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PubMed1995

Lowering of HDL2b by probucol partly explains the failure of the drug to affect femoral atherosclerosis in subjects with hypercholesterolemia. A Probucol Quantitative Regression Swedish Trial (PQRST) Report.

The aim of the Probucol Quantitative Regression Swedish Trial (PQRST) (n = 303) was to investigate whether probucol (0.5 g BID) added to diet and cholestyramine (8 g BID) could retard progression or induce regression of femoral atherosclerosis in hypercholesterolemic (> 6.86 mmol/L) subjects. Probucol did not induce regression over the 3-year trial period as estimated by change in lumen volume on quantitative arteriography of a 20-cm segment of the femoral artery. In this report we studied in a representative subgroup (n = 72) whether the reduction in HDL concentrations induced by probucol could explain the failure of the drug to be effective. We analyzed the effects of treatment on HDL particle size subclasses. Probucol lowered the relative level of HDL2b, comprising the largest HDL particles, by 53% and the protein concentration of HDL2b by 67%. The protein reduction in HDL was mainly confined to the apolipoprotein A-I moiety. The change in lumen volume correlated significantly with change in HDL, ie, HDL cholesterol (r = .34, P < .01), HDL2 cholesterol (r = .37, P < .01), HDL2b protein (r = .44, P < .001), and the relative HDL2b value (r = .51, P < .001). The corresponding values for relative HDL2b, distribution calculated on the active (n = 35) and placebo (n = 37) groups separately were also significant (r = .39 and .32, respectively; both P < .05). The correlation between drug-induced change in the relative HDL2b concentration and change in atherosclerosis was independent of the alteration in triglyceride concentration and could not be explained by treatment interaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein A-I↗

PubMedDate not supplied

Homozygous familial hypercholesterolemia occurring with apoprotein E3 deficiency. Report of two cases.

This is the first report of homozygous familial hypercholesterolemia (FH) occurring together with dysbetalipoproteinemia. The former was demonstrated by deficiency of specific receptors for apoprotein B of low density lipoproteins and the latter by isoelectric focusing of the E isoapoproteins and the presence of a broad-beta band on electrophoresis. Two young boys of Lebanese extraction had extensive tuberous and tendinous xanthomata, serum cholesterol concentrations of 29.9 and 28.4 mmol/liter, respectively, and mildly raised serum triglycerides due to an accumulation of lipoprotein remnant particles. Homozygosity for FH was demonstrated in both boys by the deficiency of specific binding of low density lipoprotein to cultured skin fibroblasts (less than 15% and less than 10% of normal, respectively). The E apoprotein phenotypes showed E3/E2 in one boy and E2/E2 in the other. The treatment of both boys with cholestyramine and probucol reduced the serum cholesterol concentration to between 15 and 18 mmol/liter and dramatically lessened the severity of xanthomatosis.

Apolipoprotein E3↗

PubMed1978

Effects of dietary and pharmacologic alteration of serum lipids on platelet survival time.

Platelet survival time (SURV) (autologous labelling with 51Chromium) was shortened (3 +/- 0.03 days; average t 1/2 +/- SEM; normal t 1/2 3.7 +/- 0.03 days) in 88 out of 128 (69%) men with coronary disease. In 35 out of 47 men with hyperprebetalipoproteinemia, SURV was shortened (3 +/- 0.09 days) (74%). Of 30 men with hyperbetalipoproteinemia, SURV was shortened (2.5 +/- 0.10 days) in 26 (87%). Of 51 men without hyperlipoproteinemia, SURV was normal (3.3 +/- 0.10 days) in 24 (47%). Dietary alteration of serum triglyceride was undertaken in 12 men with hyperprebetalipoproteinemia, and in eight a decrease of triglyceride of more than 75 mg% was achieved (324 +/- 21-219 +/- 18 mg%; P less than 0.001) with an increase of SURV (2.2 +/- 0.11-2.8 +/- 0.13 days; P less than 0.001). In four, serum triglyceride increased by more than 75 mg% (279 +/- 14-451 +/- 28 mg%) and SURV decreased (2.7 +/- 0.16-2.3 +/- 0.21 days). Cholestyramine (16 g g.d.) and diet decreased serum cholesterol (348 +/- 7.6-319 +/- 6.3 mg%; P less than 0.001) in 15 men with hyperbetalipoproteinemia and SURV increased (2.3 +/- 0.08-2.7 +/- 0.07 days; P less than 0.001). Results suggest that SURV is shortened in men with coronary disease, particularly in those with hyperlipoproteinemia, and that alteration of triglyceride and cholesterol are associated with alteration of SURV.

Adult↗

PubMed1968

The role of bile salts in controlling the rate of intestinal cholesterogenesis.

According to current concepts, the liver and gastrointestinal tract are considered to be the major, if not the sole, sources of circulating serum cholesterol. While several mechanisms have been described which control the rate of hepatic cholesterogenesis, only biliary diversion is known to alter the rate of sterol synthesis in the intestine. The present study was designed to identify the inhibitory constituent of bile and to define its anatomic and biochemical sites of action. After either biliary diversion or cholestyramine feeding, there is a marked enhancement of cholesterogenesis at every level of the small intestine; this effect is specific for sterol synthesis since acetate incorporation into fatty acids and CO(2) is unaffected by these experimental manipulations. In the present investigation bile salt has been shown to be the constituent of whole bile responsible for the inhibited rate of sterol synthesis found in the intact animal, and in addition, an inverse relationship has been shown to exist between the steady-state intraluminal bile salt concentration and the rate of cholesterogenesis in the adjacent bowel wall. The inhibitory effect of bile salt is directed at the cells of the intestinal crypt, the major anatomic site for sterol synthesis in the small bowel. This feedback inhibition has been localized in the biosynthetic sequence to a step between acetyl CoA and mevalonic acid and, presumably, is at the enzymatic step mediated by hydroxymethylglutaryl reductase. These studies emphasize the close interrelationship which exists between the mechanisms of control of cholesterogenesis in the liver and small intestine. Sterol synthesis in the liver is regulated by exogenous cholesterol intake, whereas the rate of intestinal sterol synthesis is controlled by bile salt, the major end product of the hepatic catabolism of cholesterol.

Acetates↗

PubMed1969

Very low density lipoproteins in intestinal lymph: origin, composition, and role in lipid transport in the fasting state.

The transport of endogenous lipids in the lipoproteins of mesenteric lymph was studied in fasting rats with mesenteric lymph fistulas. The lymph was found to contain, in addition to chylomicrons (S(f) >400), a significant amount of another, more dense, triglyceride-rich fraction, the very low density lipoproteins (VLDL), which showed a peak S(f) of 102. The VLDL differed from chylomicrons not only in flotation, but also in per cent lipid composition and electrophoretic mobility in agarose gel. The VLDL fraction was found to contain 47% of the triglyceride and 54% of the cholesterol of fasting lymph and, in the fasting state, was the major lipoprotein species present. When cholestyramine resin was administered intraduodenally, or bile flow was acutely diverted from the intestine, it was demonstrated that the lipids in lymph VLDL, like those in chylomicrons, were derived from the intestine and bile. These data indicate that the VLDL in intestinal lymph are not derived from the plasma but are of intestinal origin. Because certain properties of lymph VLDL were similar to those reported for plasma VLDL (per cent lipid composition, flotation coefficient, and continuing entry into plasma in the fasting state), additional comparisons between these fractions were made. Although lymph VLDL moved to the alpha(2) region in agarose gel, when they were mixed with VLDL-free serum immediately before electrophoresis they showed the alpha(2) mobility of rat serum VLDL. Furthermore, immunoelectrophoretic comparison of partially delipidated lymph and serum VLDL revealed that these fractions shared in common their major apoprotein, and possibly others as well. The fatty acid composition of lymph and serum triglycerides, as determined by gas-liquid chromatography, revealed that although they were generally similar, differences existed which most likely reflected the presence in serum of triglycerides of hepatic origin. These experiments demonstrate the importance of intestinal VLDL in the transport of endogenous lipids in mesenteric lymph in the fasting state. The similarities between intestinal lymph VLDL and plasma VLDL suggest that the latter may be derived in part from the former.

Animals↗

PubMed1973

Estimation of cholesterol and bile acid turnover in man by kinetic analysis.

The kinetics of cholesterol and bile acid turnover were determined from an analysis of the biliary lipids after a single intravenous injection of labeled cholesterol. A compartmental model was designed for the system, and the fractional metabolic rates and fluxes were determined in one lean and two obese normal humans. Each of the normals converted about 3% per day of their rapidly miscible cholesterol pool to cholic acid and 1% per day or less to chenodeoxycholate. Cholate was catabolized at about twice the rate of the dihydroxy bile acids in these normals. Two of the normals were fed corn oil with little change in their kinetic parameters from the control state. The other normal received cholestyramine and dramatically increased the bile acid flux with little change in neutral sterol catabolism. A cirrhotic patient was also studied by this technique and noted to have kinetic parameters quite different from the normals.

Adult↗

PubMed1975

The urinary concentrating defect in the Gunn strain of rat. Role of bilirubin.

The role of high serum and tissue levels of unconjegated bilirubin in the pathogenesis of the impaired urinary concentrating ability was investigated in homozygous (jj) Gunn rats with the congenital absence of hepatic glucuronyl transferase. Continuous phototherapy with blue fluorescent lights at a wave length of 460 nm or oral cholestyramine feeding or both reduced serum levels of unconjugated hilirubin to levels consistently below 3.0 mg/100 ml for several weeks in both weanling and adult jj Gunn rats. The renal concentrating defect was already present in weanling jj Gunn rats by 21 days of age. In treated weanling jj animals, maximum concentrating ability and the concentration of urea and nonurea solutes in the papilla and medulla, determined after 24 h of fluid deprivation, were normal when compared to unaffected heterozygous (Jj) littermates. Solute-free water reabsorption which is reduced in jaundiced jj Gunn rats was restored to normal in treated weanling jj rats. The tissue concentration of unconjugated bilirubin was reduced throughout the papilla and inner and outer medulla in the treated jj rats in comparison with untreated jj littermates. The defect in urinary concentrating ability was only partially reversible and sometimes irreversible in adult jj rats, probably because of permanent renal parenchymal damage occurring secondary to massive crystalline deposits in the papilla and medulla. It is concluded that unconjugated bilirubin is directly involved in the pathogenesis of the concentrating defect in jaundiced jj Gunn rats.

Animals↗

PubMed1983

Effect of dietary fat on sympathetic nervous system activity in the rat.

Previous studies from our laboratory have demonstrated that dietary intake affects the sympathetic nervous system (SNS); carbohydrate intake, in particular, has been shown to stimulate sympathetic activity. The present studies were undertaken to characterize the effect of dietary fat on SNS activity in the rat. Sympathetic activity was assessed by measurement of norepinephrine (NE) turnover in heart, interscapular brown adipose tissue (IBAT), and pancreas and by excretion of NE in the urine. When fed a fat-enriched diet (50% chow, 50% lard), fractional NE turnover in heart (k) increased from 6.3 +/- 0.6% h in ad lib. fed controls to 14.7 +/- 1.3% h in the high-fat group (P less than 0.001); calculated NE turnover rate increased from 24.5 +/- 2.4 ng/heart per h to 36.8 +/- 3.5 (P less than 0.05). Urinary NE excretion more than doubled after 6 d of the same high fat diet (P less than 0.001). Ganglionic blockade produced a greater effect on NE turnover in fat-fed, as compared with chow-fed animals, consistent with increased sympathetic activity in the fat-fed group. When fat absorption was blocked with a bile acid binding resin (cholestyramine), the same high-fat diet did not increase cardiac NE turnover, indicating that fat absorption is required for the stimulatory effect on sympathetic activity. In another series of experiments, in which chow (and hence protein) intake was held constant, the effect of fat and isocaloric sucrose supplements on NE turnover was assessed in heart, IBAT, and pancreas. The caloric value of the supplements was 50, 100, and 335% of the chow in the different experiments. An effect of fat on NE turnover in heart and IBAT was demonstrable at the lowest level of fat supplement. Fat increased pancreatic NE turnover when added in amounts sufficient to double the caloric intake. The stimulatory effect of sucrose and fat on NE turnover in heart and IBAT was similar. These experiments demonstrate that fat increases SNS activity in the rat and that the magnitude of the effect is similar to that of sucrose. The results imply that fat may contribute to dietary thermogenesis in this species.

Adipose Tissue, Brown↗

PubMed1982

The mechanism of action of lipid-lowering drugs.

In conclusion, many drugs have been used as lipid lowering agents. Only five currently combine efficacy and acceptable side effects. None of these, nicotinic acid, clofibrate, probucol, cholestyramine or colestipol, is without serious drawbacks. In using lipid lowering drugs, it is important to bear in mind the following. First, no patient should be committed to an indefinite period of drug therapy without an adequate trial of diet therapy. For overweight patients, caloric restriction and weight reduction should always be therapeutic goals. Second, as our understanding of lipoprotein metabolism increases, evaluation of new drugs must include not only their effects on triglyceride but also on lipoprotein and apoprotein levels. Third, our drug armamentarium is currently quite limited and there is a pressing need for the development of new, safe and effective hypolipidemic agents.

Cholestyramine Resin↗

PubMed1993

Blind comparison of patient preference for Flavored Colestid Granules and Questran Light.

OBJECTIVE: To compare the sensory and mixability characteristics of Flavored Colestid Granules (a new colestipol formulation) with Questran Light (the most recent cholestyramine formulation). METHODOLOGY: Seventy-two nonsmoking adults between the ages of 25 and 64 years were enrolled in the study. Subjects assessed the sensory and mixability characteristics of each product in chilled bottled water and orange juice after at least a one-hour fast. Products were administered in a double-blind, randomized fashion. The sensory characteristics that were rated included overall rating, aftertaste, appearance, aroma, color, consistency, flavor, sweetness, mouthfeel, and thickness. Each characteristic was rated with a nine-point hedonic scale. Mixability of the products was assessed on a five-point scale. Subjects also were asked to choose which product they preferred as to sensory and mixability characteristics in each vehicle. RESULTS: Fifty-three of the 72 subjects preferred the sensory characteristics of Flavored Colestid Granules in water (p < 0.001). Questran Light was preferred by 61 subjects when mixed in orange juice (p < 0.001). The sensory characteristic rating scores also supported subject preferences for Flavored Colestid Granules in water and Questran Light in orange juice. Mixability of Flavored Colestid Granules was rated significantly better (p < 0.001) than Questran Light in water. There was no significant difference for mixability between the products in orange juice. CONCLUSIONS: Questran Light was significantly preferred on a sensory basis when mixed in orange juice. Flavored Colestid Granules was significantly preferred over Questran Light for both sensory and mixability characteristics with water as the vehicle.

Adult↗

PubMed2005

Niemann-Pick C1 expression is not regulated by the amount of cholesterol flowing through cells in the mouse.

The Niemann-Pick C1 (NPC1) protein functions to regulate the transport of cholesterol from late endosomes/lysosomes to other cellular compartments after lipoprotein uptake through the coated-pit pathway. The present study examines the relative expression of NPC1 mRNA and NPC1 protein in different tissues of the mouse in relation to the uptake of total cholesterol carried in chylomicron remnants (CMr-TC), low density lipoproteins (LDL-TC), cholesteryl ester carried in high density lipoproteins (HDL-CE), and cholesterol synthesis. Results from this study demonstrate that the highest relative expression of NPC1 is in the liver, which is also the tissue with the highest uptake of CMr-TC, LDL-TC, HDL-CE, and cholesterol synthesis. However, there was no similar relation in the remaining tissues. To examine the relative expression of NPC1 in relation to the amount of cholesterol that flowed through the coated-pit pathway, mice were fed a diet supplemented with increasing amounts of cholesterol or cholestyramine. The results from this study demonstrated that there was no relation between the relative expression of NPC1 and the amount of cholesterol that flowed through the coated-pit pathway. We conclude that the relative expression of NPC1 is not regulated by the flow of cholesterol through cells in the mouse and is therefore constitutive.

Animals↗

PubMed1977

Influence of intravenous nutrients on bilirubin transport. II. Emulsified lipid solutions.

The effects of an emulsified intravenous fat preparation (Intralipid) on bilirubin transport were analyzed by cholestyramine extraction, spectrophotometric analysis, Sephadex gel filtration, peroxidase assay, bilirubin uptake by red blood cells, and by toxicity in tissue culture (L-929) cells. Intralipid is capable of binding bilirubin, but does not compete effectively with bilirubin bound to high affinity sites on albumin. The emulsified fat appears to have a higher affinity for bilirubin than for cell membranes. Red blood cells become coated with Intralipid, resulting in an increased association of bilirubin with the cell surface, but a decrease in pigment actually incorporated into the red cell membrane. In tissue culture experiments, Intralipid protected the cells from bilirubin toxicity. It is concluded that Intralipid may enhance the carrying capacity of serum for bilirubin, and thus exert a protective effect on tissues.

Albumins↗

PubMed2002

Regulation of hepatic low-density lipoprotein receptor, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and cholesterol 7alpha-hydroxylase mRNAs in human liver.

To characterize the coordinate regulation of cholesterol metabolism in human liver, we simultaneously quantified mRNA levels of cholesterol 7alpha-hydroxylase (CYP7A1), 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR), and low- density lipoprotein receptors (LDLRs) in liver biopsies from 76 patients undergoing cholecystectomy. The three transcript levels were not different between untreated gallstone and gallstone-free patients and not significantly altered by 10-d exclusion of dietary cholesterol. Treatment with chenodeoxycholic acid suppressed CYP7A1 and to a lesser extent HMGR mRNA levels. Cholestyramine treatment increased CYP7A1, but also HMGR and LDLR mRNA, and statins only increased HMGR mRNA. Resin + statin treatment increased all mRNA species. In untreated patients, the mRNA levels of HMGR and LDLR were more strongly correlated (r = +0.60) than those of CYP7A1 and HMGR (r = +0.49) or CYP7A1 and LDLR (r = +0.21). In the treated patients, in whom bile acid synthesis was suppressed or stimulated, mRNA levels of CYP7A1 and HMGR (r = +0.84) as well as CYP7A1 and LDLR (r = +0.62) were more strongly correlated than those of HMGR and LDLR (r = +0.59). The coordinate control of HMGR and LDLR mRNA levels reflects their common regulation by shared transcriptional activation. In contrast, following changes in bile acid flux through the liver, CYP7A1 gene expression becomes a strong modulator of hepatic cholesterol metabolism.

Adult↗

PubMed1985

Role of gastric acid and bile acids in the pathogenesis of compound 48/80-induced gastric lesions in rats.

We studied the effects of various agents, which influence gastric acidity and bile acids, on compound 48/80 (48/80)-induced gastric lesions in rats. 48/80-Induced gastric lesions were produced by repeated intraperitoneal administration of 48/80 at 0.75 mg/kg once daily for 4 days. Test agents were given orally twice daily (30 min before and 9 hr after 48/80 administration) for 4 days. AI(OH)3 and sucralfate at 2000 mg/kg/day, a weak antacid dose, significantly inhibited (about 50-60%) the development of 48/80-induced lesions. Propantheline at 60 mg/kg/day and omeprazole at 60 or 200 mg/kg/day, which reduced gastric secretion for more than 12 hr, also significantly inhibited (about 30-40%) these lesions. Cimetidine at 200 mg/kg/day, which reduced gastric secretion for only 5 hr, had little effect on the lesion formation. Cholestyramine, which is a potent bile acids binding agent, had no effect on 48/80-induced lesions in doses of 600 or 2000 mg/kg/day. These results suggest that gastric acid, but not bile acids, is partly involved in the pathogenesis of 48/80-induced gastric lesions.

Animals↗

PubMedDate not supplied

Metabolism of meso-2,3-dimercaptosuccinic acid in lead-poisoned children and normal adults.

Meso-2,3-dimercaptosuccinic acid (DMSA, or succimer) is an oral chelating agent for heavy-metal poisoning. While studying the urinary elimination of unaltered DMSA, altered DMSA (i.e., its mixed disulfides), and lead in children with lead poisoning, we observed a pattern of urinary drug elimination after meals suggestive of enterohepatic circulation. The excretion of lead in urine patterned the elimination of altered DMSA rather than the parent molecule. In addition, the half-life of elimination of DMSA via the kidney was positively associated with blood lead concentration. Two additional crossover studies of DMSA kinetics were conducted in normal adults to confirm the presence of enterohepatic circulation of DMSA after meals. In one, increases in plasma total DMSA concentration were observed after meals in all six subjects; these increases were prevented by cholestyramine administration 4, 8, and 12 hr after DMSA. In the second, the administration of neomycin also prevented increases in DMSA after meals. These studies indicate that 1) a metabolite(s) of DMSA undergoes enterohepatic circulation and that microflora are required for DMSA reentry; 2) in children, moderate lead exposure impairs renal tubular drug elimination; and 3) a metabolite of DMSA appears to be an active chelator.

Adult↗

PubMedDate not supplied

In vivo and in vitro studies on the regulatory link between 3-hydroxy-3-methylglutaryl coenzyme A reductase and cholesterol 7 alpha-hydroxylase in rat liver.

The activities of 3-hydroxy-3-methylglutaryl CoA reductase (HMGCoA reductase; EC 1.1.1.34), rate-limiting enzyme of cholesterol biosynthesis, and cholesterol 7 alpha-hydroxylase (EC 1.14.13.17), key enzyme of the neutral bile acid synthesis pathway, were measured in the microsomal fraction of rat liver and in rat liver cells to investigate the coordinate regulation of the two pathways. Both enzyme activities exhibited the same diurnal rhythm and responded in a coordinate fashion to fasting or bile acid-feeding (decrease) and to cholestyramine-feeding (increase). Cholesterol-feeding decreased the activity of HMGCoA reductase, increased that of cholesterol 7 alpha-hydroxylase, and concomitantly increased free cholesterol in microsomes. In an ex vivo setting using primary hepatocytes from animals fed a high cholesterol diet the activity of HMGCoA reductase was initially low and that of cholesterol 7 alpha-hydroxylase was elevated. Release of cholesterol into the medium with ongoing incubation caused HMGCoA reductase activity to increase, and that of cholesterol 7 alpha-hydroxylase to decline. Incubation of hepatocytes with a cholesterol-containing lipoprotein fraction stimulated the activity of cholesterol 7 alpha-hydroxylase, but left HMGCoA reductase activity unaffected. The results confirm the idea of a joint regulation of the two key enzymes of cholesterol metabolism in response to the levels of substrate and metabolites, and support the notion that with respect to bile acid and cholesterol levels, respectively, regulation of HMGCoA reductase activity may be secondary to that of cholesterol 7 alpha-hydroxylase. The in vitro studies supply evidence that the effects of cholesterol and bile acid excess or deficiency are direct and do not involve accessory changes of hormone levels or mediators.

Animals↗

PubMed1999

Effects of superoxide dismutase on the acetylcholine-induced relaxation response in cholesterol-fed and streptozotocin-induced diabetic mice.

High concentration of acetylcholine (ACh) caused a rapid and long lasting relaxation response in age-matched controls, whereas this response was significantly weaker in streptozotocin (STZ)-diabetic and cholesterol fed mice. The levels of basal and ACh-stimulated cyclic GMP in the aorta was also significantly smaller in STZ-diabetic and cholesterol-fed mice. The attenuated relaxation responses to ACh in both STZ-diabetic and cholesterol-fed mice were ameliorated by the chronic administration of cholestyramine. A prior incubation of aortic strips with superoxide dismutase (SOD, 60 U/ml) improved the recovery phase of the relaxation of diabetic aorta after single administration of ACh, whereas SOD had no effects on ACh-induced relaxation of aortic strips from cholesterol fed mice. These results suggest that superoxide anion may be responsible for an impairment of endothelium-dependent relaxation of aorta from STZ induced diabetic mice. It is further suggested that impairment of endothelium-dependent relaxation in STZ-diabetic and cholesterol fed mice may be caused by different mechanisms.

Acetylcholine↗

PubMedDate not supplied

A comparative review of the adverse effects of treatments for hyperlipidaemia.

Various lipid-lowering drugs have been shown to reduce serum cholesterol and serum triglycerides effectively. In view of trials indicating that lipid-lowering drugs may reduce cardiac morbidity and mortality but not the overall mortality in the study group, increased attention must be focused on potential harmful side effects during treatment with these agents. The adverse effects of many of the principal drugs in this category are discussed. Gastrointestinal symptoms, usually self-limited and reversible, are the most common side effects. Potential harmful adverse effects include drug interactions (cholestyramine), myopathy and hepatic injury (HMG-CoA reductase inhibitors), and increased gallstone formation and ventricular arrhythmias (clofibrate). Not all lipid-lowering drugs have been studied adequately on a long term basis, so that medications given for an indefinite period must be reevaluated frequently. However, there are several agents that lower serum lipid levels effectively and that have been used for more than 20 years without serious side effects.

Cholestyramine Resin↗