Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Colestipol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources
PubMed1988

Regulation of biliary cholesterol secretion. Functional relationship between the canalicular and sinusoidal cholesterol secretory pathways in the rat.

The functional interrelationship between biliary cholesterol secretion, sinusoidal lipoprotein cholesterol secretion and bile salt synthesis was studied in the rat. Diosgenin, fructose, and colestipol in the diet were used to, respectively, influence biliary cholesterol output, VLDL production and bile salt synthesis. In the acute bile fistula rat, biliary cholesterol output was 700% increased by diosgenin and 50% decreased by fructose. In the rats fed both diosgenin and fructose, biliary cholesterol secretion was increased only by approximately 200%, whereas biliary bile salts and phospholipid outputs were unchanged. In the isolated perfused liver, VLDL-cholesterol output was 50% reduced by diosgenin alone, but was unchanged following feeding of diosgenin plus fructose. However, the livers of rats fed diosgenin plus fructose exhibited a 700% increase in VLDL-triglyceride production and a 200% increase in VLDL-cholesterol output. A significant reciprocal relationship between VLDL-cholesterol secretion and the coupling ratio of cholesterol to bile salts in bile was observed. Colestipol added to the diet maintained both sinusoidal and biliary cholesterol outputs within the normal range. In the chronic bile fistula rat, colestipol increased bile salt synthesis by 100% while diosgenin and fructose diets had no effect. Similarly, the addition of fructose to the colestipol diet did not decrease bile salt synthesis. These data suggest a reciprocal relationship between biliary cholesterol secretion and hepatic secretion of cholesterol as VLDL particles. The free cholesterol pool used for bile salt synthesis seems functionally unrelated to the pool from which VLDL-cholesterol and biliary cholesterol originate. These findings support the idea that metabolic compartmentalization of hepatic cholesterol is a major determinant of the quantity of cholesterol available for recruitment by the bile salt-dependent biliary cholesterol secretory mechanism.

Animals↗
PubMed2002

A randomized crossover trial of combination pharmacologic therapy in children with familial hyperlipidemia.

We sought to determine whether a low-dose combination of a bile acid-binding resin (colestipol) with an hydroxymethylglutaryl CoA reductase inhibitor (pravastatin) would result in improved acceptability, compliance, and effectiveness in lipid-lowering compared with conventional therapy with a higher dose of a bile acid-binding resin only, with fewer side effects. We performed a randomized, crossover open-label clinical trial with two 18-wk medication regimens separated by an 8-wk washout period in 36 children and adolescents with familial hypercholesterolemia or familial combined hyperlipidemia. The regimens included colestipol 10 g/d (10 pills) versus a combination of colestipol 5 g/d with pravastatin 10 mg/d (six pills). All patients were maintained on a fat-reduced diet. Acceptability was better with the combination regimen. Mean compliance was similar and suboptimal (approximately 60%) with all medication components. Mean relative LDL cholesterol lowering was significantly better with the combination regimen (-17 +/- 16% versus -10 +/- 13%; p = 0.045), although insufficient to achieve recommended target values in the majority of patients on either regimen. Both regimens were equally free of adverse effects, with no important effect on chemistry or hematologic values. Patient-reported adverse effects were more common with the conventional-dose colestipol-only regimen. Compliance with medication regimens using the bile acid-binding resins is suboptimal, although combination with a low dose of a statin may result in better lipid lowering.

Adolescent↗
PubMed1985

Weight loss improves lipoprotein lipid profiles in patients with hypercholesterolemia.

Risk for coronary artery disease is directly related to plasma levels of total and low-density lipoprotein (LDL) cholesterol and inversely related to high-density lipoprotein (HDL) cholesterol concentrations. Weight gain in four of five patients with hypercholesterolemia given colestipol for 37 +/- 6 months was associated with a decrease in HDL cholesterol levels and an increase in LDL cholesterol/HDL cholesterol ratios. Weight loss (-7 +/- 2 kg) in these five and two other patients given colestipol increased plasma HDL cholesterol (17% +/- 6%) and lowered total cholesterol (-8% +/- 1%), LDL cholesterol (-13% +/- 2%), and total triglyceride (-20% +/- 4%) concentrations. However, in six patients given treatment by diet alone (no colestipol), comparable weight loss (-6 +/- 1 kg) did not alter plasma HDL cholesterol or total triglyceride concentrations, but reduced total cholesterol (-9% +/- 3%) and LDL cholesterol (-11% +/- 3%) levels. These results suggest that weight reduction increases plasma HDL cholesterol levels only in those patients with hypercholesterolemia given colestipol but not in those given treatment by diet alone. Nevertheless, the effects of weight loss on plasma total cholesterol and LDL cholesterol levels were comparable in the two groups of patients. This indicates that weight loss is an important adjunct in the treatment of moderately obese patients with hypercholesterolemia and may reduce their risk for coronary artery disease by improving their lipid profiles.

Adult↗
PubMed1984

Electrocardiographic effects of probucol. A controlled prospective clinical trial.

Probucol is known to prolong QT intervals in some patients and to produce fatal arrhythmias in selected animal species. To assess the prevalence and clinical relevance of this effect in a controlled manner, we analyzed electrocardiograms (ECGs) and medical events in patients during a placebo-controlled crossover trial comparing single or combined administration of probucol and colestipol. Forty-two Type II hyperlipoproteinemic patients were studied for eighteen to twenty-four months. Two cardiologists independently read the tracings which were previously arranged randomly without names or dates. There were no statistical differences between the reports of the ECG parameters by the two cardiologists. The mean QTc interval of the entire patient population was lengthened after probucol administration without reaching statistical significance when compared to placebos or colestipol treatments. Forty-eight % of the patients showed lengthening of the QTc interval during probucol treatment by 11 to 70 msec increment over baseline placebo. The remaining had either no change or shortening of the interval. There were no statistically significant differences in means of R-R, PR, QRS, QTc or QoT intervals among placebo, probucol., colestipol and probucol plus colestipol treatments. It is concluded that probucol prolonged QT intervals in the electrocardiograms of about one half of patients receiving the drug with no other clinical or statistically significant evidence of cardiotoxicity or electrocardiographic effects.

Adult↗
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↗
PubMed1994

Effect of bile salt binding or protease inactivation on plasma cholecystokinin and gallbladder responses to bombesin.

BACKGROUND/AIMS: Bombesin-stimulated plasma cholecystokinin levels decrease after an initial increase despite continuous infusion of bombesin. The aim of this study was to determine if a feedback mechanism, mediated by bile salts or proteolytic enzymes, is responsible for this decline. METHODS: Bombesin (1.0 ng.kg-1.min-1) was infused into volunteers for 180 minutes on separate occasions. Cholestyramine, colestipol, camostate, or saline were perfused intraduodenally during the second hour of the tests. Cholestyramine was also administered without infusion of bombesin. RESULTS: Colestipol and cholestyramine, dependent on their bile salt-binding capacity, markedly enhanced (P < 0.05) bombesin-stimulated plasma cholecystokinin from 2.1 +/- 0.5 pmol/L to 6.4 +/- 2.2 pmol/L and 12.1 +/- 3.3 pmol/L (P < 0.05 vs. colestipol), respectively, and further decreased gallbladder volume (P < 0.05) from 9.4 +/- 1.6 mL to 2.0 +/- 0.4 mL and 2.2 +/- 0.5 mL, respectively. The protease inhibitor camostate had no effect. Bile salt precipitation also enhanced plasma pancreatic polypeptide responses (P < 0.01) but did not alter gastrin responses. Plasma cholecystokinin responses to cholestyramine without bombesin infusion varied considerably, but increments were highly correlated to decreases in gallbladder volume (r = 0.91; P < 0.005). CONCLUSIONS: Bile salt sequestration but not protease inactivation enhances plasma cholecystokinin and gallbladder responses to bombesin infusion in humans.

Adult↗
PubMed1990

Long-term maintenance of therapeutic response to lovastatin in patients with familial and non-familial hypercholesterolemia: a 3-year follow-up.

The 3-year efficacy of lovastatin alone or in combination with colestipol was evaluated in 54 patients with type 2 hyperlipoproteinemia (22 non-familial and 32 familial hypercholesterolemic patients). A sufficient and sustained reduction in LDL cholesterol was achieved in non-familial hypercholesterolemia with lovastatin alone (average dose 74 mg/day, range 40-80 mg/d), whereas combination therapy with lovastatin 80 mg/d and colestipol (average dose 11.9 g/d, range 5-20 g/d) was required in familial hypercholesterolemia. The percentage changes from baseline at 3 years in serum LDL cholesterol, HDL cholesterol and total triglycerides were in the lovastatin-only group -53%, +10% and -15%, respectively, and in the two-drug group -58%, +22% and -18%, respectively. A subgroup analysis in patients with non-familial hypercholesterolemia indicated that the lipid-modifying effects of lovastatin were similar in type 2A and 2B phenotypes, except for a greater triglyceride lowering effect in type 2B. The lovastatin-alone regimen was well tolerated, whereas addition of colestipol caused subjective side effects in many patients. Serious side effects or discontinuations due to therapies did not occur. Both therapies caused slight but significant increases (within normal limits) in average serum transaminase levels. After 36 months a significant rise of 1.7 kg in mean body weight was observed in the lovastatin-only group. The ophthalmological follow-up did not reveal any cataractogenic effect attributable to treatment during the 3.8-year follow-up period.

Adult↗
PubMed1992

Growth during treatment of familial hypercholesterolemia.

Treatment of hypercholesterolemic children with restriction of dietary saturated fat may result in an inadequate supply of energy for normal somatic growth. We examined the growth of 30 children with familial hypercholesterolemia, some of whom were also treated with colestipol, a bile acid-binding resin. The median duration of treatment was 8.5 years in 13 patients on diet only, and 5.5 years + 3.5 years in 17 patients treated with diet followed by diet and colestipol. Statistically significant reductions in serum total cholesterol were obtained in both groups. The SD scores for both height/age and weight/age decreased by approximately 0.4 during dietary treatment (p < 0.05), but were not affected by treatment with colestipol. These results document the risk of growth retardation during dietary treatment of children with familial hypercholesterolemia.

Child↗
PubMed1985

Activation of rat liver microsomal 3-hydroxy-3-methylglutaryl coenzyme A reductase by NADPH. Effects of dietary treatments.

The sigmoidal curves observed for rat liver microsomal 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase with NADPH as the varied substrate were markedly affected by feeding the animals diets containing colestipol, mevinolin and colestipol or cholesterol. Feeding of mevinolin and colestipol decreased the S0.5 for NADPH from 270 to 40 microM, while cholesterol feeding increased the value to 1.3 mM. Immuno-blotting analysis revealed that the Mr 100,000 form of HMG-CoA reductase predominated in cases where the S0.5 value was lowest, and the Mr 200,000 species was the major form where the S0.5 values were highest. Activation of HMG-CoA reductase by NADPH was not due to conversion of the Mr 200,000 form to the 100,000 form.

Allosteric Regulation↗
PubMed1980

Therapeutic trials of antibiotic associated colitis.

Since September 1977 we have seen 63 patients with Clostridium difficile and a faecal toxin, but only 33 had histological evidence of pseudomembranous colitis. We have conducted separate double blind trials of an antibiotic, vancomycin and an anion-exchange resin, colestipol, in patients with post-operative diarrhoea. Vancomycin was extremely effective at eradicating the organism and its faecal toxin. These changes were associated with a marked symptomatic improvement. Colestipol proved ineffective in absorbing the faecal toxin and caused no change in numbers of Clostridial difficile. There was no associated symptomatic response. Neither drug had any effect on diarrhoea not related to Clostridium difficile. A carrier state was created by those patients who continued to excrete the organism after Colestipol or placebo treatment. This was eradicated by subsequent treatment with vancomycin. Our brief experience with metronidazole is discussed and a rational basis for treatment advocated.

Anti-Bacterial Agents↗
PubMed1982

[Behavior of high-density lipoproteins in drug lipid-lowering treatment].

Changes in serum lipids, the individual lipoprotein fractions after ultracentrifugation and the apoproteins B, A1 and A2 were studied in 66 patients with primary hypercholesterolemia under treatment with different lipid-lowering agents. After 3 months with dietary treatment alone and a 4-week placebo period the patients were given bezafibrate (3 X 200 mg daily), colestipol (2 X 10 g per day) or probucol (2 X 500 mg daily) for 12 months, followed by another 4-week placebo period at the end of the study. Colestipol showed the best lipid-lowering effect (total and LDL cholesterol were decreased by 20% and 23% respectively) but satisfactory total and LDL cholesterol lowering results were also obtained with the other substances. However, the changes in HDL differed widely among the three substances: bezafibrate increased HDL cholesterol and the HDL apoproteins A1 and A2 significantly, colestipol did not alter these parameters, while probucol treatment was followed by a significant decrease in both HDL-cholesterol and the apoproteins A1 and A2.

Adult↗
PubMed1998

Use of niacin, statins, and resins in patients with combined hyperlipidemia.

Patients in the original Familial Atherosclerosis Treatment Study (FATS) cohort were subgrouped into those with triglyceride levels < or = 120 mg/dL (n = 26) and those with triglyceride levels > or = 190 mg/dL (n = 40). Their therapeutic responses to niacin plus colestipol, lovastatin plus colestipol, colestipol alone, or placebo were determined. Therapeutic response was also determined in the same 2 triglyceride subgroups (n = 12 and n = 27, respectively) of patients selected for low levels of high-density lipoprotein (HDL) cholesterol and coronary artery disease. These triglyceride criteria were chosen to identify patient subgroups with high likelihood of "pattern A" (normal-size low-density lipoprotein [LDL] particles and triglyceride < or = 120 mg/dL) or "pattern B" (small dense LDL and triglyceride > or = 190 mg/dL). Our findings in these small patient subgroups are consistent with the emerging understanding that coronary artery disease patients presenting with high triglyceride levels have lower HDL-C, smaller less buoyant LDL-C, and greater very low-density lipoprotein (VLDL) cholesterol and VLDL apolipoprotein B, and are more responsive to therapy as assessed by an increase in HDL-C and reduction in triglycerides, VLDL-C, and VLDL apolipoprotein B. In the FATS high-triglyceride subgroup with these characteristics, a tendency toward greater therapeutic improvement in coronary stenosis severity was observed among those treated with either of the 2 forms of intensive cholesterol-lowering therapy. This improvement is associated with therapeutic reduction of LDL-C and elevation of HDL-C, but also appears to be associated with drug-induced improvement in LDL buoyancy.

Anticholesteremic Agents↗
PubMed1977

Conjugated dihydroxy bile salt inhibition of glucose influx in rat jejunum in vitro.

Effects of bile salts on intestinal transfer differ in diverse animal preparations exposed to various bile acids. Radiolabeled glucose influx into rat jejunum in vitro was studied in buffer and compared to taurodeoxycholate, taurochenodeoxycholate, taurocholate, and deoxycholate. Jejunum was obtained from intact, bile-diverted, and colestipol-treated rats and in similar categories after abdominal x-irradiation. Taurodeoxycholate but not taurocholate inhibited glucose influx only in bile-fistula and colestipol-treated rats. Bile diversion increased and colestipol decreased glucose uptake from buffer. Added inhibitory effects of irradiation and bile salts were seen in bile-fistula animals. These data suggest that normal exposure to bile is chronically inhibiting jejunal glucose transport and that dihydroxy bile salts are responsible for this effect. They do not provide an explanation for the role of bile in the intestinal radiation syndrome.

Abdomen↗
PubMed1989

New horizons in combination drug therapy for hypercholesterolemia.

A modest number of hypolipidemic drugs are currently available, and their use as single agents frequently fails to adequately control patients with severe hypercholesterolemia. Combined-drug regimens afford the opportunity to maximize the cholesterol-lowering effects of drugs that have different mechanisms of action and, at the same time, minimize potential side effects. The bile acid sequestrants (cholestyramine and colestipol) enhance fecal sterol excretion and are nonsystemically acting; they have provided the cornerstone for the majority of the established combined-drug regimens. The most effective regimens have used bile acid sequestrants in combination with nicotinic acid, or more recently, lovastatin or simvastatin. Combinations in which fenofibrate, bezafibrate, or probucol have been used with cholestyramine or colestipol have also been shown to be useful although the low-density-lipoprotein-lowering effect of probucol appears quite variable. The use of low doses of bile acid sequestrants (4-8 g/day of cholestyramine or 5-10 g/day of colestipol) in combination with lovastatin, simvastatin, or probucol provides a therapeutic regimen that is usually well tolerated, shows additive lipid lowering, and is cost effective.

Anticholesteremic Agents↗
PubMed1995

Effects of lowering elevated LDL cholesterol on the cardiovascular risk of lipoprotein(a).

OBJECTIVE: To determine if lowering elevated low-density lipoprotein cholesterol (LDL-C) levels offsets the adverse effect of raised lipoprotein(a) (Lp[a]) levels on coronary artery disease (CAC) in men. DESIGN: Randomized, double-blind, placebo-controlled trial of lipid lowering for CAD. SETTING: Post hoc analysis of the Familial Atherosclerosis Treatment Study. PARTICIPANTS: A total of 146 men aged 62 years or younger with CAD and apolipoprotein B levels of at least 125 mg/dL. INTERVENTION: Patients received a Step II Diet and lovastatin (40 mg daily) plus colestipol (30 g daily), niacin (4 g daily) plus colestipol, or placebo (plus colestipol if LDL-C > 90th percentile) for 2.5 years. They were grouped by their LDL-C responses: "minimal" if LDL-C decreased by 10% or less from baseline (mean [SD] change, +6% [13%]) and "substantial" if LDL-C decreased more than 10% (mean [SD] change, -40% [16%]). MAIN OUTCOME MEASURE: Impact of lowering elevated LDL-C on the cardiac event rate (death, myocardial infarction, and revascularization for refractory ischemia) and CAD change associated with elevated Lp(a). RESULTS: In multivariate analyses, the best correlate of baseline CAD severity was Lp(a) (r = 0.30; P < .001). For 36 patients with minimal LDL-C reduction, CAD progression correlated only with in-treatment Lp(a) levels (r = 0.45; P < .01), but for 84 patients with substantial LDL-C reduction, disease regressed and its change correlated with in-treatment LDL-C (r = 0.24; P < .05) but not with Lp(a) (r = -0.05). Lipoprotein(a) levels were not significantly altered in either group. For 40 patients with Lp(a) at the 90th percentile or higher, events were frequent (39%) if reduction of LDL-C was minimal, but were few (9%) if reduction was substantial (relative risk, 0.23; 95% confidence interval, 0.06 to 0.99). CONCLUSIONS: In men with CAD and elevated LDL-C, Lp(a) levels were dominant correlates of baseline disease severity, its progression, and event rate over 2.5 years. However, with substantial LDL-C reductions, persistent elevations of Lp(a) were no longer atherogenic or clinically threatening. This provides a possible direction for treatment in such patients with elevated Lp(a) and LDL-C.

Adult↗
PubMed1978

Abnormal low density lipoproteins in children with familial hypercholesterolemia--effect of polyanion exchange resins.

In 20 children and adolescents with familial Type II a hyperlipoproteinemia, serum lipids and lipoproteins were examined before and during treatment with polyanion exchange resins. The composition of LDL was compared to that of helthy siblings. The patients were given Colestyramine (0.6 g/kg body weight) and Colestipol (0.5 g/kg body weight) in a cross-over study for 8 weeks each, after they had been under dietary treatment for at least 12 months. In 6 children, drug treatment had to be stopped due to side-effects. The most common complaints were gastrointestinal discomfort and constipation. Cholesterol, triglycerides and phopholipids were measured in whole serum and cholesterol, triglycerides and Apolipoprotein-B in isolated lipoprotein fractions after ultracentrifugation. Apo-B was determined by radial immunodiffusion. The Apo-B: cholesterol ratio in whole serum and in the LDL fraction was identical in the patients and in the controls. The LDL triglyceride: Apo-B ratio, however, was about 50% lower in the patients. This abnormal LDL composition was not altered by therapy with polyanion exchange resins. HDL cholesterol levels were significantly lower in the patients than in healthy children, and remained low during therapy. The decrease of total and LDL cholesterol (25%) and Apo-B (20%) was similar under both Colestipol and Colestyramine. Triglycerides and phospholipids showed no significant changes in therapy.

Adolescent↗
PubMed1984

Plasma and lipoprotein lipid responses to four hypolipid drugs.

The responses of 14 hyperlipidemic subjects to 4 hypolipidemic agents were compared by measuring cholesterol and triglyceride in whole plasma, very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL) monthly for 2 months before and 3 months during treatment with each of 4 drugs: clofibrate, 2 g/d; colestipol, 20 g/d; para-aminosalicylic acid-ascorbate (PAS-C), 6-8 g/d; and oxandrolone, 7.5 mg/d. Lipid responses proved to be stable by the first monthly evaluation both off and on each drug. Mean adherence was high and similar for all agents (81-92% of the prescribed dose). Clofibrate was associated with significant decreases in mean plasma cholesterol (-16%, p less than .01), plasma triglyceride (-51%, p less than .005), VLDL-cholesterol (-61%, p less than .005) and VLDL-triglyceride (-61%, P less than .005), while HDL cholesterol increased (+20%, p less than .01), and the LDL-cholesterol/HDL ratio declined (-24%, p less than .05). Colestipol was associated with decreases in mean plasma cholesterol (-15%, p less than .01) and LDL-cholesterol (-22%, p less than .05), while VLDL-triglyceride increased (+41%, p less than .05), and the LDL-cholesterol/HDL-cholesterol radio declined (-25%, p less than .05). PAS-C was associated with decreases in VLDL-cholesterol (-30%, p less than .05), and VLDL-triglyceride (-29%, p less than .05), while the LDL-cholesterol/HDL-cholesterol ratio remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Hyperviscosity syndrome in a hypercholesterolemic patient with primary biliary cirrhosis.

A 45-yr-old woman with primary biliary cirrhosis, xanthomatosis, and marked hypercholesterolemia developed symptoms of the hyperviscosity syndrome on three separate occasions. On presentation, she had a plasma total cholesterol concentration of 53.40 mM (2065 mg/dl) and a relative serum viscosity of 2.9. Following three courses of plasma exchange in a 5-day period, the total cholesterol level decreased to 6.75 mM (261 mg/dl) and the viscosity to 1.3. The cutaneous xanthomata were markedly diminished 1 wk following plasma exchange. Despite therapy with colestipol (30 g/d), the hyperviscosity syndrome developed 147 days later. This cycle recurred again 137 days after colestipol was discontinued. Serum viscosity and total cholesterol concentration were highly correlated during the postexchange or accumulation phases (R = 0.95, 95% CI: 0.85, 0.98) and during the exchange or interventional phases (R = 0.95, 95% CI: 0.84, 0.99). Serum viscosity was less significantly correlated with total serum protein (R = 0.84; 95% CI: 0.55, 0.95) or with plasma triglyceride (R = 0.63; 95% CI: 0.26, 0.81). There were no significant correlations of red cell mass, plasma fibrinogen levels, or serum bile salts with viscosity. Subfractionation of plasma into lipoprotein classes showed 45% of total cholesterol in the lipoprotein X fraction and a presumptive slow alpha-lipoprotein species. It is postulated that both the hyperviscosity syndrome and rapid resolution of xanthomata in the patient may be attributable to the physiology of her abnormal lipoprotein particles.

Blood Viscosity↗