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)

The formation of deoxycholic acid (D) was studied in 8 patients with Type II hyperlipoproteinaemia and in 6 with Type IV hyperlipoproteinaemia, using orally administered [2.4--3H]cholic acid and [24--14C]deoxycholic acid. The diet was standardized and of natural type. The mean values for fractional turnover, pool size and D synthesis in the patients with Type II pattern were 0.23 days-1, 331 mg and 75 mg/day, respectively; in Type IV they were 0.39 days-1, 587 mg and 191 mg/day. Compared with a group of healthy subjects, the pool size and formation of D were normal in Type IV, but significantly reduced in Type II. The mean conversion of cholic acid into the circulating pool of D was calculated to be 37% in Type II, and 38% in Type IV patients. Both these values are within normal limits.
Atherosclerosis
PMID:The formation of deoxycholic acid in patients with type II and IV hyperlipoproteinaemia. 18 86

Determination of serum cholesterol values in three populations of children and adolescents, totalling 4013 subjects aged 1 month to 20 years, revealed 16 cases of primary hyperbetalipoproteinemia (overall frequency, 1:251) and led to the detection of the disorder in 12 asymptomatic siblings. The upper limit of normal for serum cholesterol concentration was approximately 200 mg/dl at all ages studied. Dietary treatment was instituted in patients whose serum cholesterol value exceeded this limit and in whom a primary lipid defect was confirmed; the serum cholesterol value decreased in all patients who adhered to the diet. However, since the potential hazards and long-term results of dietary treatment, with or without drug therapy, in growing children are not known, such treatment should be reserved for affected children with a family history of premature atherosclerosis, and follow-up is essential.
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PMID:Primary hyperlipoproteinemia in childhood and adolescence: identification and treatment of persons at risk for premature atherosclerosis. 18 9

Some patients with familial hypercholesterolemia (FHC, type II) are highly responsive to the cholesterol-lowering effect of clofibrate, while others are not only resistant to this effect but may even show an increase in plasma beta-lipoproteins. In an attempt to find an explanation for these striking differences, we have studied the pharmacokinetics of clofibrate in FHC patients at both extremes of responsiveness. The results disclosed several major differences between the two groups. Plasma clofibric acid (CPIB) measured during the chronic administration of the drug was significantly higher in the responders than in the non-responders, whether all patients in each group or only those with tendon xanthomas were considered. Plasma CPIB concentrations were negatively correlated with body weight in the responders but not in CPIB-resistant patients. They were also inversely proportional to decreases in plasma beta-lipoprotein cholesterol after chronic clofibrate administration in the responsive group, but directly proportional to increases in the non-responders. Increasing the dose of clofibrate from 2 to 3 g/day in CPIB-resistant patients always resulted in an increase in plasma CPIB levels, but this was followed in some patients by a decrease and in others by an increase in plasma beta-lipoprotein cholesterol concentrations, so that the overall effect was not statistically significant. The half-life of plasma CPIB was measured over 48 h after a single 1-g dose of clofibrate in patients who had not received this drug for at least 3 weeks. Half-life was significantly longer in the responsive patients. In addition, the bioavailability and the rate of absorption of clofibrate tended to be higher in this group than in the resistant patients. We suspect that both groups differ not only in the metabolic handling of clofibrate but also in some aspect of their beta-lipoprotein cholesterol metabolism.
Atherosclerosis 1977 Apr
PMID:Pharmacokinetics of clofibrate in familial hypercholesterolemia. 19 24

The examination was conducted in 1048 patients with the ischaemic heart disease. Both males, and females displayed most frequently Type II hyperlipidemia. Type IV was more frequent in males, than in females. The incidence of Types IIa and IIb depended on the stage of coronary atherosclerosis, the age and sex of the patients. The concomitant diseases were found to influence the incidence of hyperlipidemia. Among the tested drugs administered in a course of therapy of 4 weeks atromidine proved to be most effective for the examined types of hyperlipidemia (IIa, IIb, IV). Hyperlipidemia relapsed in 1/3 of the patients within 1 year.
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PMID:[Drug treatment of hyperlipemia in middle-aged and old persons with ischemic heart disease]. 19 32

The author studied the influence of testosterone metabolite--5alpha-androstan-3beta,17beta-diol--on the development of hyperlipidemia and atherosclerosis in chinchilla rabbits given cholesterol-free semisynthetic atherogenic diet. The metabolite under study inhibited the development of hypercholesterolemia and hyperbetalipoproteinemia and decreased blood phospholipid content in the blood serum of experimental animals below the initial level. Lipid content in the sum total fraction of pre-beta and beta-lipoproteins decreased under the effect of the mentioned metabolite; there was also a fall in the amount of lipoproteins of low density and their greater saturation with cholesterol. Development of experimental atherosclerosis was intensified.
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PMID:[Effect of 5alpha-androstan-3beta, 17beta-diol on serum lipids and lipoproteins and the development of experimental atherosclerosis]. 19 69

Plasmapheresis was studied as a means of reducing the serum cholesterol concentration in 3 hypercholesterolemic patients who each underwent courses of intensive plasmapheresis with removal of 250--500 ml of plasma each day for 5--9 days. In one homozygous Type II patient, the serum cholesterol concentration decreased from 609 +/- 45 mg/100 ml (mean +/- SEM) to 365 +/- 17 mg/100 ml (40% decrease, P less than 0.05) with two different courses of plasmapheresis. In the two other patients with non-homozygous hyperbetalipoproteinemia the serum cholesterol concentration decreased from 289 +/- 27 mg/100 ml to 205 +/- 19 mg/100 ml (29% decrease, p less than 0.05). After cessation of treatment, the cholesterol concentration returned to pre-treatment levels in 10--13 days in the homozygous patient and 7 days in one non-homozygous hyperbetalipoproteinemic patient; clofibrate (2 g/day) in this patient was associated with a smaller reduction of the cholesterol concentration with plasmapheresis and an increased rate of return of pre-treatment levels after plasmapheresis was stopped. Sustained plasmapheresis for 6 days in the other non-homozygous hyperbetalipoproteinemic patient resulted in a new approximate "steady state" with a serum cholesterol concentration of 176--199 mg/100 ml compared with a pre-plasmapheresis value of 227 mg/100 ml. The response of the plasma cholesterol levels to plasmapheresis was subjected to kinetic analysis based on a current model of the regulation of lipoprotein metabolism.
Atherosclerosis 1978 Oct
PMID:Effect of intessive plasmapheresis on the plasma cholesterol concentration with familial hypercholesterolemia. 21 70

Coronary arteriographic findings, plasma lipid and lipoprotein levels, and cigarette smoking history are reported for the first 101 male post myocardial infarction survivors who have been entered into the POSCH clinical trial. Estimates of the extent of stenosis in the major coronary arteries were made using 4 models ranging from a simple determination of the number of the 3 major vessels having significant (i.e. 50% or greater stenosis) disease to more complex methods of determining overall extent of disease in 14 major segments of the coronary arteries. Age was shown to be an important factor in the extent of vessel disease. When controlling for age, plasma cholesterol and LDL-cholesterol levels were shown to be related to the extent of disease, especially in Type II hyperlipoproteinemia subjects. Multiple linear regression analysis demonstrated that age and LDL-cholesterol had positive associations and HDL-cholesterol had an inverse association with the coronary artery disease indices. In this comparatively "healthy" subgroup of the overall population of first MI survivors the major CHD risk factors are limited to plasma lipids and cigarette smoking. This preliminary report of 10% of the recruitment objective of the project supports the currently held views of the lipid--atherosclerosis hypothesis regarding the effects of age-total plasma cholesterol, LDL--cholesterol, and HDL--cholesterol on the extent of coronary atherosclerotic plaques, as determined by coronary arteriography.
Atherosclerosis 1979 Feb
PMID:Plasma lipoproteins and coronary arteriography in subjects in the program on the surgical control of the hyperlipidemias. Preliminary report. 22 1

Seventeen ambulant outpatients with familial Type IIa or Type IIb hyperlipoproteinaemia were treated with Cynarin, the 1,5-dicaffeyl ester of quinic acid, the constituent of the artichoke (Cynara scolymus). The dose tested was 250 mg and 750 mg daily. The mean serum cholesterol and triglyceride concentrations were not significantly changed within 3 months. Cynarin, administered per os, has no hypolipidaemic effect in familial Type II hyperlipoproteinaemia.
Atherosclerosis 1977 Feb
PMID:Inefficiency of cynarin as therapeutic regimen in familial type II hyperlipoproteinaemia. 57 9

Individuals with familial hyperbetalipoproteinemia are at increased risk of premature atherosclerosis and thrombosis. Although there is controversy whether platelet survival is shortened or normal in this disease, several in vitro tests of platelet function are abnormal including a decreased threshold concentration for stimulation of aggregation by ADP, epinephrine and collagen and increased release of nucleotides to the same agents. These functional changes are accompanied by an increase of cholesterol to phospholipid ratio in the platelet membrane and in low density lipoprotein in individuals with type IIa hyperlipoproteinemia. Clofibrate and halofenate reverse some of the abnormalities in vitro and the former drug, when administered for 6 weeks to patients with type IIa hyperlipoproteinemia decreases platelet sensitivity to ADP and epinephrine. The platelet hypersensitivity to aggregating agents can be reproduced in vitro by increasing the cholesterol to phospholipid rather in normal platelets. These artificially hypersensitive platelets can be returned to normal by halofenate in vitro. Incorporation of cholesterol into platelet membranes increases the basal level of the membrane associated enzyme adenylate cyclase. However, the enzyme no longer responds to stimulation by prostaglandin E1, and this is associated with relative resistance of the platelet to inhibition by this pharmacologic agent. These functional alterations produced by cholesterol enrichment of platelet membranes occur is parallel with an increase in platelet membrane microviscosity suggesting that the more rigid membrane can alter the behavior of membrane associated enzymes and receptors. A correlation appears to exist between the ability of certain drugs to induce phase separation in model membranes and the potency in inhibitory platelet aggregation.
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PMID:Platelet function in hyperbetalipoproteinemia. 58 Sep 82

This chapter has demonstrated the diagnostic capability and feasibility of documenting functional abnormalities during dynamic stress in a pediatric population. The overview confirms that a controlled exercise procedure can be performed routinely in ambulatory children with or without cardiovascular disease and should be included in the clinical evaluation of specific lesions. It now appears that the primary indications for noninvasive exercise testing in the pediatric population include the following disorders: 1. Left ventricular outflow obstructions, a. Subvalvar obstructions, b. Valvar obstructions, c. Supravalvar obstructions, d. Idiopathic hypertrophic subaortic stenosis, e. Coarctation of the aorta; 2. Chronic left or right ventricular volume overload, a. Atrioventricular or semilunar valve incompetence, b. Left-to-right shunts; 3. Rhythm and conduction disturbances, a. Postoperative ventriculotomy, b. Bradytachyarrhythmias, c. Arrhythmias in patients with or without symptoms. The role of the exercise procedure is not yet established in the following areas: 1. Patients with family history of premature atherosclerosis or Type II hyperlipoproteinemia; 2. Patients with elevated blood pressure; 3. The evaluation of syncope, chest pain, or atypical findings on physical examinations (especially in athletes). Consequent upon increased interest and improved technology, the role of this technique will soon be established in the invasive and noninvasive evaluation of pediatric patients with or without overt cardiovascular disease.
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PMID:Exercise testing in children and young adults: an overview. 70 68


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