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At least 451 records · Page 25Linked to original sources
PubMed1992

Ask the Pharmacist.

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Cholestyramine Resin↗
PubMed1992

A retrospective review of the use of lipid-lowering agents in combination, specifically, gemfibrozil and lovastatin.

We conducted a retrospective review examining lipid profiles, creatine phosphokinase (CK) levels, and alanine aminotransferase levels (ALT) in patients receiving the combination of gemfibrozil and lovastatin. Serum lipid levels were significantly improved with therapy over those before therapy. Of the 70 patients receiving the combination, 5 experienced mild elevations in CK, 1 a mild elevation in ALT, and 1 mild elevations in both. No patient reported muscle weakness or muscle pain. The combination of these two medications appeared to be at least additive, highly effective, and well tolerated. The mean total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels decreased from 278, 306, and 180 mg% to 200, 151, and 129 mg%, respectively, and the mean high-density lipoprotein cholesterol levels increased from 34 to 40 mg%. This retrospective data analysis suggests that the combination of gemfibrozil and lovastatin may be safe in patients with normal renal function when the dosage of lovastatin is limited and when CK and ALT levels are monitored carefully.

Aged↗
PubMed2005

A bitter tale.

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Anion Exchange Resins↗
PubMed1991

[Small doses of the resin Colestid in the treatment of hyperlipoproteinemia].

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

Colestipol↗
PubMed1990

Regression of coronary atherosclerosis during treatment of familial hypercholesterolemia with combined drug regimens.

We conducted a randomized, controlled trial in 72 patients with heterozygous familial hypercholesterolemia to test whether reducing plasma low-density lipoprotein levels by diet and combined drug regimens can induce regression of coronary lesions. Four hundred fifty-seven lesions were measured before and after a 26-month interval by computer-based quantitative angiography. The primary outcome variable was within-patient mean change in percent area stenosis. Mean low-density lipoprotein cholesterol levels decreased from 7.32 +/- 1.5 to 4.45 +/- 1.6 mmol/L. The mean change in percent area stenosis among controls was +0.80, indicating progression, while the mean change for the treatment group was -1.53, indicating regression (P = .039 by two-tailed t test for the difference between groups). Regression among women, analyzed separately, was also significant. The change in percent area stenosis was correlated with low-density lipoprotein levels on trial. We conclude that reduction of low-density lipoprotein cholesterol levels can induce regression of atherosclerotic lesions of the coronary arteries in patients with familial hypercholesterolemia. The anticipation of benefit from treatment applies to women and men alike.

Adult↗
PubMed1990

The effects of simvastatin on serum lipoproteins in severe hypercholesterolaemia.

The effects of simvastatin, an inhibitor of cholesterol synthesis, on serum lipids, lipoprotein composition and apolipoproteins were evaluated in a total of 50 patients with hypercholesterolaemia. In the first study, 24 patients (mean serum cholesterol 10.74 +/- 1.59 mmol/l) were treated with simvastatin 40 mg daily for 24 wk. Serum cholesterol and low density lipoprotein (LDL) cholesterol decreased to average values 29-36% and 35-42% below the basal value, respectively. Serum triglycerides decreased by 16-28%, and high density lipoprotein (HDL) cholesterol increased by 6-11%. Apolipoprotein A-I concentration increased 6-8% and that of apolipoprotein B decreased 29-33%. The composition of LDL remained unchanged whereas the very low density lipoproteins became enriched in triglycerides. Lipoprotein Lp(a) was not affected. In the second study 26 patients (mean serum cholesterol 12.35 +/- 2.05 mmol/l) were treated with simvastatin 40 mg daily as monotherapy or combined with a bile acid binding resin for 2 yr. Serum cholesterol levels decreased to values which remained stable throughout the entire study period; after 2 yr this decrease amounted to 43%. Compared to monotherapy, combination therapy yielded a further 12% decrease of cholesterol. In the entire group, triglycerides decreased by 16% and HDL cholesterol increased by 9%. Side effects were limited to slight increases in alanine aminotransferase and creatine phosphokinase in some patients. Simvastatin appears to be an important asset in the treatment of hypercholesterolaemia.

Adult↗
PubMedDate not supplied

Treatment of familial hypercholesterolemia with drugs in children.

We assessed plasma lipid levels in children and adolescents who were on various drug regimens and who were attending a specialized lipid treatment center. All subjects had familial hypercholesterolemia (FH), and the study group included 30 subjects with heterozygous (He) and three with homozygous (Ho) FH. In the 30 He FH subjects treated with 5 to 30 g/day of a bile-acid-binding resin, plasma lipid levels were still substantially above optimal (less than or equal to 50th percentile for age and sex), although statistically significant (p less than 0.001) reductions in total and low density lipoprotein (LDL) cholesterol of 15% and 21% compared with baseline were achieved. In eight subjects who received resin plus niacin, additional reductions in total and LDL cholesterol of 15% and 17%, respectively, were achieved. Even though the combination therapy produced reductions in total, LDL, and LDL/high density lipoprotein cholesterol of 29%, 37%, and 47%, respectively, compared with baseline, resulting absolute levels were still well above optimal. Six subjects with severe He FH received a 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor (lovastatin, 80 mg/day or simvastatin, 40 mg/day), and substantial total and LDL cholesterol reductions on the order of 35% and 41%, respectively, were found compared with diet alone. The decreases were substantially greater than those achieved with either resin or resin plus niacin. In a number of these subjects, absolute lipid levels were approaching optimal levels. In the three Ho FH subjects, the response to HMG CoA reductase inhibitors was variable but generally poor.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗