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PubMed1981

Measurement of gastrointestinal transit of solid food using a colestipol-phenol red complex as a marker.

The present study was undertaken to determine whether colestipol-phenol red complexes can be used as markers for gastrointestinal transit of solid food. Colestipol (1.0g) bound completely with phenol red (10 mg) to form a stable complex in water (pH 7.0) Phenol red was more readily eluted from colestipol with 20 ml of 1 N HCl than 1 N NaOH, but was not eluted with 0.1 N HCL (pH 1.0). It was therefore assumed that the complex would remain stable in the gastrointestinal tract. Also, phenol red in the gastrointestinal tract was quantitatively eluted from the complex with 20 ml of 1N HCl. In a study on gastric emptying, phenol red solution (liquid food) was excreted from the stomach in a zero-order manner, and the colestipol-phenol red complex (solid food) in a first-order manner. It was concluded that colestipol-phenol red complexes can be used as markers of gastrointestinal transit.

Animals↗
PubMed1992

[Colestipol in the treatment of heterozygous familial hypercholesterolemia].

In the specialized clinic for disorders of the lipid metabolism 27 patients, 8 men and 19 women, heterozygotes with familial hypercholesterolaemia were treated for 8 weeks with Colestid (colestipol bags a 5 g, Upjohn, Belgium). The administered dose was 15 g colestipol per day. After colestipol treatment the authors recorded a statistically significant decline of total cholesterol by 18% and of LDL-cholesterol by as much as 27%. The apolipoprotein B concentration declined during treatment by 9% and concurrently there was a favourable rise of apolipoprotein A-1 by 20%. The authors recorded also a slight rise of the HDL-cholesterol concentration which, however, was not statistically significant. The serum triglyceride level increased slightly after colestipol treatment. It did not prove possible to influence the lipoprotein(a) level by colestipol administration. As compared with other hypolipidaemic agents from the group of ion exchange resins, the patients tolerated Colestid surprisingly well. Only one female patient discontinued treatment because of dyspeptic complaints, severe constipation.

Adolescent↗
PubMed1987

Acceptability of cholestyramine or colestipol combinations with six vehicles.

Preferences for cholestyramine or colestipol in combination with orange drink, orange juice, grape juice, apple juice, water, or apple sauce were evaluated in 40 healthy adults. Each subject evaluated the taste, texture, and smell of 30-mL samples of 12 drug-vehicle combinations (two drugs, six vehicles) using modified five-point wine-tasting scales. Samples were prepared to contain either cholestyramine 1.0 g or colestipol hydrochloride 1.3 g. The products were tested at room temperature and were administered in a random order. Subjects and observers were blinded to the identity of the products. Acceptability scores for taste, texture, and smell were significantly higher for cholestyramine than for colestipol. Total mean preference scores for cholestyramine-vehicle combinations ranged from 9.9 to 11.7; for colestipol, 6.3 to 8.9. Orange drink, apple juice, grape juice, and orange juice were the preferred vehicles for cholestyramine. The preferred vehicles for colestipol were orange drink, apple sauce, and apple juice.

Adult↗
PubMed1982

Comparative efficacy of colestipol and clofibrate in type IIa hyperlipoproteinemia.

A multiclinic study was performed comparing colestipol hydrochloride, clofibrate, and placebo in 245 patients with type IIa hyperlipoproteinemia. Eighty-five subjects took colestipol hydrochloride in progressive doses of 15, 20, and 30 g/day; 87 took 2.0 g/day of clofibrate; and 73 took placebo over the six months of study. Colestipol lowered total cholesterol level 20.9% in comparison with clofibrate (14.6%) (statistically significant at months 3, 5, and 6), and lowered low-density lipoprotein cholesterol level 28.8% in comparison with clofibrate (14.8%) (significant at months 2, 4, and 6, all times measured). High-density lipoprotein cholesterol level remained unchanged in all groups. Clofibrate lowered total triglyceride levels 22.5%, compared with an increase of 12.5% in the colestipol group and 11.1% in the placebo group (significant at all time intervals). Colestipol was more effective than clofibrate in lowering the cholesterol fractions associated with increased cardiovascular risk.

Adolescent↗
PubMed1994

The effect of colestipol and cholestyramine on ibuprofen bioavailability in man.

The purpose of this study was to determine whether a concomitant single oral dose of one of the anion exchange resins colestipol hydrochloride (10 g) or cholestyramine (8 g) administered with ibuprofen (400 mg) would alter the bioavailability of this non-steroidal anti-inflammatory agent. The study was performed according to a randomized three-way crossover design in six healthy male volunteers. After dosing, serial blood samples were collected for a period of 10 h. Plasma harvested from blood was analysed for ibuprofen by a sensitive high-performance liquid chromatographic method. There were no significant differences between colestipol treatment and control for peak plasma concentration (Cmax), time to peak concentration (Tmax), area under the plasma concentration-time curve (AUC), mean residence time (MRT), elimination rate constant (Kel), or elimination half-life (t1/2). Cholestyramine treatment resulted in a significant decrease in AUC (26%, p < 0.05) and Cmax (34.4%, p < 0.01) and a significant increase in Tmax (80%, p < 0.01) and MRT (20.2%, p < 0.05). Cholestyramine administration showed no significant effect on the Kel and t1/2 values. A significant correlation was obtained between the increase in MRT and the increase in Tmax. The confidence intervals (90%) of the mean values of the pharmacokinetic parameters (AUC0-infinity and Cmax) for the colestipol: control ratio were well within the acceptable range of 100 +/- 20, whereas those for the cholestyramine: control ratio were outside it. Colestipol treatment was found to be bioequivalent to the control treatment by Schuirmann's two one-sided t tests, while cholestyramine treatment was found to be bioinequivalent.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1982

Randomized controlled trial of colestipol in antibiotic-associated colitis.

Thirty-eight patients with severe antibiotic-associated postoperative diarrhoea were entered into a randomized controlled trial to compare colestipol (an ion exchange resin) in 17 patients with placebo (sherbet) in 21 patients. Clostridium difficile or its toxin was present before treatment in 12 of the colestipol group, compared with only 5 in the placebo group. Because of the low incidence of Cl. difficile or its toxin, the placebo group data from 22 patients receiving placebo in a previous trial (9 of whom had Cl. difficile or toxin) were included for comparison. Neither colestipol nor placebo had any influence on the faecal excretion of Cl. difficile or its toxin. Colestipol was clinically no better than placebo. In view of the persistent faecal excretion of Cl. difficile toxin, ion exchange resins cannot be recommended for the treatment of antibiotic-associated colitis.

Anti-Bacterial Agents↗
PubMed1988

The effect of encapsulated, low-dose colestipol in patients with hyperlipidemia.

Colestipol is an effective cholesterol (C)-lowering agent, but it must be taken in large doses and the palatability is poor. In an open-label study, the effects of low doses (2-10 g) of encapsulated colestipol (size: 1 g or 0.65 g) were investigated. There were 16 men and 16 women with an average age of 59 +/- 11 years and with hyperlipidemias IIA, IIB, or IV. Patients were on AHA I diet and stayed in the study for up to 2 years with regular follow-up every 3 to 4 months. Colestipol was started after several months of dietary baseline; it was tolerated well with only two patients reporting mild constipation. A group mean for total cholesterol (T-C), LDL-C, HDL-C, VLDL-C and triglycerides (TG) was calculated at each of four daily dose intervals, i.e., 2 to 4 g, 4 to 6 g, 6 to 8 g and 8 to 10 g. Each patient usually received more than one of the four dosage intervals. A paired t test and a rank sum test were performed to test for significant (P less than or equal to .05) differences between baseline and drug treatment. With the exception of the lowest dose, total C was significantly decreased by all dosage ranges and LDL-C changes were similar. There was no significant effect on HDL-C and VLDL-C whereas TG levels increased at 4 to 6 g and 8 to 10 g dose. The use of diet and low colestipol doses may be considered in patients with moderate hypercholesterolemia who do not respond to diet alone.

Capsules↗
PubMed1999

The effect of the apolipoprotein E phenotype on cholesteryl ester transfer protein activity, plasma lipids and apolipoprotein A I levels in hypercholesterolaemic patients on colestipol and lovastatin treatment.

BACKGROUND: Apolipoprotein E (apo E) allele E 4 is associated with high atherogenic lipid levels and coronary heart disease. Cholesteryl ester transfer protein (CETP) transfers cholesteryl esters from (high density lipoprotein) HDL to other lipoproteins. CETP gene expression is enhanced in hypercholesterolaemia and correlates with plasma apo E concentration. OBJECTIVE: The effect of the apo E phenotype on plasma CETP activity and the hypolipidaemic efficacy of colestipol and lovastatin was studied in patients with type II a or II b hypercholesterolaemia. RESULTS: The baseline mean plasma total, low density lipoprotein (LDL) and HDL cholesterol, triglyceride, apolipoprotein A I (apo A I) concentrations and CETP activity were 8.89 mmol x l(-1), 6.78 mmol x l(-1), 1.39 mmol x l(-1), 1.59 mmol x l(-1), 1.49 g x l(-1) and 114 nmol x h(-1) x ml(-1), respectively. The colestipol-induced changes were -26%, -36%, +5%, + 12%, -1% and -17%, and the lovastatin-induced changes -34%, -44%, +6%, -18%, +1% and -19%. The lipid and apo A I concentrations or the CETP activity did not differ statistically significantly according to the apo E phenotype, although the HDL cholesterol and apo A I levels were lowered in patients with apo E 4/4 but elevated in patients with the other phenotypes. The CETP activity correlated with the LDL cholesterol concentration (r = 0.52, P = 0.01) and the change in the LDL cholesterol during colestipol (r = 0.51, P = 0.02) and lovastatin (r = 0.65, P = 0.001) treatment, but only in patients without the apo E 4 allele. CONCLUSION: Colestipol and lovastatin reduced CETP activity to the same amount, regardless of the apo E phenotype. The apo E phenotype seems to modify the interaction between CETP activity and LDL cholesterol in hypercholesterolaemia and during pharmacological lowering of cholesterol.

Adult↗
PubMedDate not supplied

Clofibrate-induced low density liporotein elevation. Therapeutic implications and treatment by colestipol resin.

Plasma lipid and lipoprotein responses to clofibrate were assessed in fifteen hypertriglyceridemic patients for the purpose of ascertaining low-density lipoprotein (LDL) changes. Subjects were grouped into either Type IV (11) or IIB (4) subgroups according to initial LDL level. Clofibrate was without effect on LDL in the IIB group, but consistent, often large, elevations were noted in Type IV cases (mean increase, 37.6%, P less than 0.001). In the IIB subgroup, addition of the bile-acid sequestrant, colestipol, lowered LDL (27.8%, P less 0.02) and total cholesterol (21.3%, P less 0.01) below pre-treatment values. In the Type IV subgroup, LDL fell to 19.5% above baseline (P great than 0.05). Significant LDL elevations induced by clofibrate in three of six subjects were restored to initial levels. In both groups, triglycerides and very-low density lipoproteins (VLDL) were not affected. The efficacy of colestipol in reducing LDL levels, expressed as either absolute or percentage reductions, increased as a function of increasing post-clofibrate LDL concentration (r = 0.84, P less than 0.001). In these subjects the level of LDL after treatment with clofibrate depended upon their LDL level prior to drug therapy, the effect of clofibrate on this level, and lipoprotein phenotype. Thus colestipol was most effective in IIB subjects, Type IV subjects with the lowest baseline VLDL and hence reciprocally highest LDL, and Type IV individuals who exhibited the largest LDL induction by clofibrate. The reported ineffectiveness of clofibrate on mortality and morbidity in patients with established coronary heart disease might be related to elevations and infrequent reductions of LDL. From the perspective of lipoprotein lowering, the combination with colestipol appears more favorable.

Adult↗
PubMed1978

Long-term trial with colestipol plus clofibrate in familial hypercholesterolemia.

Twenty subjects with familial hypercholesterolemia (12 Type IIa and 8 Type IIb), previously treated with Colestipol for 16 months, were subjected to therapy with Colestipol (15 g/day) + clofibrate (2 g/day) for 15 months. During the second treatment period these patients continued to follow the isocaloric hypocholesterolemic diet initiated during the original trial. In Type IIa patients, the association of these drugs enhanced the decrease in plasma cholesterol levels. The total mean decrease was -40 +/- 17 mg/dl (P less than 0.05). In Type IIb patients, on the other hand, the association of clofibrate with Colestipol induced an increase in plasma cholesterol levels. The total mean increase was +24 +/- 7 mg/dl (P less than 0.05). A markedly significant decrease in plasma triglyceride levels was observed in this group (- 107 +/- 30; P less than 0.01). These results seem to indicate that, in Type IIa, clofibrate increased the resin's hypocholesterolemic effect. In Type IIb, on the other hand, the association of these drugs did not seem to be indicated since a marked hypotriglyceridemic effect was accompanied by an increase in plasma cholesterol levels. These results are briefly discussed in the light of recent data obtained on the effects of Colestipol and clofibrate on lipoprotein metabolism.

Adult↗
PubMed1981

Effect of colestipol and clofibrate on plasma lipid and lipoproteins in type IIa hyperlipoproteinemia.

The effects of 2.0 g of clofibrate and 15, 20 and 30 g of colestipol on plasma lipid and lipoprotein levels were evaluated in adult patients with Type IIa hyperlipoproteinemia. Clofibrate treatment was associated with decreases in 11.0% in plasma cholesterol. 15.2% in LDL cholesterol, 26.1% in triglycerides, and an 11.3% increase in HDL cholesterol. The reductions in total cholesterol with the various doses of colestipol ranged from 11.9 to 17.8% and reductions in LDL cholesterol ranged from 16.1 to 27.3%. Colestipol treatment was not associated with any significant change in HDL cholesterol levels and minor increases in triglycerides. The addition of clofibrate to patients receiving colestipol resulted in a significant increase in HDL cholesterol and a decrease in triglycerides, but no additional reduction in total or LDL cholesterol.

Adult↗
PubMed1981

Effect of colestipol and clofibrate, singly and in combination, on plasma lipid and lipoproteins in type IIb hyperlipoproteinemia.

The effect of colestipol, clofibrate and a combination of these two drugs on plasma lipid and lipoprotein levels was evaluated in 14 adult male patients with Type IIb hyperlipoproteinemia. A crossover design with each patient receiving all three treatments was utilized. Twenty g of colestipol per day reduced total and LDL cholesterol by 39.1 and 51.5 mg/dl, respectively (p less than 0.001). There was an associated rise in total triglycerides of 63.5 mg/dl (p less than 0.01) with no significant change in HDL cholesterol. Clofibrate, 2.0 g per day, did not significantly lower either total (-7.9 mg/dl) or LDL cholesterol (+8.7 mg/dl). There was marked interpatient variability in terms of the LDL cholesterol response to clofibrate, but the majority of patients demonstrated an increase. HDL cholesterol levels increased by 6.7 mg/dl (p less than 0.01) and total triglycerides were reduced by 94.6 mg/dl (p less than 0.001). Utilizing the same dosages of both drugs, the combination of colestipol and clofibrate were less effective in lowering total and LDL cholesterol than colestipol therapy alone, and increases in HDL cholesterol and decreases in triglycerides similar to those obtained with clofibrate were observed.

Adult↗
PubMed1989

In vitro adsorption of bile salts by colestipol hydrochloride.

The acid-base titration of colestipol hydrochloride exhibits no sharp inflection points, indicating a weakly basic anion-exchange copolymer. The swelling of colestipol hydrochloride in water and the adsorption of cholate anion are inversely related to pH and are, therefore, related to the ionization state of the copolymer. The Langmuir adsorption parameters at pH 7.5 and 37 degrees C are similar for cholate, glycocholate, and taurocholate anions. Adsorption capacity was not related to particle size and exceeded the adsorptive capacity of the external surface by three orders of magnitude. Therefore, it is believed that the swelling of colestipol hydrochloride makes extensive internal surface area available for adsorption of bile salts. The rate of adsorption depends on the concentration of sodium cholate to which the colestipol hydrochloride is exposed. Adsorption was complete within 5 min when the concentration was below the adsorptive capacity. In contrast, adsorption at levels of sodium cholate at or above the adsorptive capacity was not complete within a 3-hr test period.

Adsorption↗
PubMed1994

Colestipol at varying dosage intervals in the treatment of moderate hypercholesterolaemia.

1. Bile acid sequestrants such as colestipol are effective lipid lowering agents but have a poor reputation for tolerability particularly when administered at the originally recommended doses. We have investigated a low dosage regimen with varying dosage intervals in order to assess efficacy and tolerability. 2. This double-blind, placebo controlled, parallel group study was conducted to investigate the effect of varying administration schedules of colestipol (10 g daily), against placebo in reducing LDL cholesterol levels in patients with moderate hypercholesterolaemia on the American Heart Association step 1 diet. 3. Colestipol or matched placebo, was administered as 5 g twice daily (COL am/pm) or 10 g once daily in the morning (COL am) or evening (COL pm) at fixed times with meals. 4. All 98 patients who entered the initial 16 week dietary phase, subsequently entered the 12 week active treatment phase and were randomised to placebo or active treatment and to one of the three treatment schedules. Fasting lipid profiles were performed every 4 weeks during both phases. 5. All active treatments significantly reduced LDL and total cholesterol compared with placebo (COL am: 17% and 10%, COL pm: 18% and 10%, COL am/pm: 19% and 12% (P = 0.0001)). HDL cholesterol rose significantly with COL am (5% (P = 0.021)) and COL am/pm (7% (P = 0.002)) when compared with placebo while a marginal increase was seen with COL pm (4% (P = 0.063)). Colestipol tended to increase serum triglyceride concentrations but the changes were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1978

Colestipol hydrochloride for treatment of hypercholesterolemia in a family practice: five-year study.

Colestipol hydrochloride (Colestid) lowered the serum cholesterol level significantly more than did placebo in hypercholesterolemic patients (21 colestipol, 19 placebo) treated for up to 5 years. In the 21 colestipol-treated patients, the average decrease in serum cholesterol levels was 19 percent during the first year and 23 percent during the second through fifth years. Seven patients (age range, 44 to 59 years) took colestipol for the full 5 years. The data showed a consistent lowering of the serum cholesterol level. The only side effect was constipation.

Adult↗
PubMed1989

Intensive combination drug therapy of familial hypercholesterolemia with lovastatin, probucol, and colestipol hydrochloride.

Patients with familial hypercholesterolemia (FH) have had a life-long sustained elevation of low-density lipoprotein (LDL) cholesterol levels. Consequently, there is a need to maximally lower their elevated levels, and this usually requires lowering LDL levels more than 50%. Because no single hypolipidemic drug will consistently produce such degrees of lowering, combination drug therapy with two or even three agents is required to produce the desired degree of cholesterol lowering. A prospective trial was designed to determine if combination therapy using three hypolipidemic agents could effectively lower LDL levels in 17 severely affected FH subjects. Colestipol hydrochloride (10 g b.i.d.), probucol (500 mg b.i.d.), and lovastatin (20 or 40 mg b.i.d.) were given to each patient, in varying combinations, over a 25-month period. Lovastatin (40 mg/day) uniformly lowered LDL levels 36%. Probucol lowered LDL only 14% and in a variable manner. The combination of lovastatin and probucol lowered LDL no better than lovastatin alone. Lovastatin plus colestipol lowered LDL 52%; probucol added as a third agent produced no further lowering. Lovastatin (80 mg/day) plus colestipol lowered LDL 56%. Lovastatin increased high-density lipoprotein (HDL) cholesterol levels 6%, whereas probucol decreased HDL 29%. In all patients there was an effective lowering of LDL levels, ranging from 40% to 70%. Thus, lovastatin plus colestipol is an effective hypolipidemic regimen for producing marked decreases in LDL levels in FH subjects. The addition of probucol as a third hypolipidemic agent adds little to the therapeutic regimen as measured by lowering of LDL levels.

Cholesterol↗
PubMed1990

The effect of feeding lovastatin and colestipol on production and cholesterol content of eggs.

The purpose of the present study was to determine whether feeding lovastatin or colestipol, or both, to laying hens would decrease the concentration of cholesterol in eggs. Forty-eight White Leghorn hens (69 wk of age) were allocated randomly to one of four groups. For 5 wk, the birds were fed: 1) a control diet; 2) diets supplemented with 35 mg of lovastatin per kg of feed; 3) 11.7 g of colestipol per kg of feed; or 4) both 35 mg of lovastatin and 11.7 g of colestipol per kg of feed. Drug feeding did not affect egg production or the concentration of cholesterol in the yolk, muscle, or liver. Lovastatin residue was found in liver samples from hens receiving lovastatin, but no lovastatin residue was found in the muscle, egg-white, or egg-yolk samples from hens on any treatment. These findings suggest that lovastatin or colestipol, or both, fed at relatively low amounts do not decrease the concentration of cholesterol in egg yolk and do not depress egg production.

Animal Feed↗
PubMed1992

Successful management of primary hypercholesterolaemia with simvastatin and low-dose colestipol.

OBJECTIVE: To examine whether a small dose of bile acid sequestrant used in combination with a hydroxymethylglutaryl coenzyme A reductase inhibitor is more effective in reducing serum and low-density lipoprotein (LDL) cholesterol levels than inhibitor used alone. DESIGN: A randomised, double-blind study. SETTING: Subjects receiving tertiary care at a hospital lipid clinic. PATIENTS: Subjects with severe primary hypercholesterolaemia (types IIa and IIb), already stabilised on a cholesterol-lowering diet, with serum cholesterol levels of 7.0 mmol/L or more and triglyceride levels of 6.0 mmol/L or less. Sixty-four subjects were randomly assigned to the treatment groups; three withdrew before any outcome observations; 61 completed the trial and their results were analysed. INTERVENTIONS: Subjects were randomly assigned to receive either colestipol placebo or colestipol 5 g or 10 g each morning in fixed dosage for 18 weeks. They simultaneously received incremental doses of simvastatin: placebo for six weeks, then 20 mg/night for six weeks, then 40 mg/night for a final six weeks. MAIN OUTCOME MEASURES: Lipids, lipoproteins, and haematological and biochemical safety parameters were measured at the end of each treatment period. Adverse events were monitored. RESULTS: Respective maximum reductions (95% confidence intervals) in serum cholesterol, LDL cholesterol and apolipoprotein B (apo-B) values in subjects taking combination therapy were 41% (38%-45%), 50% (46%-53%) and 43% (39%-46%), compared with lesser reductions of 32% (26%-37%), 38% (31%-45%) and 37% (32%-41%) in those taking simvastatin monotherapy. The percentage changes in LDL cholesterol with combination therapy were independent of baseline cholesterol level or lipid phenotype. Combination therapy reduced serum triglyceride levels by up to 24% (15%-32%) and increased high-density lipoprotein (HDL) cholesterol levels by up to 9% (3%-15%). Three subjects withdrew within a few weeks because of severe gastrointestinal side effects related to colestipol; 19 experienced milder gastrointestinal side effects, 15 were taking combination therapy. CONCLUSIONS: A combination of low-dose colestipol and simvastatin was found to be more effective in reducing serum and LDL cholesterol than simvastatin used alone. Such combination therapy offers the possibility of improved cholesterol lowering without the need for full dosage of either drug.

Anticholesteremic Agents↗