cholestyramine. When the men in this cohort were compared, each 1 mg/dl increment in baseline HDL-C (mean 44.3 mg/dl) was associated with a 5.5% decrement in risk of "definite" CHD death or myocardial infarction (Z = -5.4), and each 1 mg/dl increase from baseline HDL-C levels (mean increase = 1.6 mg/dl) during the trial was associated with a 4.4% risk reduction (Z = -2.2). In the 1899 participants receiving placebo, the corresponding risk decrements were 3.4% and 1.1%. Although baseline HDL-C level (mean = 44.4 mg/dl) remained a significant risk predictor (Z = -3.8) in the placebo cohort, increases in HDL-C (mean increase 0.5 mg/dl) were not significantly predictive of CHD (Z = -0.6) unless "suspect" as well as "definite" end points were analyzed (Z = -2.0). When the associations between HDL-C (baseline plus change) and incidence of definite CHD end points within each treatment cohort were compared, their difference approached nominal significance (Z = 1.9). The results suggest a synergistic interaction, in which cholestyramine treatment reduced CHD risk most substantially in men maintaining the highest HDL-C levels.

Adult↗

PubMed2000

Maternal hypercholesterolemia enhances atherogenesis in normocholesterolemic rabbits, which is inhibited by antioxidant or lipid-lowering intervention during pregnancy: an experimental model of atherogenic mechanisms in human fetuses.

Maternal hypercholesterolemia during pregnancy is associated with a marked increase in aortic fatty streak formation in human fetuses and faster progression of atherosclerosis during normocholesterolemic childhood. However, the mechanisms responsible are unknown, and the contribution of genetic differences is difficult to assess in humans. The goal of this study was to determine whether maternal hypercholesterolemia per se may cause enhanced fatty streak formation in offspring and whether interventions during pregnancy can reduce it. During pregnancy, 1 group of New Zealand White rabbits was fed control chow and 8 groups were fed hypercholesterolemic diets Chol 1 (yielding plasma cholesterol of 153 mg/dL) or Chol 2 (yielding 359 mg/dL) without or with cholestyramine, vitamin E, or both. Offspring (n=15 to 25 per group) were killed at birth. Maternal hypercholesterolemia enhanced mean lesion size in the aorta of their offspring at birth from 44+/-18x10(3) micrometer(2) per section in controls to 85+/-26x10(3) in Chol 1 and 156+/-49x10(3) in Chol 2 groups (P<0.0001 for both). Cholestyramine or vitamin E treatment of mothers significantly reduced atherosclerosis at birth by up to 39% compared with controls on the same diet. Oxidized fatty acids and malondialdehyde in aortic atherosclerotic lesions and plasma were similarly affected by diets and treatment as atherosclerosis. Our results establish the causal role of hypercholesterolemia and peroxidation in fetal atherogenesis and demonstrate that both lipid-lowering and antioxidant interventions during pregnancy can reduce it. If it can be established that interventions in mothers also affect progression of lesions after birth, this may indicate a novel approach for the prevention of atherosclerosis.

Animals↗

PubMed2001

Maternal hypercholesterolemia and treatment during pregnancy influence the long-term progression of atherosclerosis in offspring of rabbits.

Maternal hypercholesterolemia during pregnancy is associated with enhanced fatty streak formation in human fetuses and faster progression of atherosclerosis during childhood even under normocholesterolemic conditions. A causal role of maternal hypercholesterolemia in lesion formation during fetal development has previously been established in rabbits. The same experimental model is now used to establish that maternal hypercholesterolemia or ensuing pathogenic events in fetal arteries enhance atherogenesis later in life. Five groups of rabbit mothers were fed chow, cholesterol-enriched chow, or cholesterol-enriched chow plus 1000 IU vitamin E, 3% cholestyramine, or both during pregnancy. Offspring of all groups (n=136) were fed a mildly hypercholesterolemic diet for up to a year and had similar cholesterol levels. Aortic lesion sizes and lipid peroxidation products in plasma and lesions in offspring were determined at birth, 6 months, or 12 months. Lesion progression in offspring of hypercholesterolemic mothers was greater than in all other groups. At each time point, offspring of hypercholesterolemic mothers had 1.5- to 3-fold larger lesions than offspring of normocholesterolemic mothers (P<0.01), with the greatest absolute differences at 12 months. Maternal treatment reduced lesions by 19% to 53%, compared with offspring of untreated hypercholesterolemic mothers (P<0.01), with the greatest effect in the vitamin E groups. At 12 months, lesions in offspring of all vitamin E and cholestyramine-treated mothers were similar to those of normocholesterolemic mothers. Lipid peroxidation end-products in lesions and plasma showed analogous differences between groups as lesions (P<0.01). Thus, pathogenic programming in utero increases the susceptibility to atherogenic risk factors later in life and maternal intervention with cholesterol-lowering drugs or antioxidants reduce postnatal lipid peroxidation and atherosclerosis in their offspring.

Animals↗

PubMed1998

Aminated polysaccharides as bile acid sorbents: in vitro study.

Dextran, pullulan, and microcrystalline cellulose were cross-linked with 1-chloro-2,3-epoxypropane and reacted with N-(1-chloroethyl)-N,N-diethylamine or N-glycidyl-N,N,N-trialkylammonium chloride in order to obtain sorbents containing tertiary amino and/or quaternary ammonium groups. In vitro equilibrium sorption of cholic acid on these sorbents was studied in comparison with Cholestyramine, and in vitro dissociation of ionic complexes of cholic acid-sorbents was determined under dynamic conditions. The sorption capacity and the affinity of these sorbents for cholic acid were investigated in relation to the nature of the polymeric support, the swelling porosity of sorbent, the basicity of amino groups, and the nature of the substituents at the nitrogen atom. The maximum sorption capacity increases with the increase in amino group content, their basicity, and the length of alkyl substituents at the nitrogen atom. The affinity for cholic acid of all polysaccharide-based sorbents is higher than that of Cholestyramine. Dextran-based sorbents display the highest sorption affinity. It was found that there exists an optimum swelling porosity for the polysaccharide sorbents to attain the highest affinity for cholic acid. The dissociation rate of ionic complexes depends also on the nature of the polysaccharide and the swelling porosity and its lower for sorbents with higher sorption affinity.

Absorption↗

PubMed1980

Effect of neonatal modulation of cholesterol homeostasis on subsequent response to cholesterol challenge in adult guinea pig.

Experiments were designed to study whether or not the mechanism of handling dietary cholesterol in adulthood can be modulated by the manipulation of cholesterol homeostasis during neonatal period. The effects of enhancing cholesterol degradation (cholestyramine feeding), high dietary cholesterol intake, and early weaning during neonatal period of guinea pigs on their subsequent plasma cholesterol levels and the response to dietary cholesterol challenged in adulthood were investigated. Pretreatment of neonatal guinea pigs with cholestyramine resulted in (a) a lower plasma cholesterol level, (b) an increased excretion rate of fecal bile acids and total steroids, (c) an expanded bile acid pool, (d) an increased activity of cholesterol 7 alpha-hydroxylase, and (e) no change in the hepatic 3-hydroxy-3-methylglutaryl coenzyme A (CoA) reductase activity when challenged with cholesterol in adulthood. Cholesterol pretreatment during neonatal period resulted in (a) no alteration in the plasma cholesterol level, (b) no alteration in the fecal excretion of steroids, or (c) no alteration in the cholesterol 7 alpha-hydroxylase activity when they were challenged with a high cholesterol diet. Early weaning did not influence the fecal excretion of steroids or cholesterol 7 alpha-hydroxylase activity but resulted in a slight decrease in the hepatic 3-hydroxy-3-methylglutaryl-CoA reductase activity when they were challenged with a high cholesterol diet. These results suggest that stimulation of cholesterol catabolism rather than cholesterol feeding or early weaning during neonatal period can influence the response to dietary cholesterol challenge in adulthood.

Aging↗

PubMed1994

Regulation of hepatic 7 alpha-hydroxylase expression by dietary psyllium in the hamster.

Soluble fiber consistently lowers plasma total and low density lipoprotein (LDL)-cholesterol concentrations in humans and various animal models including the hamster; however, the mechanism of this effect remains incompletely defined. We performed studies to determine the activity of dietary psyllium on hepatic 7 alpha-hydroxylase, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase and LDL receptor expression in the hamster. In animals fed a cholesterol-free semisynthetic diet containing 7.5% cellulose (avicel) as a fiber source, substitution of psyllium for avicel increased hepatic 7 alpha-hydroxylase activity and mRNA levels by 3-4-fold. Comparable effects on 7 alpha-hydroxylase expression were observed with 1% cholestyramine. Psyllium also increased hepatic 7 alpha-hydroxylase activity and mRNA in animals fed a diet enriched with cholesterol and triglyceride. Activation of 7 alpha-hydroxylase was associated with an increase in hepatic cholesterol synthesis that was apparently not fully compensatory since the cholesterol content of the liver declined. Although dietary psyllium did not increase hepatic LDL receptor expression in animals fed the cholesterol-free, very-low-fat diet, it did increase (or at least restore) receptor expression that had been downregulated by dietary cholesterol and triglyceride. Thus, 7.5% dietary psyllium produced effects on hepatic 7 alpha-hydroxylase and LDL metabolism that were similar to those of 1% cholestyramine. Induction of hepatic 7 alpha-hydroxylase activity by dietary psyllium may account, in large part, for the hypocholesterolemic effect of this soluble fiber.

Animals↗

PubMed1993

The effect of cholesterol-lowering agents on hepatic and plasma cholesterol in Niemann-Pick disease type C.

Niemann-Pick disease type C (NP-C) is a neurovisceral lipidosis characterized by defective intracellular trafficking of cholesterol and lysosomal accumulation of unesterified cholesterol, believed to be an offending metabolite. We studied the effect of cholesterol-lowering agents on hepatic and plasma cholesterol levels in NP-C by randomly assigning 25 patients with NP-C to one of five treatment regimens containing different combinations of cholestyramine, lovastatin, nicotinic acid, or dimethyl sulfoxide (DMSO). Unesterified cholesterol content was measured in liver biopsies before and after 4 months' treatment. All drug regimens except DMSO alone reduced hepatic and plasma cholesterol levels. Toxicity was limited and did not prevent any patient from completing the study. The combination of cholestyramine, lovastatin, and nicotinic acid lowered cholesterol levels in liver and blood with minimal side effects. A controlled clinical study will be necessary to determine if this regimen influences the rate of neurologic progression.

Adolescent↗

PubMed2001

Possible estuary-associated syndrome: symptoms, vision, and treatment.

The human illness designated as possible estuarine-associated syndrome (PEAS) by the Centers for Disease Control and Prevention (CDC) has been associated with exposure to estuaries inhabited by toxin-forming dinoflagellates, including members of the fish-killing toxic Pfiesteria complex (TPC), Pfiesteria piscicida and Pfiesteria shumwayae. Humans may be exposed through direct contact with estuarine water or by inhalation of aerosolized or volatilized toxin(s). The five cases reported here demonstrate the full spectrum of symptoms experienced during acute and chronic stages of this suspected neurotoxin-mediated illness. The nonspecific symptoms most commonly reported are cough, secretory diarrhea, headache, fatigue, memory impairment, rash, difficulty in concentrating, light sensitivity, burning skin upon water contact, muscle ache, and abdominal pain. Less frequently encountered symptoms are upper airway obstruction, shortness of breath, confusion, red or tearing eyes, weakness, and vertigo. Some patients experience as few as four of these symptoms. The discovery that an indicator of visual pattern-detection ability, visual contrast sensitivity (VCS), is sharply reduced in affected individuals has provided an objective indicator that is useful in diagnosing and monitoring PEAS. VCS deficits are present in both acute and chronic PEAS, and VCS recovers during cholestyramine treatment coincident with symptom abatement. Although PEAS cannot yet be definitively associated with TPC exposure, resolution with cholestyramine treatment suggests a neurotoxin-mediated illness.

Adult↗

PubMed2005

Reduction in fecal excretion of Giardia cysts: effect of cholestasis and diet.

Bile is a major growth factor for the proliferation of Giardia spp. trophozoites in the small intestine and, at high concentrations, stimulates encystment of trophozoites. This report demonstrates that surgical cholestasis to interrupt the flow of bile from liver to intestine or the use of bile-binding resins in the diet can both dramatically decrease the fecal excretion of Giardia muris cysts. Cholestasis produced a 3 log reduction in excretion of G. muris cysts within 24 hr of surgery and a 4 log reduction after 3 days. Sham controls showed no difference in cyst excretion from presurgical control values. Two isocaloric diets were studied: a control diet (N) of Purina mouse chow containing 5% celufil and an experimental diet (CR) containing 5% cholestyramine, a resin that binds bile. Compared with the N diet, the CR diet was associated with reductions in cyst excretion of 3 logs within 1 day. Despite lowered excretion of G. muris cysts in mice fed the cholestyramine diet, the trophozoite recovery from the duodenum was similar with both diets. Cyclic feeding of the CR diet and the N diet at 3-day intervals produced significant oscillations (changes of 3-4 logs) in fecal cyst shedding. The significant reductions in fecal excretion of cysts observed with agents that bind bile suggests that diets capable of binding bile might be a therapeutic means to minimize the fecal excretion of cysts and thereby may help to reduce the risk of spreading giardiasis through fecal-oral contamination.

Animals↗

PubMed1990

Pharmacological intervention for altering lipid metabolism.

Pharmacological intervention for altering plasma levels of lipoproteins is usually aimed at reducing atherogenesis and preventing coronary heart disease (CHD). Drug therapy should be attempted only after other nonpharmacological methods (such as elimination of smoking, weight reduction and exercise) have been tried. An overview of the metabolism of low density lipoprotein (LDL) and high density lipoprotein (HDL) particles is the basis of this paper. Various sites suitable for pharmacological intervention are identified. LDL metabolism can be altered at 2 potential sites, with a consequent reduction in the plasma level of this atherogenic lipoprotein. Hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors (such as lovastatin) and cation-exchange resins (e.g. cholestyramine) reduce LDL levels by stimulating the hepatic synthesis of apolipoprotein (apo) B,E receptors. Very low density lipoprotein (VLDL) secretion is inhibited by nicotinic acid (niacin) and gemfibrozil, leading to a secondary decrease in LDL production from VLDL. Probucol also reduces the LDL concentration and inhibits the oxidative modification of LDL. Gemfibrozil and other fibrates stimulate lipoprotein lipase activity, thereby decreasing VLDL concentration. Reduction of the LDL concentration is effective in reducing CHD incidence, whether this is achieved by stimulation of catabolism or inhibition of production of the lipoprotein. In contrast, the mechanism of raising plasma HDL-cholesterol levels is probably relevant to the potential clinical benefits associated with drug therapy. Gemfibrozil and cholestyramine stimulate synthesis of apoprotein A1, the major protein constituent of HDL particles. Both drugs have been shown to reduce the incidence of CHD in clinical trials, via mechanisms that are related in part to their HDL-raising activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Cost-effectiveness of drug therapy for hypercholesterolaemia: a review of the literature.

In this article we review published studies of the cost-effectiveness of drug therapy for hypercholesterolaemia to take stock of the principal findings that have been reported to date. We identified 9 studies that met all criteria for inclusion in our review, including 3 of bile-acid sequestrants (cholestyramine, colestipol), 2 of HMG-CoA reductase inhibitor (lovastatin), and 4 that considered both an HMG-CoA reductase inhibitor (simvastatin) and a bile-acid sequestrant (cholestyramine). While these studies were largely consistent in methodological approach, some differences were noted in the costs attributed to drug therapy. The cost-effectiveness of therapy with bile-acid sequestrants was found to range from $100 000 to $209 000 per year of life saved (1991 $US) for middle-aged men (42 to 55 years of age) with moderately high cholesterol levels (280 to 290 mg/dl) and otherwise average coronary risk characteristics. Corresponding cost-effectiveness ratios that have been reported for lovastatin range from $64 000 to $82 000, while those for simvastatin range from $45 000 to $65 000. Studies to date therefore suggest that therapy with HMG-CoA reductase inhibitors (i.e. lovastatin and simvastatin) is substantially more cost-effective than treatment with bile-acid sequestrants.

Age Factors↗