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Cholesterol Studies
From 1985 through 1987

Results for your query:

Words in abstract only: cholesterol

Published in 1985 through 1987

Only select references with abstracts available

Show references published in English only

Show references pertaining to humans

In journal subset: Abridged Index Medicus Journals

With an article type of: REVIEW

Documents: 1 to 56 of 56

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NLM database Document

Record 1 from database: MEDLINE
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Title

Structure and biochemical effects of fenofibrate.

Author

Kloer HU

Address

Department of Medicine, University of Giessen, Federal Republic of Germany.

Source

Am J Med, 1987 Nov, 83:5B, 3-8

Abstract

The structures of various fibric acid derivatives are compared. Fenofibrate inhibits de novo hepatic fatty acid synthesis and seems to inhibit hepatic very low-density lipoprotein synthesis, but it enhances mitochondrial and peroxisomal fatty acid oxidation and lipoprotein lipase activity. It produces a very significant reduction in the plasma triglyceride concentration. Fenofibrate also inhibits cholesterol synthesis prior to processing mevalonate, indirectly causing significant reduction of hydroxymethylglutaryl coenzyme A reductase activity. The drug may inhibit acyl-coenzyme A-cholesterol transferase activity, reducing cholesterol ester accumulation within cells. Fenofibrate significantly increases the fractional rate of lecithin-cholesterol acyltransferase activity in normolipidemic and hypercholesterolemic patients. This may explain the increase in cholesterol ester levels observed in high-density lipoproteins. It may stimulate bile acid synthesis from exogenous cholesterol. It causes a marked reduction of increased spontaneous platelet aggregation. Fenofibrate also markedly diminishes the effect of platelet-derived growth factor upon DNA synthesis in vitro, an effect that might impede a key event in early atherogenesis. Thus, fenofibrate has effects not directly related to its lipid- and lipoprotein-lowering action.

Language of Publication

English

Unique Identifier

88074434

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MeSH Heading (Major)

Fatty Acids|*BI; Procetofen|*PD; Propionates|*PD; Triglycerides|*ME

MeSH Heading

Chemistry; Cholesterol|BI/ME; DNA|BI; Human; Phosphatidylcholine-Sterol O-Acyltransferase|ME; Platelet Aggregation|DE; Platelet-Derived Growth Factor|AI

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9343

Country of Publication

UNITED STATES

Record 2 from database: MEDLINE
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Title

Fibric acids: effects on lipids and lipoprotein metabolism.

Author

Grundy SM; Vega GL

Address

University of Texas Health Science Center, Center for Human Nutrition, Dallas 75235-9052.

Source

Am J Med, 1987 Nov, 83:5B, 9-20

Abstract

The major effect of the fibrates on triglycerides is to promote triglyceride-rich lipoprotein catabolism through increased lipoprotein lipase activity. Fibrates also enhance lipolysis of plasma triglycerides by a means different from that of caloric restriction. Their effect on very low-density lipoprotein metabolism also differs from that of nicotinic acid. The effect of fibrate therapy upon low-density lipoprotein-cholesterol concentrations depends upon the patients' overall lipoprotein status. The responsible mechanisms are not understood. In hypertriglyceridemic patients, fibrates often reverse abnormal changes in low-density lipoprotein composition; low-density lipoprotein heterogeneity is reduced and small dense low-density lipoproteins are eliminated, apparently secondary to reduced levels of triglyceride-rich lipoproteins. Kinetic studies indicate that fibrates do not enhance low-density lipoprotein formation rates, thus contradicting the idea that fibrate therapy causes increased low-density lipoprotein cholesterol levels via increased conversion of very low-density lipoprotein to low-density lipoprotein. Though enhanced low-density lipoprotein catabolism in hypertriglyceridemia could occur via several mechanisms, the responsible factors are largely reversed by fibrate therapy. In non-hypertriglyceridemic patients, fibrates may actually enhance the fractional clearance of low-density lipoprotein and thus reduce low-density lipoprotein levels. Fibrate therapy reverses the typical high-density lipoprotein pattern of hypertriglyceridemic patients, producing more high-density lipoprotein2a and less high-density lipoprotein2b. Such treatment also increases high-density lipoprotein cholesterol levels in patients without definite hypertriglyceridemia. Synthesis rates of apolipoproteins AI and AII may be affected by fibrates. The fibrates' major effects on sterol metabolism are interference with cholesterol and bile acid synthesis and increased cholesterol secretion into bile. Although bile saturation increases in most patients, in only a relatively small percentage do gallstones actually develop; super-saturated bile is not sufficient to induce gallstone formation in most patients. Available data strongly imply that fibrates mobilized cholesterol out of tissue pools, perhaps by altering tissue cell membranes to allow cholesterol release from the cell surfaces.

Language of Publication

English

Unique Identifier

88074443

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MeSH Heading (Major)

Clofibrate|*AA/PD; Triglycerides|*ME

MeSH Heading

Antilipemic Agents|PD; Bezafibrate|PD; Bile Acids and Salts|BI; Cholesterol|BI; Human; Lipoproteins, HDL|ME; Lipoproteins, LDL|BI/ME; Lipoproteins, VLDL|BI; Liver|ME; Pentanoic Acids|PD; Procetofen|PD

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9343

Country of Publication

UNITED STATES

Record 3 from database: MEDLINE
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Title

Effect of fibric acid derivatives on blood lipid and lipoprotein levels.

Author

Hunninghake DB; Peters JR

Address

Heart Disease Prevention Clinic, Variety Club Heart and Research Center, Minneapolis, Minnesota 55455.

Source

Am J Med, 1987 Nov, 83:5B, 44-9

Abstract

The literature for the last seven years was reviewed in terms of the effect of the various fibric acid derivatives on blood lipid and lipoprotein levels. The criteria for review resulted in a greater focus on three of the newer fibric acid derivatives: bezafibrate, ciprofibrate, fenofibrate. In type II A hyperlipoproteinemia, all fibric acid derivatives produce modest reductions in total plasma cholesterol and low-density lipoprotein cholesterol. The evidence suggests that bezafibrate, ciprofibrate, and fenofibrate may produce greater reductions in low-density lipoprotein cholesterol than those usually observed with clofibrate and gemfibrozil. All fibric acid derivatives produce modest reductions in triglycerides and modest increases in high-density lipoprotein cholesterol in type II A hyperlipoproteinemia. In type II B hyperlipoproteinemia, the low-density lipoprotein cholesterol lowering effect of fibric acid derivatives is generally less than that observed in type II A hyperlipoproteinemia. In type II B hyperlipoproteinemia, there is a mean decrease in low-density lipoprotein cholesterol for all patients studied. However, there is a considerable interpatient variation ranging from significant decreases to significant increases in low-density lipoprotein cholesterol. Further studies are required to assess whether the low-density lipoprotein cholesterol lowering effect is greater with the newer fibric acid derivatives. All fibric acid derivatives produce clinically significant decreases in triglyceride levels in type II B. There is also an associated increase in high-density lipoprotein cholesterol. In type IV hyperlipoproteinemia, all fibric acid derivatives produce clinically significant reductions in triglyceride. There is also an associated increase in high-density lipoprotein cholesterol and generally also an increase in low-density lipoprotein cholesterol levels. The available data do not suggest a clinically significant difference in the hypotriglyceridemic effect of the various fibric acid derivatives in type IV hyperlipoproteinemia. The lipid-altering effects of the various fibric acid derivatives were usually less in those studies that contained placebo and dietary controls. Additional controlled clinical trials are needed to accurately discriminate the relative lipid-and lipoprotein-altering effects of the various fibric acid derivatives.

Language of Publication

English

Unique Identifier

88074436

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MeSH Heading (Major)

Clofibrate|*AA/PD/TU; Hypercholesterolemia, Familial|BL/*DT; Lipids|*BL; Lipoproteins|*BL

MeSH Heading

Anticholesteremic Agents|TU; Bezafibrate|TU; Clofibric Acid|AA/TU; Comparative Study; Human; Pentanoic Acids|TU; Procetofen|TU

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE

ISSN

0002-9343

Country of Publication

UNITED STATES

Record 4 from database: MEDLINE
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Title

3-Hydroxy-3-methylglutaryl--coenzyme A reductase inhibitors in the treatment of hypercholesterolemia.

Author

Hoeg JM; Brewer HB Jr

Address

Molecular Disease Branch, National Heart, Lung, and Blood Institute, Bethesda, Md 20892.

Source

JAMA, 1987 Dec, 258:24, 3532-6

Abstract

A new class of drugs, which inhibit de novo cholesterol biosynthesis, significantly reduces the blood cholesterol concentrations in hypercholesterolemic patients. Four separate inhibitors have lowered plasma total cholesterol and low-density lipoprotein (LDL) levels in humans by 20% to 40%: mevastatin (Compactin), lovastatin (mevinolin), pravastatin (CS-514, Eptastatin, and SQ 31000), and simvastatin (Synvinolin, MK-733). In addition to lowering total and LDL cholesterol concentrations, the plasma concentration of the potentially atherogenic B apolipoprotein is also reduced by 20% to 40%. The reduction in the levels of circulating atherogenic lipoprotein particles occurs as a result of decreased synthesis and enhanced removal of LDLs by the LDL receptor pathway in hepatocytes. Moreover, the levels of high-density lipoprotein cholesterol, which are inversely related to atherosclerosis, increase in concentration with treatment by these drugs. If the short-term safety of these drugs extends to ongoing long-term studies and if cardiovascular morbidity and mortality are affected by their use, this class of hypolipidemic agent will markedly facilitate the effective treatment of hypercholesterolemia.

Language of Publication

English

Unique Identifier

88063146

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MeSH Heading (Major)

Anticholesteremic Agents|AE/*TU; Hydroxymethylglutaryl CoA Reductases|*AI; Hypercholesterolemia|*DT

MeSH Heading

Adult; Animal; Child; Human; Lipoproteins, LDL Cholesterol|BL; Lovastatin|TU

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0098-7484

Country of Publication

UNITED STATES

Record 5 from database: MEDLINE
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Title

Low density lipoprotein receptor regulation and the cellular basis of atherosclerosis: implications for nutritional and pharmacologic treatment of hypercholesterolemia.

Author

Heber D; Koziol BJ; Henson LC

Address

Department of Medicine, University of California, Los Angeles School of Medicine.

Source

Am J Cardiol, 1987 Oct, 60:12, 4G-8G

Abstract

Blood levels of lipids and lipoproteins are prominent among the factors identified as contributing to the development of coronary artery disease. Studies have demonstrated that reduction of low density lipoprotein (LDL) levels lowers the risk of coronary events and retards the progression of atherosclerotic lesions. LDL receptors play a central role in the metabolism of LDL: they maintain cellular cholesterol homeostasis by effects on cholesterol synthesis, modulate the plasma level of lipoproteins by clearing LDL from the circulation and deliver cholesterol to the adrenal glands and gonads for steroid hormone synthesis and to the liver for bile acid synthesis. The 2 major strategies that have been developed so far to lower LDL levels involve the use of bile acid-binding resins, which bind cholesterol in the intestinal lumen, thereby leading to a decrease in intracellular cholesterol, which increases the rate of synthesis of LDL receptors and increases the rate of LDL clearance; and, more recently, the use of inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the key enzyme in the biosynthesis of cholesterol. Further studies are required to assess whether HMG-CoA reductase inhibitors, used alone or concomitantly with bile acid-binding resins, are safe and effective for long-term use in patients with elevated LDL levels.

Language of Publication

English

Unique Identifier

88046556

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MeSH Heading (Major)

Arteriosclerosis|*PA; Atherosclerosis|*PA; Hypercholesterolemia|DH/*DT; Receptors, LDL|*PH

MeSH Heading

Human

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 6 from database: MEDLINE
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Title

Plasma lipid concentrations: the concept of "normality" and its implications for detection of high cardiovascular risk.

Author

Lewis B

Address

Department of Chemical Pathology and Metabolic Disorders, United Medical School of St Thomas's Hospital, London.

Source

J Clin Pathol, 1987 Sep, 40:9, 1118-27

Abstract

The relation between serum cholesterol concentrations and the incidence of coronary heart disease is continuous and curvilinear; there is neither epidemiological nor biological evidence to support the existence of a threshold value. There is a clinical need, however, for an acceptable definition of action limits and desirable ranges, based on the evidence that raised cholesterol concentrations are causally related to atherosclerotic heart disease. The European Atherosclerosis Society has proposed a set of cut off points, which, together with age and the presence of other risk factors, direct the clinician to an appropriate level of treatment. Because the changes of serum cholesterol during adult life appear unphysiological, these action limits do not require adjustment for age. The distribution of serum cholesterol in the United Kingdom population is such that a case finding strategy is required to identify the many persons at very high risk of coronary disease. Measurements of triglyceride, high density lipoprotein, apolipoproteins, and the investigation of hyperlipoproteinemia are informative but less mandatory.

Language of Publication

English

Unique Identifier

88033749

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MeSH Heading (Major)

Cholesterol|*BL; Coronary Disease|BL/*PC

MeSH Heading

Adult; Disease Susceptibility; Female; Human; Hyperlipidemia|PC; Lipoproteins|BL; Male; Middle Age

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

0021-9746

Country of Publication

ENGLAND

Record 7 from database: MEDLINE
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Title

Dietary fiber, lipids and atherosclerosis.

Author

Anderson JW

Address

Medical Service, Veterans Administration Medical Center, Lexington, Kentucky 40511.

Source

Am J Cardiol, 1987 Oct, 60:12, 17G-22G

Abstract

Dietary fiber has important hypocholesterolemic effects and may reduce risk for coronary artery disease. Careful clinical studies indicate that foods such as oat bran or beans, rich in water-soluble fiber, can decrease serum total cholesterol by 19% while decreasing serum low density lipoprotein cholesterol by 22%. Food supplements rich in soluble fiber such as psyllium mucilloid are well tolerated and may lower serum cholesterol by 15%. Thus, high fiber foods or soluble fiber food supplements may decrease serum cholesterol by 15% to 19% and decrease estimated risk for coronary heart disease by greater than 30%.

Language of Publication

English

Unique Identifier

88046553

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MeSH Heading (Major)

Arteriosclerosis|*DH; Atherosclerosis|*DH; Dietary Fiber|*TU

MeSH Heading

Adult; Aged; Cereals; Human; Hypercholesterolemia|DH; Legumes; Middle Age; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 8 from database: MEDLINE
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Title

The influence of non-beta-blocking drugs on the lipid profile: are diuretics outclassed as initial therapy for hypertension?

Author

Ames RP

Address

Columbia University College of Physicians and Surgeons, New York, NY.

Source

Am Heart J, 1987 Oct, 114:4 Pt 2, 998-1006

Abstract

Diuretic drugs, when used in the treatment of hypertension, raise the blood concentrations of total cholesterol and low-density or very low-density lipoprotein cholesterol. Triglycerides often increase as well. Thiazide, phthalimidine, loop, potassium-sparing, and methylindoline drugs produce a similar effect. Only indapamide, a methylindoline agent with vasodilator activity, has been free of adverse lipid effects. It remains unclear whether it is the low dose of indapamide or some other quality that frees it of this effect. In long-term diuretic therapy, total cholesterol returns to, or below, baseline values, suggesting that the lipid elevations are transitory. However, in studies with adequate control groups, total cholesterol declines below baseline valves in control subjects such that an adverse differential in lipid values persists in long-term treatment. Selective alpha-1-adrenoceptor-blocking drugs cause no change or favorable alterations in lipid concentrations in short-term and long-term (1 year) treatment. Among all antihypertensive drugs, this class of agents, and especially prazosin, has produced the most consistently salutary lipid and metabolic effects. Although less well examined, guanabenz, clonidine, guanfacine, and diltiazem have been associated with favorable lipid changes. Captopril and nifedipine have caused no change in lipid-lipoprotein values in limited investigations. These agents are preferable to diuretics and certain beta blockers with respect to short-term effects on lipids and lipoproteins. Their ultimate superiority as monotherapy depends on whether they lower blood pressure equally well. Lowering of the probability of coronary heart disease in hypertensive patients depends as much on blood pressure control as on lipid effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

88020726

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MeSH Heading (Major)

Antihypertensive Agents|*TU; Hypertension|*DT; Lipids|*BL

MeSH Heading

Adrenergic alpha-Antagonists|TU; Diuretics|TU; Human

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW LITERATURE

ISSN

0002-8703

Country of Publication

UNITED STATES

Record 9 from database: MEDLINE
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Title

Cholesterol metabolism and aging.

Author

Kreisberg RA; Kasim S

Address

Source

Am J Med, 1987 Jan, 82:1B, 54-60

Abstract

Changes occur in lipid and lipoprotein concentrations with age that increase the risk of developing atherosclerotic disease. In children and young adults (less than 20 years of age), the plasma total cholesterol concentration decreases between the ages of 10 and 20 years. After age 20, the plasma total cholesterol concentration increases progressively, and in men reaches a plateau between the ages of 50 and 60 years, whereas in women, it reaches a peak between 60 and 70 years of age. The low-density lipoprotein cholesterol concentration increases progressively in men and women after age 20, but more rapidly in men, accounting for most of the overall gender difference in total cholesterol. The rate at which the low-density lipoprotein cholesterol concentration increases in women begins to accelerate between 40 and 50 years of age, and the concentration exceeds that in men by 55 to 60 years. High-density lipoprotein cholesterol concentrations decrease in males during puberty and early adulthood, and thereafter remain lower than those in women at all comparable ages. The high-density lipoprotein cholesterol concentrations remain constant in women throughout their lifetime. Beyond 30 years of age, women taking estrogen preparations have higher high-density lipoprotein cholesterol concentrations than women who are not taking estrogens. The triglyceride concentration increases progressively in men, reaching peak values between 40 and 50 years of age, and then declining slightly thereafter. In women, the triglyceride concentration increases throughout their lifetime, but is always higher in those using estrogens. Whether these changes in lipoprotein concentrations merely accompany the increasing prevalence of atherosclerotic vascular disease that occurs with age, or contribute to it, is unknown at this time.

Language of Publication

English

Unique Identifier

87124882

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MeSH Heading (Major)

Aging|*ME; Cholesterol|*ME; Coronary Disease|*ME

MeSH Heading

Adult; Aged; Female; Human; Lipoproteins, HDL Cholesterol|ME; Lipoproteins, LDL Cholesterol|ME; Male; Middle Age; Triglycerides|ME

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-9343

Country of Publication

UNITED STATES

Record 10 from database: MEDLINE
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Title

Effect of ursodeoxycholic acid and chenodeoxycholic acid on cholesterol and bile acid metabolism.

Author

Tint GS; Salen G; Shefer S

Address

Source

Gastroenterology, 1986 Oct, 91:4, 1007-18

Abstract

Orally administered UDCA dramatically reduces the secretion of cholesterol into the bile. During UDCA therapy cholesterol balance is maintained by a reduction in both the relative and absolute absorption of cholesterol and, perhaps, by a combined moderate enhancement of bile acid synthesis and a suppression of cholesterol production. The percentage of UDCA in the bile is limited by the inability of UDCA to suppress bile acid synthesis from cholesterol and by the conversion of UDCA to CDCA by the intestinal bacteria.

Language of Publication

English

Unique Identifier

86301701

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MeSH Heading (Major)

Bile Acids and Salts|*ME; Chenodeoxycholic Acid|PD/*TU; Cholelithiasis|*DT/ME; Cholesterol|*ME; Deoxycholic Acid|*AA; Ursodeoxycholic Acid|PD/*TU

MeSH Heading

Animal; Human; Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0016-5085

Country of Publication

UNITED STATES

Record 11 from database: MEDLINE
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Title

Changing perspectives in the prevention of coronary artery disease.

Author

Levy RI

Address

Source

Am J Cardiol, 1986 May, 57:14, 17G-26G

Abstract

Today the question is no longer whether cholesterol reduction is beneficial for those at risk for coronary artery disease; the questions now are when, whom and how to treat. Areas of great interest include extrapolation of current trial results to low density lipoprotein reduction by diet and drugs, and assessment of the value of increasing high density lipoprotein levels by pharmacologic means. We will need to decide what measurements (total cholesterol, lipoprotein cholesterol or lipoprotein apoprotein levels) are of most value to the diagnosis, treatment and follow-up of the at-risk patient. Recommendations, including those of the recently published National Institutes of Health Consensus Panel on Cholesterol Lowering, suggest that our index for diagnosis and treatment should be set considerably lower than it is today. To be successful with a more aggressive approach to cholesterol lowering, we will need to better support, educate and motivate the at-risk patient. Physicians need to become more knowledgeable about what plasma cholesterol is and how to change it. Methods that enhance patient adherence to diet and drug therapy must be developed. We will need to alter lifetime habits and will need the help of both the food industry and better informed consumers, knowledgeable on how to read food labels, if we are to succeed. Ultimately, we will need a 2-pronged approach, focusing on both the physician and the public at large.

Language of Publication

English

Unique Identifier

86239019

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MeSH Heading (Major)

Coronary Disease|BL/ET/*PC

MeSH Heading

Animal; Atherosclerosis|ET/PC; Cholestyramine|TU; Clinical Trials; Double-Blind Method; Female; Health Promotion; Human; Lipids|BL; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Long-Term Care; Male; Motivation; Patient Education; Random Allocation; Risk

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 12 from database: MEDLINE
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Title

Comparative toxicity and safety profile of fenofibrate and other fibric acid derivatives.

Author

Blane GF

Address

Laboratoires Fournier, Centre de Recherches de Daix, Dijon, France.

Source

Am J Med, 1987 Nov, 83:5B, 26-36

Abstract

It is estimated that there are approximately six million patient-years of clinical experience with fenofibrate among physicians outside of the United States. A review of the European literature and unpublished studies supplied by the manufacturer (Laboratoires Fournier, Dijon, France) has been compiled with the data recently reported from a double-blind, placebo-controlled study completed in the United States. In general, fenofibrate has been found to reduce serum triglyceride levels by 30 to 60 percent in patients with type II B and IV hyperlipoproteinemia. Serum cholesterol levels were also reduced by 20 to 25 percent in this group of hypertriglyceridemic patients. A similar reduction in serum cholesterol levels was also found in type II A patients (normal triglyceride levels). Low-density lipoprotein levels were usually reduced in those patients with elevated levels and high-density lipoprotein levels increased when baseline levels were low. Fenofibrate also produced a 10 to 28 percent reduction in uric acid that was sustained for years. The incidence of unwanted effects ranged from 2 to 15 percent in the open trials lasting from a few months up to six years. Gastrointestinal problems (abdominal discomfort, diarrhea, and constipation) are most common, occurring in approximately 5 percent of patients. Reports including fatigue, headache, loss of libido, impotence, dizziness, and insomnia were grouped as neurologic and occurred with a total incidence of 3 to 4 percent. In about 1 percent of patients, muscle tenderness developed, often accompanied by elevated creatine phosphokinase levels. These and the gastrointestinal problems occurred with a similar frequency in the placebo-treated cohort in controlled studies. In approximately 2 percent of patients, a skin rash developed, an incidence that appears significantly higher than that of placebo control groups. Liver changes in rodents have included marked peroxisome proliferation and increased hepatic carcinomas with very high doses. In humans, only a small increase in incidence of elevated levels of serum glutamic oxaloacetic transaminase and serum glutamic pyruvic transaminase seems to be present and is not clearly different from that of the control groups. Alkaline phosphatase, gamma-glutamyl transferase, and bilirubin levels are often decreased with no known undesirable effects. Investigations into the lithogenicity of bile indicated a significant increase in five studies. However, there has been no evidence of a significant rise in the incidence of cholelithiasis in the clinical trials completed to date.

Language of Publication

English

Unique Identifier

88074433

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MeSH Heading (Major)

Clofibrate|*AA/AE/TO; Procetofen|*AE/TO; Propionates|*AE

MeSH Heading

Animal; Clinical Trials; Double-Blind Method; Drug Screening; Human; Random Allocation

Publication Type

CLINICAL TRIAL; CONTROLLED CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE

ISSN

0002-9343

Country of Publication

UNITED STATES

Record 13 from database: MEDLINE
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Title

Metabolic effects of oral contraceptives.

Author

Gaspard UJ

Address

Department of Obstetrics and Gynecology, State University of LiÄege, Belgium.

Source

Am J Obstet Gynecol, 1987 Oct, 157:4 Pt 2, 1029-41

Abstract

Combination oral contraceptives (OCs) are probably not an independent risk factor for cardiovascular disease but through their metabolic actions, may partly amplify the effects of known risk factors for cardiovascular disease. This review of the literature and our own data indicate that use of high-dose, progestogen-dominant OCs induces a potentially atherogenic lipoprotein profile (high low-density lipoprotein-cholesterol:high-density lipoprotein-cholesterol ratio), mostly attributable to the antiestrogenic action of the progestogen content of these OCs. In contrast, lower-dose combination OCs with reduced amounts of progestogens and slight estrogen dominance, either monophasic or multiphasic, produce strikingly fewer adverse effects on lipoproteins. Moreover, use of low-dose, as opposed to high-dose, OCs results in almost unchanged glucose tolerance, marginally increased or unchanged insulin and glucagon responses to glucose, and probably unchanged levels and activity of peripheral insulin receptors. Further in-depth studies of low-dose OC formulations are mandatory to ascertain reduced metabolic risk of these OCs.

Language of Publication

English

Unique Identifier

88047041

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MeSH Heading (Major)

Contraceptives, Oral, Combined|AE/*PD; Glucose|*ME; Lipoproteins|*ME

MeSH Heading

Cardiovascular Diseases|CI; Diabetes Mellitus|ME; Estrogens, Synthetic|PD; Female; Glucose Tolerance Test; Human; Insulin|BL; Insulin Resistance|DE; Progesterone|PD; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

0002-9378

Country of Publication

UNITED STATES

Record 14 from database: MEDLINE
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Title

Agents for gallstone dissolution.

Author

Pitt HA; McFadden DW; Gadacz TR

Address

Source

Am J Surg, 1987 Feb, 153:2, 233-46

Abstract

Numerous methods are presently available for gallstone dissolution, including oral bile salts; cholesterol solvents such as mono-octanoin and methyl tert-butyl ether; calcium or pigment solvents such as EDTA and polysorbate; mechanical extraction techniques through a T-tube tract or after endoscopic sphincterotomy; or fragmentation methods such as ultrasonography or electrohydraulic lithotripsy, lasers, and extracorporeal shock waves. Which, if any, of these methods will be appropriate for an individual patient depends on the type of stones, whether they are in the gallbladder or bile ducts, whether access to the biliary tree is available, the patient's age and general medical condition, and the availability of expert radiologists, endoscopists, and newer equipment. In the United States, the only available oral bile salt for cholesterol gallstone dissolution is chenodeoxycholate. Ursodeoxycholate, which is more rapid and less toxic, has not been approved by the Federal Drug Administration. These agents are most effective in thin women with small, floating, radiolucent cholesterol gallstones in a functioning gallbladder. Only about half of this small subset of patients, however, will experience partial or complete dissolution of stones in 6 to 12 months. Moreover, recurrence is very likely, and the potential toxicity of long-term therapy is unknown. Thus, for most patients, cholecystectomy remains the most cost-effective and, perhaps, safest option. Intragallbladder instillation of methyl tert-butyl ether and extracorporeal shock wave therapy are also likely to be applicable to only small subsets of patients and to be associated with high recurrence rates. In patients with retained ductal cholesterol stones and access to the biliary tree, mono-octanoin therapy is advantageous in that it can be begun as soon as cholangiography demonstrates no extravasation. In properly selected patients, a 90 percent success rate with mono-octanoin infusion can be expected within a week. Radiologic or endoscopic extraction techniques require maturation of a relatively straight T-tube tract but are not dependent on the type of stone. In the hands of experts, these techniques are highly successful. In postcholecystectomy patients without access to the biliary tree, endoscopic sphincterotomy has become the preferred method of management and can be expected to succeed in more than 90 percent of patients. At this point, the exact role for ultrasonic or electrohydraulic lithotripsy and lasers is unknown. However, these techniques may be applicable in the future in patients with retained bile duct stones in whom extraction and infusion techniques have failed.

Language of Publication

English

Unique Identifier

87125529

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MeSH Heading (Major)

Cholelithiasis|*TH

MeSH Heading

Administration, Topical; Bile Acids and Salts|AD; Human; Lithotripsy

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-9610

Country of Publication

UNITED STATES

Record 15 from database: MEDLINE
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Title

Regulation of plasma cholesterol by hepatic low-density lipoprotein receptors.

Author

Kovanen PT

Address

Source

Am Heart J, 1987 Feb, 113:2 Pt 2, 464-9

Abstract

The endogenous lipoprotein system (very low-density lipoprotein [VLDL], intermediate-density lipoprotein [IDL], low-density lipoprotein [LDL] cascade) holds the key to understanding the mechanisms by which hormones, diet, and drugs interact to regulate the plasma cholesterol level. Crucial components of this system are hepatic LDL receptors that mediate the uptake and degradation of plasma LDL. With experimental animals, it has been possible to demonstrate that hepatic LDL receptors are sensitive to hormonal, dietary, and pharmacologic manipulation. The decrease in number of hepatic LDL receptors in hypothyroidism or after cholesterol feeding leads to elevation of plasma LDL cholesterol levels. Conversely, the increase in number of hepatic LDL receptors results in lowering of plasma LDL cholesterol levels. This can be observed in hyperthyroidism, during administration of pharmacologic doses of 17 alpha-ethinyl estradiol, or during treatment with cholesterol-lowering drugs such as the bile acid-binding resins and cholesterol-synthesis inhibitors. Since cholesterol excretion from the body occurs via the liver, the increased efficiency of disposal of plasma cholesterol by increasing hepatic LDL receptors will ultimately lead to depletion of excessive body cholesterol. Pharmacologic regulation of hepatic LDL receptors should be a valuable tool in the prevention and therapy of atherosclerosis.

Language of Publication

English

Unique Identifier

87124368

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MeSH Heading (Major)

Cholesterol|*BL; Liver|*PH; Receptors, LDL|*PH

MeSH Heading

Animal; Cholesterol, Dietary|AD; Disease Models, Animal; Dogs; Human; Hypercholesterolemia, Familial|BL; Lipoproteins, LDL Cholesterol|BL; Rabbits; Rats

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-8703

Country of Publication

UNITED STATES

Record 16 from database: MEDLINE
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Title

Serum-cholesterol response to dietary cholesterol: a re-evaluation.

Author

Hegsted DM

Address

Source

Am J Clin Nutr, 1986 Aug, 44:2, 299-305

Abstract

The data from the literature in which the serum-cholesterol response has been measured following a change in cholesterol intake have been re-evaluated. The overall data appear to be best explained by exponential equations. However, very large differences in response have been reported for similar changes in cholesterol intake and no predictive equation can explain such values. It is concluded that over the range of cholesterol intakes of practical interest--0 to 400 mg/1000 kcal--the usual response is approximately linear, each 1 mg/1000 kcal resulting in an expected increase of serum cholesterol of approximately 0.1 mg/dl. With a 2500 kcal diet, an increase in intake of 100 mg/day would be expected to increase serum cholesterol by approximately 4 mg/dl.

Language of Publication

English

Unique Identifier

86265431

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MeSH Heading (Major)

Cholesterol|*BL; Cholesterol, Dietary|*ME

MeSH Heading

Human; Regression Analysis; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 17 from database: MEDLINE
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Title

Role of risk factor management in progression and regression of coronary and femoral artery atherosclerosis.

Author

Glueck CJ

Address

Source

Am J Cardiol, 1986 May, 57:14, 35G-41G

Abstract

The results of 3 recently completed studies usher in a new era in the treatment of coronary atherosclerosis and its sequelae. In aggregate, these results show that reductions in low density lipoprotein (LDL) cholesterol or reductions in the ratio of total to high density lipoprotein (HDL) cholesterol by either diet or drugs or both are effective in primary and secondary prevention of coronary artery disease (CAD). In the Lipid Research Clinics' Coronary Primary Prevention Trial, reducing levels of LDL cholesterol, regardless of whether the primary intervention was diet or drug, correlated with a reduction in CAD events. In the National Heart, Lung, and Blood Institute's Type II Coronary Intervention Study, CAD progression at 5 years was inversely related to a change in the ratio of HDL cholesterol to total cholesterol. In the Leiden Intervention Trial, cessation of coronary artery atherosclerotic lesion growth correlated with the ratio of total cholesterol to HDL cholesterol. Several trials now under way will test the effects of much more substantial reductions of LDL cholesterol (up to 50%) and increments in HDL cholesterol (up to 25%) on interrupting the progression or inducing the regression of coronary artery atherosclerosis. Even small reductions in the progression of coronary artery lesions or induction of their regression should produce major reductions in morbidity and mortality from CAD. The importance of secondary prevention also extends to patients after coronary artery bypass surgery, because the likelihood of graft occlusion is likewise related to the patient's lipid profile. Further, the importance of primary prevention of atherosclerosis through modification of lipids and lipoprotein cholesterol in the first-degree relatives of young victims of atherosclerosis cannot be overemphasized.

Language of Publication

English

Unique Identifier

86239023

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MeSH Heading (Major)

Arteriosclerosis|*TH; Atherosclerosis|CO/*TH; Coronary Disease|ET/PC/*TH; Femoral Artery|*

MeSH Heading

Cholesterol|BL; Cholesterol, Dietary|AD; Coronary Artery Bypass; Female; Human; Hyperlipidemia|TH; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Male; Primary Prevention; Risk; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 18 from database: MEDLINE
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Title

Treatment of hyperlipidemia.

Author

Gotto AM Jr

Address

Source

Am J Cardiol, 1986 May, 57:14, 11G-16G

Abstract

The correlation between elevated cholesterol and coronary artery disease (CAD) has emerged slowly, with the strongest statistical links appearing recently. Every major epidemiologic study carried out to date has verified the association between the concentration of serum cholesterol and the risk of CAD. Despite this, much of the medical profession continues to underrate the significance of cholesterol and lipoproteins. Programs to increase physicians' awareness of this problem are essential. The National Heart, Lung, and Blood Institute's Coronary Primary Prevention Trial showed that diet and drug therapy lower cholesterol by 9% and low density lipoprotein (LDL) cholesterol by 12.5%, on average, in at-risk patients compared with control subjects. CAD death or nonfatal myocardial infarctions were reduced collectively by 19%. Significant decreases also occurred in the incidence of angina pectoris, new positive electrocardiograms and coronary artery bypass surgery. Data from a number of important secondary prevention trials also support lowering cholesterol and LDL to retard the growth of atherosclerotic plaque. The risk from LDL elevations depends on the extent of the increase, the concentration of high density lipoprotein cholesterol and the presence of other major risk factors (e.g., hypertension and smoking). The ratio of total cholesterol or LDL to the high density lipoprotein concentration is the best indicator for CAD risk. Monitoring cholesterol levels should become an annual routine in the physician's office. A simple, economical blood test for cholesterol, which should be widely available soon, will make screening programs possible, but before such screening begins, plans must be in place for follow-up. The identification of high risk persons and their treatment with diet and, when necessary, drugs are essential.(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

86239018

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MeSH Heading (Major)

Hyperlipidemia|BL/DT/*TH

MeSH Heading

Adult; Arteriosclerosis|BL/PC; Cholesterol, Dietary; Cholestyramine|TU; Coronary Disease|BL/ET/PC; Female; Human; Lipoproteins, HDL|BL; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Liver|ME; Male; Receptors, LDL|BL; Risk; Smoking

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 19 from database: MEDLINE
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Title

Review of lipid-lowering clinical trials in relation to observational epidemiologic studies.

Author

Tyroler HA

Address

Source

Circulation, 1987 Sep, 76:3, 515-22

Abstract

A review of the experimental clinical trials and observational cohort evidence relating serum cholesterol level and its reduction to risks of coronary heart disease (CHD) discloses strong similarities among the quantitative and qualitative relationships found in these studies. Not only are the risk functions similar, but the percent reduction observed is the same as that predicted from the population experience and is proportional to the degree of cholesterol lowering. Furthermore, the risk function is continuous from the highest to the lowest serum cholesterol levels studied. These findings confirm the lipid hypothesis and indicate that lowering serum cholesterol reduces CHD risk. The understanding and control of CHD requires a dual approach: (1) identification and treatment of high-risk individuals, and (2) modification of environmental and behavioral determinants to achieve more favorable distributions of serum cholesterol in populations.

Language of Publication

English

Unique Identifier

87302141

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MeSH Heading (Major)

Antilipemic Agents|*TU; Cholesterol|*BL; Coronary Disease|EP/*ET; Hypercholesterolemia|EP/*PC/TH

MeSH Heading

Adolescence; Adult; Age Factors; Aged; Cholestyramine|TU; Clinical Trials; Comparative Study; Diet; Double-Blind Method; Human; Male; Middle Age; Random Allocation; Risk

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW

ISSN

0009-7322

Country of Publication

UNITED STATES

Record 20 from database: MEDLINE
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Title

Hypolipidemic effects of HMG-CoA reductase inhibitors in patients with hypercholesterolemia.

Author

Illingworth DR; Bacon S

Address

Department of Medicine, Oregon Health Sciences University, Portland 97201.

Source

Am J Cardiol, 1987 Oct, 60:12, 33G-42G

Abstract

Hypercholesterolemia with increased plasma concentrations of low density lipoproteins (LDL) is a major risk factor for the premature development of coronary atherosclerosis in humans and is best exemplified by patients with familial hypercholesterolemia. The recent development of several specific competitive inhibitors of the rate-limiting enzyme in cholesterol biosynthesis (3-hydroxy-3-methylglutaryl-coenzyme A reductase, HMG CoA reductase) has opened up an important new avenue of therapy for patients with hypercholesterolemia who are not responsive to dietary treatment alone. Three drugs, lovastatin (mevinolin), simvastatin (synvinolin) and pravastatin (CS 514), are currently undergoing clinical trials in North America and Europe; the former has recently been approved for general use. Experience with lovastatin and simvastatin in the treatment of patients with primary and secondary causes of hypercholesterolemia is reviewed. The relative potency of simvastatin appears to be greater than that of lovastatin and pravastatin but, with each drug, decreases in the plasma concentrations of LDL cholesterol of 30% to 50% can be achieved. The hypocholesterolemic effects of HMG CoA reductase inhibitors can be potentiated by combination therapy with other approved lipid-lowering medications including the bile acid sequestrants and nicotinic acid. If long-term safety can be satisfactorily established, specific inhibitors of HMG CoA reductase represent a major advance in the therapy of hypercholesterolemia and afford the potential to reduce substantially the high incidence of premature atherosclerosis that occurs in patients with persistent hypercholesterolemia.

Language of Publication

English

Unique Identifier

88046555

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MeSH Heading (Major)

Anticholesteremic Agents|*TU; Hydroxymethylglutaryl CoA Reductases|*AI; Hypercholesterolemia, Familial|*DT

MeSH Heading

Comparative Study; Human; Lovastatin|AA/TU; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 21 from database: MEDLINE
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Title

Antiatherogenic properties of calcium antagonists.

Author

Weinstein DB; Heider JG

Address

Source

Am J Cardiol, 1987 Jan, 59:3, 163B-172B

Abstract

A generalized accumulation of cholesterol, calcium and matrix materials (collagen, elastin and proteoglycans) occurs in an age-dependent manner in major arteries. Human atherogenesis is a disease of arteries characterized by a focal accumulation of fibrous matrix elements, lipids and calcium at lesion sites. Studies in cholesterol-fed animal models have indicated that calcium competitors and chelating agents can reduce calcium, lipid and matrix accumulation in arterial lesions and reduce the extent of lesion formation. These agents generally alter soft and hard tissue calcium pools or have deleterious side-effect profiles. Antiatherogenic studies with calcium antagonists (which have been shown to be safe in human clinical studies) have created confusion because of conflicting results. It is apparent, however, that high doses of calcium antagonists can significantly decrease atherogenic lesion development in cholesterol-fed rabbits. The antiatherogenic effects of calcium antagonists may be the result of changes in intracellular calcium pools within smooth muscle cells, which may lead to alterations in cellular metabolic activity or may be due to activities not related to calcium channel effects. Several mechanisms involving regulation of lipoprotein receptor synthesis, lipoprotein uptake or degradation, cholesterol ester hydrolytic activity and arterial matrix synthesis are discussed as potential sites of activity for calcium antagonists. A dihydropyridine channel antagonist, PN 200-110 (isradipine), has been shown to be a very potent antiatherogenic agent in the rabbit and also to be a potent inhibitor of smooth muscle cell matrix synthesis.

Language of Publication

English

Unique Identifier

87124486

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MeSH Heading (Major)

Arteriosclerosis|*DT; Atherosclerosis|*DT; Calcium Channel Blockers|PD/*TU

MeSH Heading

Animal; Calcinosis|DT; Calcium|ME; Human; Ion Channels|DE; Muscle, Smooth, Vascular|ME; Oxadiazoles|PD

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 22 from database: MEDLINE
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Title

Gallstone dissolution therapy. Current status and future prospects.

Author

Fromm H

Address

Source

Gastroenterology, 1986 Dec, 91:6, 1560-7

Abstract

Findings by several groups of investigators have provided a reliable data base that supports a nonoperative approach toward the management of so-called silent gallstones. Considerable progress has been made in the medical dissolution treatment of selected patients with cholesterol gallstones. Ursodeoxycholic acid, and, more recently, a combination of ursodeoxycholic and chenodeoxycholic acids have been shown to be both effective and safe in dissolving gallstones that are predominantly composed of cholesterol. A drawback of the bile acid dissolution therapy lies in a significant recurrence rate after treatment is discontinued. Currently, several new methods of gallstone treatment are under study, which involve either the injection of a cholelitholytic solution, such as methyl tert-butyl ether, into the gallbladder or the use of mechanical means, such as excorporeally induced shock waves, to disintegrate gallstones. These treatments, however, are effective only if the stones are composed mainly of cholesterol without significant admixtures of calcium salts, pigment, or mucus. Most of the treatment failures are probably related to the presence of calcifications that are not visible on conventional radiographs. Future improvements of gallstone dissolution therapy can be expected from the following possible developments: improvement in ability to predict gallstone composition; dissolution of calcium salt-, pigment-, and mucus-containing stones; early treatment, before calcifications occur; combination of chemical and mechanical methods of treatment; stimulation of gallbladder contraction; prevention of stone recurrence after dissolution; and synthesis of new cholelitholytic agents.

Language of Publication

English

Unique Identifier

87031362

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MeSH Heading (Major)

Cholelithiasis|DT/*TH

MeSH Heading

Bile Acids and Salts|TU; Ethers|TU; Glycerides|TU; Human; Lithotripsy; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0016-5085

Country of Publication

UNITED STATES

Record 23 from database: MEDLINE
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Title

Epidemiology of atherosclerosis: an updated overview.

Author

Criqui MH

Address

Source

Am J Cardiol, 1986 Feb, 57:5, 18C-23C

Abstract

Ongoing epidemiologic research continues to provide new insight into the multifactorial etiology of atherosclerosis and coronary artery disease (CAD). Cigarette smoking remains a primary risk factor; low tar and nicotine cigarettes have apparently not contributed to a reduced incidence of CAD and cardiovascular death. The stepwise risk of increasing levels of diastolic blood pressure to cardiovascular death is well known; however, elevated systolic blood pressure may be a more potent risk factor. The benefits of treating diastolic blood pressure greater than or equal to 115 mm Hg are indisputable; the benefits of treating milder hypertension, i.e., diastolic blood pressure between 90 and 114 mm Hg, probably outweigh the risks, but controversy persists. Low-density lipoprotein cholesterol, which comprises approximately 70% of total cholesterol, is strongly associated with CAD. Studies continue to relate hypercholesterolemia and CAD, showing approximately a 2% reduction in disease for each 1% reduction in total cholesterol. The influences of diabetes mellitus, thrombosis and psychosocial factors in the genesis of CAD are reviewed, as well as the evidence supporting the synergistic hazard presented by risk-factor clusters. High-density lipoprotein cholesterol bears an inverse, protective relation to CAD. Factors affecting high-density lipoprotein levels, e.g., obesity/exercise, cigarette smoking, alcohol consumption and postmenopausal use of estrogen in women, are also reviewed in light of recent findings. Additional investigation is necessary to clarify the benefits and risks associated with the treatment or modification of known risk factors and to identify others.

Language of Publication

English

Unique Identifier

86127055

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MeSH Heading (Major)

Arteriosclerosis|*ET; Atherosclerosis|EP/*ET

MeSH Heading

Adult; Aged; Alcohol Drinking; Coronary Disease|ET; Diabetes Mellitus|CO; Estrogens|AE; Female; Human; Hyperlipidemia|CO; Hypertension|CO; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Male; Menopause; Middle Age; Obesity|CO; Risk; Smoking; Social Support; Support, U.S. Gov't, P.H.S.; Thrombosis|CO; Type A Personality

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 24 from database: MEDLINE
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Title

Factors affecting the rate of catalyzed transfer of cholesteryl esters in plasma.

Author

Fielding CJ

Address

Source

Am Heart J, 1987 Feb, 113:2 Pt 2, 532-7

Abstract

The transfer of cholesteryl esters generated by lecithin-cholesterol acyltransferase to low- and very low-density lipoproteins is greatly modified under different physiologic and pathologic conditions. A major factor determining transfer rates is the level of unesterified cholesterol in the acceptor lipoproteins. Low cholesteryl ester transfer rates are characteristic of several groups at increased risk for coronary artery disease. This appears to reflect a systematic abnormality of free cholesterol metabolism and transport in these groups.

Language of Publication

English

Unique Identifier

87124380

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MeSH Heading (Major)

Cholesterol Esters|*BL/ME

MeSH Heading

Biological Transport; Catalysis; Coronary Disease|BL/ME; Human; Hypercholesterolemia, Familial|BL/ME; Phosphatidylcholine-Sterol O-Acyltransferase|BL/ME; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-8703

Country of Publication

UNITED STATES

Record 25 from database: MEDLINE
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Title

Lipid markers for atherosclerosis.

Author

Kottke BA

Address

Source

Am J Cardiol, 1986 Feb, 57:5, 11C-17C

Abstract

Atherogenesis results from the simultaneous occurrence of 2 important processes: platelet-endothelial interaction, with its consequences mediated by the platelet-derived growth factor, and lipid accumulation. Lipid accumulation results from the balance or imbalance of cellular uptake of lipoproteins versus the removal of cholesterol esters. Uptake results from activity of the low-density lipoprotein (LDL) receptor of smooth muscle cells and fibroblasts, modified LDL receptor and remnant receptors of macrophages. Cholesterol-ester removal is regulated by apolipoprotein A-l. Low levels of apolipoprotein A-l are found in most patients with clinically significant coronary artery disease, suggesting that defects in cellular cholesterol ester removal may play an important role in atherogenesis.

Language of Publication

English

Unique Identifier

86127054

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MeSH Heading (Major)

Arteriosclerosis|*ET; Atherosclerosis|*ET/ME; Lipids|*ME

MeSH Heading

Apolipoproteins A|AN/GE/ME; Binding Sites; Cholesterol|ME; Endothelium|ME; Human; Lipoproteins|ME; Macrophages|PH; Receptors, LDL|AN

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 26 from database: MEDLINE
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Title

Effects of fibric acid derivatives on biliary lipid composition.

Author

Palmer RH

Address

Columbia University College of Physicians and Surgeons, New York, New York.

Source

Am J Med, 1987 Nov, 83:5B, 37-43

Abstract

Fenofibrate, a potent analogue of clofibrate, causes changes in biliary lipid composition similar to those seen with clofibrate and other derivatives of fibric acid, although there is a suggestion that the increase in cholesterol content may be accompanied by an increase in phospholipid content as well as a decrease in bile acid content. This may favor liquid crystal formation, and fenofibrate may have less propensity to cause gallstones than would other derivatives. Many other factors are also important in determining whether supersaturated bile will result in gallstone formation, and the use of this compound should be monitored in the future to determine the clinical importance of these findings.

Language of Publication

English

Unique Identifier

88074435

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MeSH Heading (Major)

Clofibrate|*AA/TU; Hypercholesterolemia, Familial|*DT; Procetofen|*TU; Propionates|*TU

MeSH Heading

Antilipemic Agents|TU; Bezafibrate|TU; Clinical Trials; Clofibric Acid|AA/TU; Comparative Study; Double-Blind Method; Female; Human; Male; Random Allocation; Support, U.S. Gov't, P.H.S.

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES

ISSN

0002-9343

Country of Publication

UNITED STATES

Record 27 from database: MEDLINE
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Title

Ocular complications of Tangier disease.

Author

Pressly TA; Scott WJ; Ide CH; Winkler A; Reams GP

Address

Department of Medicine, University of Missouri-Columbia.

Source

Am J Med, 1987 Nov, 83:5, 991-4

Abstract

Tangier disease, or familial high-density lipoprotein deficiency, is an inherited disorder resulting in tissue deposition of excessive cholesterol esters. Although associated corneal clouding has been reported to produce little visual impairment, this patient with Tangier disease had corneal clouding, decreased corneal sensation, and cicatricial ectropion and experienced slowly progressive marked visual impairment. All ocular cases of Tangier disease are reviewed. Ectropion and incomplete eyelid closure may precede corneal clouding and should be recognized as signs associated with Tangier disease. The combination of exposure keratopathy and corneal infiltration can cause significant visual impairment.

Language of Publication

English

Unique Identifier

88046920

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MeSH Heading (Major)

Corneal Opacity|*ET; Ectropion|*ET; Hypolipoproteinemia|*CO; Tangier Disease|*CO/GE; Vision Disorders|*ET

MeSH Heading

Aged; Case Report; Human; Male

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES

ISSN

0002-9343

Country of Publication

UNITED STATES

Record 28 from database: MEDLINE
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Title

Mechanisms of atherogenesis.

Author

Clarkson TB; Weingand KW; Kaplan JR; Adams MR

Address

Source

Circulation, 1987 Jul, 76:1 Pt 2, I20-8

Abstract

Recently the nature of the cellular and molecular events in atherogenesis have been elucidated better. Some of these findings may be important in explaining individual differences in susceptibility to atherosclerosis that are independent of known risk factors. Nonhuman primates are valuable models for the study of mechanisms of diet-induced atherosclerosis. Cynomolgus macaques are useful for studies of male-female differences in atherosclerosis, since they share with premenopausal white women a relative protection against coronary atherosclerosis compared with males. These animals are also useful for psychosocial atherosclerosis research since social status affects the extent of atherosclerosis, and experimentally induced social stress increases extent of coronary artery atherosclerosis. Nonhuman primates have also been useful for studies of individual differences in susceptibility to diet-induced atherosclerosis and its risk factors. These studies have indicated that about 75% of the variability in the plasma cholesterol response to dietary cholesterol is attributable to genetically determined differences in cholesterol absorption and lipoprotein catabolism. There is preliminary evidence suggesting the existence of "mesenchymal susceptibility" in nonhuman primates; i.e., differences in risk of atherosclerosis that are independent of exposure to known risk factors. Efforts are being made to establish colonies of rhesus monkeys that possess contrasting degrees of mesenchymal susceptibility.

Language of Publication

English

Unique Identifier

87244813

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MeSH Heading (Major)

Arteriosclerosis|*ET; Atherosclerosis|*ET/PX; Diet, Atherogenic|*; Stress, Psychological|*CO

MeSH Heading

Animal; Cholesterol, Dietary|ME; Human; Macaca; Risk; Sex Factors; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0009-7322

Country of Publication

UNITED STATES

Record 29 from database: MEDLINE
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Title

Relationship of intermediate and low-density lipoprotein subspecies to risk of coronary artery disease.

Author

Krauss RM

Address

Source

Am Heart J, 1987 Feb, 113:2 Pt 2, 578-82

Abstract

Recent studies have shown that heterogeneity of human plasma low-density lipoproteins (LDL) is, in part, the result of production of different LDL products from two subspecies of intermediate-density lipoproteins (IDL). Cholesterol-enriched forms of both IDL species are found in plasma of patients with atherogenic dyslipidemias (familial hypercholesterolemia and type 3 hyperlipoproteinemia) and have physical properties similar to the major species in plasma of cholesterol-fed monkeys. Patients with familial combined hyperlipidemia have been shown to have increased plasma levels of IDL and of a smaller, denser LDL subclass (LDL-IIIA) that appears to be a metabolic product of the smaller IDL subspecies. Results from the NHLBI Type II Coronary Intervention study have supported a link between the small IDL-LDL pathway and coronary disease, in that 2-year changes in levels of these species were associated with disease progression. Furthermore, therapeutic reductions in IDL levels were correlated with increases in high-density lipoprotein cholesterol. Thus variation in IDL levels might influence coronary disease risk by both a direct effect and indirectly by affecting LDL particle number and possibly high-density lipoprotein metabolism.

Language of Publication

English

Unique Identifier

87124389

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MeSH Heading (Major)

Coronary Disease|BL/*ET; Lipoproteins|*BL/ME; Lipoproteins, LDL|*BL/ME

MeSH Heading

Human; Risk; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-8703

Country of Publication

UNITED STATES

Record 30 from database: MEDLINE
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Title

High-density lipoprotein turnover.

Author

Nestel PJ

Address

Source

Am Heart J, 1987 Feb, 113:2 Pt 2, 518-21

Abstract

High-density lipoprotein (HDL) metabolism has been reviewed from information derived from turnover studies in humans. The two major HDL apoproteins AI and AII have different removal rates, reflecting the faster catabolism of HDL2 than of HDL3. This is caused by the continual cycle of formation of HDL2 from HDL3 and its reversion to HDL3, in response to the need to transport cholesterol and other lipids from extrahepatic cells and catabolized triglyceride-rich lipoproteins. The conversion of HDL2 to HDL3 is mediated through a hepatic lipase. Because this lipase is inhibited by estrogen and stimulated by androgens, women have higher HDL2 levels than men. The synthesis of apoproteins AI and AII is also higher in women than in men. Nutrition also influences HDL turnover. Carbohydrates increase AI and HDL2 removal, whereas polyunsaturated fatty acids inhibit synthesis. Vegetarians show high HDL removal rates. Thus low-fat, low-cholesterol diets generally lead to lower HDL levels. Disorders that alter HDL composition (such as alcoholic liver disease or Tangier disease) accelerate HDL removal. Other HDL proteins such as apoproteins C and E show faster turnover rates than AI and AII, since the former exchange with triglyceride-rich lipoproteins and participate in their catabolism. Diminished exchange of apoprotein C from HDL to chylomicrons may be responsible for the diminished catabolism of these particles in type V hyperlipoproteinemia. The unusual turnover characteristics of HDL apoprotein AIV are reviewed, suggesting a dual role for this protein in both triglyceride and cholesterol transport. The striking relationship between very low-density lipoprotein (VLDL) and HDL metabolism is expressed in an inverse association between their respective removal rates.(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

87124377

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MeSH Heading (Major)

Lipoproteins, HDL|BL/*ME

MeSH Heading

Human; Kinetics; Lipoproteins, VLDL|BL/ME

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0002-8703

Country of Publication

UNITED STATES

Record 31 from database: MEDLINE
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Title

Thrombin binding and response in platelets from patients with dyslipoproteinemias: increased stimulus-response coupling in type II hyperlipoproteinemia.

Author

Harmon JT; Tandon NN; Hoeg JM; Jamieson GA

Address

Source

Blood, 1986 Aug, 68:2, 498-505

Abstract

Platelets were obtained from patients with various hyperlipidemias [type II, type V, lecithin-cholesterol acyltransferase (LCAT) deficiency] and hypolipidemias (abetalipoproteinemia, Tangier disease) to ascertain relationships among plasma lipids, platelet lipids, thrombin binding and thrombin-induced platelet aggregation, and to compare these data with those previously obtained on stimulus-response coupling in platelets following in vitro modification of membrane microviscosity. Washed platelets were studied for their ability to bind 125I-thrombin in the range of 10(-10) to 10(-6) mol/L (10 mU/mL to 100 U/mL) and to aggregate with thrombin at concentrations less than 10(-9) mol/L (100 mU/mL). The values for binding and aggregation in eight patients from six kindred with familial hypercholesterolemia, taken as a group, fell in the low normal range. If divided into two groups, patients with overt cardiovascular disease bound normal amounts of thrombin but were more responsive to it, whereas patients without overt cardiovascular disease bound lower amounts of thrombin but gave an aggregation response in the normal range. These results suggest that platelet hyperresponsiveness in familial hypercholesterolemia arises from an alteration in the coupling mechanism between thrombin binding and response such that platelets from patients with familial hypercholesterolemia are able to respond with lower receptor occupancy than is the case with normal platelets. Thrombin binding and aggregation were within normal ranges for platelets from abetalipoproteinemia patients (N = 4) and type V hyperlipoproteinemia (N = 2), although in the latter case the response appeared to be less at very low thrombin concentrations (less than 30 mU/mL). Thrombin binding was elevated in Tangier disease (N = 3) but with lower responsiveness at lower thrombin concentrations. Thrombin binding was also elevated in LCAT deficiency (N = 2), and one patient showed increased and another showed decreased aggregation responses. In general, increased plasma cholesterol levels resulted in increased stimulus-response coupling (type II), whereas increased triglyceride levels resulted in decreased coupling (type V, Tangier), and there was no apparent alteration in the coupling mechanism with overall reduction in plasma lipid levels as in abetalipoproteinemia.

Language of Publication

English

Unique Identifier

86270433

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MeSH Heading (Major)

Blood Platelets|*ME; Blood Protein Disorders|*BL; Lipoproteins|*BL; Thrombin|*ME

MeSH Heading

Abetalipoproteinemia|BL; Adult; Female; Human; Hypercholesterolemia, Familial|PP; Lecithin Acyltransferase Deficiency|PP; Male; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0006-4971

Country of Publication

UNITED STATES

Record 32 from database: MEDLINE
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Title

Lipoproteins and apolipoproteins. Composition, metabolism, and association with coronary heart disease.

Author

Rifai N

Address

Source

Arch Pathol Lab Med, 1986 Aug, 110:8, 694-701

Abstract

Apolipoproteins play major roles in regulating lipoprotein synthesis and catabolism. Apolipoprotein AI activates the lecithin cholesterol acyltransferase, apolipoprotein CII and CIII regulate the lipoprotein lipase, and apolipoprotein B-100, B-48, and E control the cholesterol uptake into hepatic and extrahepatic cells. Therefore, investigating the alterations of lipoprotein metabolism in disease states at the apolipoprotein level may give increased insight into the underlying mechanisms of lipoprotein changes and provide better understanding about the premature development of the atherogenic process.

Language of Publication

English

Unique Identifier

86268300

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MeSH Heading (Major)

Apolipoproteins|BI/BL/*PH; Lipoproteins|*ME

MeSH Heading

Cholesterol|AE; Coronary Disease|ET; Human; Liver|ME

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0003-9985

Country of Publication

UNITED STATES

Record 33 from database: MEDLINE
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Title

An approach to the management of hyperlipoproteinemia.

Author

Hoeg JM; Gregg RE; Brewer HB Jr

Address

Source

JAMA, 1986 Jan, 255:4, 512-21

Abstract

Recent clinical trials indicate that reduction of plasma cholesterol concentrations in individuals with increased levels of low-density lipoproteins reduces their risk of myocardial infarction and death. Therefore, the question of "whether to treat" should be shifted to "whom to treat" and "how best to treat". The understanding of normal lipid transport via the plasma lipoproteins has grown to a sophisticated level over the past 20 years. Plasma cholesterol, required for cellular membrane integrity, and plasma triglycerides, the primary mammalian energy source, are carried in lipoprotein particles that vary in size, density, lipid composition, and apolipoprotein content. Some lipoprotein particles (low-density lipoproteins) play a causal role in the atherosclerotic process, while other particles (high-density lipoproteins) appear to prevent this process. Utilizing this understanding of the plasma lipoproteins, a systematic approach to the management of the patient with hyperlipoproteinemia has been developed which may lead to the normalization of plasma lipoprotein concentrations in the majority of hyperlipoproteinemic patients.

Language of Publication

English

Unique Identifier

86089520

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MeSH Heading (Major)

Hyperlipoproteinemia|BL/DI/*TH

MeSH Heading

Anticholesteremic Agents|TU; Cholesterol|BL; Human; Hypercholesterolemia|DT; Hyperlipidemia|TH; Lipids|ME; Lipoproteins|ME; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL|BL; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0098-7484

Country of Publication

UNITED STATES

Record 34 from database: MEDLINE
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Title

Effect of alcohol on cellular membranes.

Author

Goldstein DB

Address

Source

Ann Emerg Med, 1986 Sep, 15:9, 1013-8

Abstract

Ethanol disrupts the physical structure of cell membranes. The most fluid membranes, including those that are low in cholesterol, are the most easily disordered by ethanol. Although the membrane-disordering effect is small, there is pharmacological, temporal, and genetic evidence that it is important. Animals that are resistant to ethanol intoxication because of their genetic background or because of previous exposure to ethanol are found to have brain membranes that are not easily disordered in vitro. An exception is the increased behavioral sensitivity in aging animals, which is not matched by changes in their membranes. When animals are treated chronically with ethanol, their membranes become stiffer, a response that can be regarded as adaptive. Ethanol may favor the uptake of cholesterol or saturated fatty acids into membranes, thus reducing its own effect.

Language of Publication

English

Unique Identifier

86293883

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MeSH Heading (Major)

Cell Membrane|*DE; Ethanol|*PD

MeSH Heading

Aging; Alcoholism|GE; Animal; Human; Membrane Lipids|ME; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0196-0644

Country of Publication

UNITED STATES

Record 35 from database: MEDLINE
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Title

Atherosclerosis and lipoprotein metabolism: role of reverse cholesterol transport.

Author

Roheim PS

Address

Source

Am J Cardiol, 1986 Feb, 57:5, 3C-10C

Abstract

To understand the complexity of lipoprotein metabolism and its influence on atherosclerosis, one must be aware of the physiologic characteristics and functions of the different lipoprotein classes, apolipoproteins and enzymes. Understanding of the dynamics of cholesterol and lipoprotein metabolism, especially reverse cholesterol transport, will aid in finding a means of preventing and reversing the atherosclerotic process.

Language of Publication

English

Unique Identifier

86127058

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MeSH Heading (Major)

Arteriosclero