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At least 415 records · Page 23Linked to original sources
PubMed1989

Normalization of LDL receptor function by lymphocytes of patients with heterozygous familial hypercholesterolemia after treatment with plasma cholesterol lowering agents.

Low density lipoprotein (LDL)-dependent growth of mitogen-activated lymphocytes, inhibited in their capacity to synthesize cholesterol endogenously, can be used as an assay of functional receptors for LDL. Using this technique, abnormalities can be detected in circulating lymphocytes obtained from patients with familial hypercholesterolemia (FH). Functional lymphocyte LDL receptor activity was decreased in patients with heterozygous FH. Following treatment with the specific inhibitor of cholesterol synthesis, lovastatin, alone or in combination with a bile acid-binding resin, there was increased expression of functional lymphocyte LDL receptors in five of nine patients. Plasma LDL cholesterol levels decreased in all nine patients. Three other patients who were only studied while receiving therapy also manifested increased expression of functional lymphocyte LDL receptors. The degree of improvement in plasma LDL cholesterol did not predict the effect on lymphocyte LDL receptor function. Longitudinal studies indicated that an increase in functional LDL receptor activity could be observed with 4 weeks of therapy and persisted for at least 18 months on continuous treatment. These results provide direct evidence that therapy with lovastatin and a bile acid-binding resin can lead to increased expression of functional LDL receptors by lymphocytes in the majority (eight of 12) of patients with heterozygous FH.

Anticholesteremic Agents↗
PubMed1995

Treatment of the patient with primary familial heterozygous hypercholesterolemia.

Familial heterozygous hypercholesterolemia (FH) is a genetically linked lipid disorder that involves elevations in total cholesterol and LDL cholesterol. About 5% of patients with coronary heart disease have FH. Treatment options include dietary therapy, weight optimization, exercise, and drug treatment. A case study of a patient who has undergone 4 years of treatment for FH after a diagnosis of coronary heart disease is presented. Nursing care was instrumental in the patient's compliance with and adherence to the treatment plan.

Aged↗
PubMed1986

The influence of hypercholesterolaemia on the adrenal uptake and metabolic handling of 131I-6 beta-iodomethyl-19-norcholesterol (NP-59).

The biodistribution of 131I-6 beta-iodomethyl-19-norcholesterol (NP-59) was assessed in hypercholesterolaemic patients and in a rabbit model of HC to examine the alterations in the relative distribution of NP-59 and its metabolites and to explain the changes in the patterns of adrenal cortical imaging in patients with expanded cholesterol pools. Rabbits were rendered hypercholesterolaemic with a diet supplemented with 2% cholesterol for 2 weeks prior to the intravenous administration of 240 to 570 microCi of NP-59. Adrenal, bile and serum samples were obtained from four hypercholesterolaemic rabbits at 48 h following NP-59 administration, and the distribution of 131I radioactivity was compared to that of seven rabbits maintained on a standard laboratory diet. Serum cholesterol levels were 1940 +/- 248 mg dl-1 in the hypercholesterolaemic rabbits as compared to 268 +/- 62 mg dl-1 in the controls. Adrenal cortical uptake of NP-59 was decreased in HC rabbits but no significant differences were observed in the relative proportions of NP-59 or its metabolites in the bile and adrenal tissues of hypercholesterolaemic versus control animals. Hypercholesterolaemic animals did exhibit an increase in NP-59 esters in serum as compared to controls. In three of five patients with hypercholesterolaemia, adrenal uptake of NP-59 was enhanced after successful lowering of serum cholesterol levels, while the remaining two patients who responded inadequately to cholesterol-lowering therapy showed a slight drop in NP-59 uptake.

19-Iodocholesterol↗
PubMed1994

Impact of intensive lipid modulation on angiographically defined coronary disease: clinical implications.

We reviewed all randomized, controlled angiographic trials to assess the impact of intensive lipid modulation on the progression or regression of angiographically defined coronary disease. Five of seven trials satisfied selection criteria: Cholesterol-Lowering Atherosclerosis Study, Program on the Surgical Control of the Hyperlipidemias, Familial Atherosclerosis Treatment Study, Regression of Coronary Atherosclerosis During Treatment of Familial Hypercholesterolemia, and St. Thomas' Atherosclerosis Regression Study. We compared patient selection, baseline and on-trial lipid values, changes in angiographic disease scores, and clinical outcomes. In all five trials, treatment reduced levels of low-density lipoprotein (LDL) cholesterol substantially (range -32% to -46%). Treatment reduced risk of angiographic progression by almost 50% compared to controls. Furthermore, nearly one third of drug-treated patients showed angiographic regression of disease. Regression correlated well with reduction in LDL cholesterol. Although overall improvement in stenosis was modest, reduction in clinical events was impressive. Intensive lipid modulation may "stabilize" existing lesions, making them less "active" (ie, less prone to rupture or thrombosis), thereby reducing risk of acute coronary syndromes. These studies clearly support intensive lipid modulation in patients with established coronary disease.

Angiography↗
PubMed1995

An update on lipid-lowering therapy.

New information on the effects of lipid-lowering drugs is reviewed with an emphasis on special groups that benefit from specific drug therapy. Although it has been shown that the diet may further enhance the effectiveness of lipid-lowering drugs, compliance to diet and drugs remains an important issue and the large individual variations in dietary responses should be studied more extensively. The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors are safe and effective in different populations such as in women, elderly people and in special cases of secondary hyperlipidaemia. More widespread implementation of screening programmes to identify suitable patients for lipid-lowering therapy may help prevent the excess utilization of health care resources.

Aged↗
PubMed1998

Beneficial effect of a bile acid resin binder on enteral feeding induced diarrhea.

OBJECTIVES: Diarrhea is a complication of enteral feeding, occurring in up to 68% of critically ill patients. We hypothesized that prolonged fasting results in abnormal bile acid homeostasis. Subsequent enteral feeding then causes a relative luminal excess of bile acids, which leads to choleretic diarrhea. Hence, diarrhea induced by enteral feeding should improve with the use of a bile acid binding agent, such as Colestid Granules. METHODS: We evaluated the effect of Colestid on enteral feeding-induced diarrhea in a double-blind placebo-controlled study. Nineteen patients who were nil per os (NPO) for 5 days before initiation of enteral feeding were enrolled in the study and treatment continued for 7 days. The severity and frequency of diarrhea were quantified. Fecal bile acids were measured enzymatically. Stool nutrient loss was measured by fat extraction, microkjeldahl determination of nitrogen, and bomb calorimetry of dried fecal specimens. RESULTS: Enteral feeding resulted in a high frequency of diarrhea (95%) at some time during the observation period. The majority of episodes of diarrhea in both groups were of low volume. Colestid significantly decreased the prevalence and severity of diarrhea. Colestid had no significant effect on fecal calorie or nutrient losses. The average bile acid concentration in the stool increased significantly after enteral feeding. CONCLUSION: Enteral feeding-induced diarrhea is, at least in part, due to malabsorption of bile acids. The bile acid resin binding agent Colestid improves diarrhea induced by enteral feeding.

Aged↗
PubMed1990

Biochemical changes and morphological alterations of the liver in guinea-pigs after administration of simvastatin (HMG CoA reductase-inhibitor).

Simvastatin is a potent competitive inhibitor of the 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase) which is the rate-limiting enzyme of cholesterol synthesis. In guinea-pigs, administration of a high oral dose of simvastatin (125 mg/kg/day at the beginning of the study) during 18 days had a major hepatotoxic effect whereas a lower oral dose (30 mg/kg/day) did not seem to cause any liver damage. A significant reduction in microsomal Cyt P 450 content was only observed on a high dose of simvastatin whereas HMG CoA reductase activity was reduced in the group with the low simvastatin dose. The hepatic microsomal aminopyrine N-demethylase activity remained unchanged in all groups. The liver lesion was hepatocellular necrosis accompanied in some animals by a biliary duct proliferation. It was associated with a 10-fold elevation in serum aspartate and alanine aminotransferase activities, as well as a great reduction in daily food intake and body weight (28%). The hepatotoxicity of simvastatin could result from the low basal content of HMG-CoA reductase in guinea-pig liver, the prolonged inhibition of mevalonate synthesis and probably, from the absence of HMG-CoA reductase enzyme de novo synthesis.

Aminopyrine N-Demethylase↗
PubMed1989

Review of clinical studies of fenofibrate in combination with currently approved lipid-lowering drugs.

Recent trials have investigated the usefulness of fenofibrate, alone and in combination with other lipid-lowering therapies, in the treatment of hyperlipidemia. Studies of fenofibrate + bile acid sequestrants demonstrate that these two therapies may have an additive effect in reducing total cholesterol, low-density lipoprotein (LDL) cholesterol, very-low-density lipoprotein (VLDL) cholesterol and triglyceride levels in patients with hyperlipoproteinemia or familial hypercholesterolemia. These lipoprotein changes have been associated with a regression of tendon xanthoma. Pharmacokinetic studies have shown that bile acid sequestrants do not alter the absorption or the plasma levels of fenofibrate. The combined use of fenofibrate with bile acid sequestrants has been found to be comparably effective with the new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, synvinolin, with respect to the reduction of total cholesterol and LDL. Although synvinolin was more effective in lowering LDL, VLDL cholesterol and triglycerides were reduced to a greater extent with fenofibrate. Another notable difference was that fenofibrate + bile acids more markedly increased HDL levels. The combination of fenofibrate + nicotinic acid also appears to have a beneficial effect on lipoproteins. These preliminary results indicate that fenofibrate may be a useful addition to the present lipid-lowering drug armamentarium.

Anticholesteremic Agents↗
PubMed2003

Growth hormone induces low-density lipoprotein clearance but not bile acid synthesis in humans.

OBJECTIVE: Growth hormone (GH) induces hepatic low-density lipoprotein (LDL) receptors and lowers plasma cholesterol. We characterized the influence of GH treatment on plasma LDL clearance in normal humans and investigated the relative role of LDL receptor (LDLR) activity and stimulation of bile acid synthesis in subjects with different LDLR expression. METHODS AND RESULTS: Plasma clearance of autologous 125I-LDL was measured before and during 3 weeks of treatment with GH (0.1 IU/kg per day) in 9 healthy young males. Plasma LDL cholesterol was reduced by 13% and the fractional catabolic rate of LDL increased by 27%. More marked changes were seen in a patient with hypopituitarism substituted with GH (0.07 IU/kg per day) for 3 months. In a second study, GH dose-dependently reduced LDL cholesterol and increased Lp(a) levels in 3 groups of males: younger and elderly healthy subjects and heterozygous familial hypercholesterolemia (FH). No effect on bile acid synthesis measured by the plasma marker 7alpha-hydroxy-4-cholesten-3-one was observed. In an LDLR-deficient FH homozygote, LDL cholesterol was not affected by GH. CONCLUSIONS: GH treatment reduces plasma LDL cholesterol by inducing LDL clearance. In humans, LDLR expression is a prerequisite for this effect, whereas it is not related to stimulation of bile acid synthesis.

Adult↗
PubMedDate not supplied

Evaluation of human panelists in assessing coronary atherosclerosis.

The Cholesterol Lowering Atherosclerosis Study, a randomized, angiographic clinical trial, has demonstrated the beneficial effect of niacin/colestipol therapy on coronary and femoral atherosclerosis. The primary outcome was a panel-determined consensus score evaluating global coronary changes determined angiographically at 2 years. This article presents an evaluation of interreader agreement in independently assessing the status of native coronary arteries and overall coronary condition. Parameters include 1) identification of the presence of lesions and lesion changes; 2) estimation of lesion severity (percent stenosis) and amount of change in lesion severity; and 3) global assessment of change in coronary status. Readers independently agreed on 1) presence of lesions (82%) and change in lesions (51%); 2) percent stenosis +/- 10% (76%) and change in stenosis +/- 10% (81%); and 3) global assessment of change in coronary status within one step (96%). Results of these analyses may be useful in effectively designing angiographic trials that use a panel of human evaluators as well as computerized methods for angiographic interpretation.

Adult↗