Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-five patinets with well defined Type ii hyperlipoproteinemia were treated with a divided 15 g daily dose of colestipol, a bile acid sequestrant, for periods of up to 20 months. The patients were divided into 3 groups: Those with no obvious sequelae, those with arcus corneae, xanthomas, and/or xanthelasmas only, and those with atherosclerotic complications. Colestipol lowered plasma cholesterol in all 3 groups, but reduced it to normal or near-normal levels in only 9 of the 25 patients (36%). The response of plasma triglycerides was highly varible; the mean for each group was elevated by the drug. Colestipol was well-tolerated and its effect did not diminish with time. It is a useful drug in the treatment of hypercholesterolemia.
Atherosclerosis
PMID:Results of colestipol therapy in Type II hyperlipoproteinemia. 18 81

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.
Atherosclerosis 1978 Feb
PMID:Long-term trial with colestipol plus clofibrate in familial hypercholesterolemia. 34 7

Results related to long term treatment with Colestipol (a new resin sequestering bile acids) in 23 subjects with familial hypercholesterolaemia, 12 with Type IIA, 8 with Type IIB and 3 homozygotes are reported. Patients were given 15 g/day active drug for a period of 12 months and a double dose (30 g/day) for a successive period of 4 months along with a low cholesterol, low saturated fat, polyunsaturated fat-rich diet. Mean cholesterol decrease was --42 +/- 18 mg/dl (P less than 0.05) after 12 months of 15 g/day Colestipol and --69 +/- 17 mg/dl (P less than 0.01) after the following 4 months of 30 g/day Colestipol. The difference between the two periods of treatment (15 g and 30 g/day was not statistically significant. A slight but not significant increase in triglyceride levels was observed. Serum uric acid showed a significant increase throughout the entire period of treatment. No malabsorption syndrome or signs of toxicity were seen. Most frequent side effects were constipation, nausea, and metheorism which, with the exception of 4 cases which were withdrawn from the study, were reported as being transitory and mild.
Atherosclerosis
PMID:Long-term effects of colestipol (U-26,597 A) on plasma lipids in familial type II hyperbetalipoproteinaemia. 120 Nov 45

To a group of 24 subjects with hypercholesterolaemia (hyperlipoproteinaemia type II) for a period of three months the non-absorbable resin Colestid was administered in order to reduce levels of atherogenic lipids and lipoproteins. The Colestid doses were graded from 5 g in the first month to 10-15 g during the third month. Reduction of cholesterol levels and the LDL fraction was significant already during the first month of treatment. The greatest reduction of LDL cholesterol was 25% and of total cholesterol 15%. A favourable effect was recorded also in HDL cholesterol which increased. The rise of triacylglycerols was not significant. Differences in the serum lipid response or their fractions did not depend on sex (15 women, 9 men), the clinical symptomatology (IHD) or family-history of atherosclerosis or concurrent administration of fibrates (Lipanthyl in 7 patients). In view of the small doses the symptomatology of side-effects was poor. Four patients, however, did not complete three months of treatment. With regard to the economical aspect of therapy and the favourable effect of small doses the authors draw attention to this experience which can be used as a basis also when using combinations with other preparations of antihypercholesterolemic therapy in those patients where an adequate reduction of cholesterol and its LDL fraction is not achieved.
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PMID:[Small doses of the resin Colestid in the treatment of hyperlipoproteinemia]. 200 12

The pharmacopolymer bile acid sequestrants cholestyramine and colestipol hydrochloride were mixed with a diet supplemented with 0.5% cholesterol at levels of 0.25%, 0.5%, and 1.0% for cholestyramine and 0.5% and 1.0% for colestipol and fed to young, male, SEA (Susceptible to Experimental Atherosclerosis) Japanese quail (Coturnix coturnix japonica) for a period of seven days. After treatment blood was obtained by venipuncture from non-fasted animals and analyzed for serum total cholesterol concentration. Cholestyramine significantly reduced total cholesterol concentrations at all doses in a dose dependent manner. Colestipol significantly reduced total cholesterol only at the 1.0% dose. Based on these observations, cholestyramine is significantly more potent for reducing serum cholesterol in hypercholesterolemic male SEA quail than is colestipol hydrochloride.
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PMID:Comparison of hypocholesterolemic activities of the bile acid sequestrants cholestyramine and colestipol hydrochloride in cholesterol fed SEA quail. 239 2

The hyperlipidemia of the nephrotic syndrome is often associated with elevated total and low-density lipoprotein (LDL) cholesterol levels and low or normal high-density lipoprotein (HDL) cholesterol levels. This pattern of hyperlipidemia has been associated with an increased risk of accelerated atherosclerosis in other populations. Despite extensive studies of diet and drug therapy in other populations, few such therapeutic studies exist in patients with the nephrotic syndrome. To investigate the effect of diet and lipid-lowering drugs on the lipoprotein-lipid profile of patients with unremitting nephrotic syndrome and marked hyperlipidemia, we conducted a controlled trial using two such drugs: colestipol and probucol. Colestipol lowered the mean total fasting plasma cholesterol of seven patients from 397 +/- 27 to 317 +/- 37 mg/dL, a 20.2% decrease, and lowered the LDL cholesterol from 398 +/- 28 to 203 +/- 18 mg/dL, a 31.9% decrease. It did not affect the HDL cholesterol level, and thus lowered the LDL-to-HDL cholesterol ratio. Probucol lowered the mean total cholesterol from 439 +/- 72 to 339 +/- 60 mg/dL, a 22.6% decrease, and the LDL cholesterol from 282 +/- 43 to 215 +/- 26 mg/dL, a 23.8% decrease. Although the HDL cholesterol was lowered from 49 +/- 9 to 43 +/- 7 mg/dL by probucol, a 12.2% decrease, the LDL-to-HDL cholesterol ratio still declined. Both drugs were well tolerated and proved safe in this short-term trial. Antihyperlipidemic therapy may well be indicated in certain patients with unremitting nephrotic syndrome.
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PMID:Treatment of the hyperlipidemia of the nephrotic syndrome: a controlled trial. 354 20

Twenty-two patients suffering from hyperlipidemia and receiving therapy consisting of a lipid-lowering diet and clofibrate (1 g X 2) were in addition given colestipol hydrochloride (5 g X 3) (Colestid, Upjohn) in a randomized, cross-over study for 2 periods of 6 weeks. Both the cholesterol and the triglyceride concentrations in very low density lipoproteins remained unchanged during the colestipol treatment. The cholesterol concentration in low density lipoproteins decreased by 23% (P < 0.001) and increased in high density lipoproteins by 4% (P < 0.01). In a second part of the project, the effects on the lipoprotein lipids of 15 g of colestipol divided into 1, 2 or 3 daily doses were studied when added to ongoing therapy with clofibrate (1 g X 2) and lipid-lowering diet. When the colespitol was divided into 2 or 3 daily doses, the effects were manifested equally but were less pronounced when 1 dose per day was given. In a third study, 14 patients who were treated with a combination of lipid-lowering diet, clofibrate (1 g X 2) and colestipol hydrochloride (15 g daily) were followed over a 2-year period, during which time the serum cholesterol and triglyceride concentrations were maintained at a reduced level. The fasting blood glucose and serum insulin concentrations were increased during colestipol treatment. Such treatment should therefore not be given to patients with impaired glucose tolerance.
Atherosclerosis 1980 Oct
PMID:The effects of colestipol when combined with clofibrate in the treatment of severe hyperlipidemia. Short-term and long-term studies. 700 89

Colestipol is a safe, effective, cholesterol-lowering, bile-acid sequestrant that lowers low-density-lipoprotein (LDL) and total plasma cholesterol levels without consistently affecting high-density-lipoprotein (HDL) cholesterol levels. Long-term colestipol therapy in conjunction with diet may reduce xanthoma size, arrest progression of coronary artery atherosclerosis, and may reduce mortality from coronary heart disease. Probucol, a bisphenol cholesterol-lowering drug, is an effective cholesterol-lowering agent that reduces levels of HDL cholesterol, HDL cholesterol, and apoprotein A-1, the major apolipoprotein of HDL. Because HDL cholesterol is independently and inversely associated with development of coronary heart disease, the ramifications of simultaneous lowering of LDL and HDL cholesterol levels by probucol treatment need further study. Long-term, placebo-controlled studies of repetitive coronary arteriography, coronary heart disease morbidity and mortality, or both are needed to ascertain the efficacy of long-term probucol use in relation to development of atherosclerosis.
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PMID:Colestipol and probucol: treatment of primary and familial hypercholesterolemia and amelioration of atherosclerosis. 703 45

This study contrasts the sensitivity of four quantitative coronary angiography (QCA) measures (percent diameter stenosis [%S], minimum lumen diameter, average segment diameter, and percent involvement) in detecting 2-year treatment effects of two lipid-lowering therapies and reports on the longitudinal pattern after 4 years of treatment on the primary QCA trial endpoint (%S) for all, mild/moderate (<50%S), and severe lesions (> or =50%S). Patient cohorts were followed up from two randomized, placebo-controlled clinical trials of lipid-lowering therapies-colestipol/niacin in the Cholesterol Lowering Atherosclerosis Study (CLAS) and lovastatin in the Monitored Atherosclerosis Regression Study (MARS). Identical QCA methodology was used. In CLAS, the largest 2-year treatment effect size (=0.60) was noted for %S. In MARS, equivalent 2-year effect sizes (=0.15) were noted for three QCA measures. The largest 2-year effect size in %S was found in CLAS for mild/moderate lesions (=0.55) and in MARS for severe lesions (=0.31). Treatment in CLAS led to regression of disease in the first 2 years; treatment in MARS slowed progression of disease in the first 2 years and led to regression of disease after 4 years. Colestipol/niacin reduced progression of mild/moderate and severe lesions over the first 2 years of therapy; lovastatin reduced the progression of severe lesions over the last 2 years of therapy. We conclude that reducing the progression of atherosclerosis is not a simple proposition; maximal therapy for reducing and stabilizing atherosclerosis most likely will result from the selection of agents targeted at specific lesions.
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PMID:Efficacy of two lipid-lowering treatments on quantitative coronary angiographic endpoints. 1099 48