No abstract available.
Humans ; Hypercholesterolemia* ; Lovastatin*

No abstract available
Fluorouracil* ; Lovastatin* ; Stomach Neoplasms* ; Stomach* ; Thymidylate Synthase

BACKGROUND: This study was designed to evaluate the clinical efficasy of lovastatin, HMG-CoA reductase inhibitor, in patients with hypercholesterolemia. METHODS AND RESULTS: Lovastatin 20 to 80 mg were administered once daily for 12 weeks in twenty five patients(11 male, 14 famale ; nine patients with familial hypercholesterolemia) with hypercholesterolemia(>240mg/dl). Compared with pretreatment levels, lovastatin significantly decreased levels of total cholesterol(309+/-46mg/dl versus 201+/-37mg/dl) by 35%, LDL-cholesterol(230+/-48mg/dl versus 125+/-40mg/dl) by 46% and triglyceride(170+/-76 versus 142+/-66mg/dl) by 11% (p<0.05) with significantly decreased levels of total-cholesterol/HDL-cholesterol ratio(7.4+/-2.1 versue 4.6+/-1.5) and LDL-cholesterol/HDL-cholesterol ratio(5.6+/-1.9 versue 2.9+/-1.4) (p<0.005 except triglyceride, respectively). The level of Apo B(183+/-32mg/dl versus 114+/-26mg/dl) was decreased significantly by 37%(p<0.005) with significantly decreased level of Apo A-1(115+/-22 to 122+/-26mg/dl) was increased significantly by 6%(p<0.05). No serious side effects were found. CONCLUSIONS: Results from the present study show that lovastatin is an effective and well-tolerated cholesterol-lowering agent.
Humans ; Hypercholesterolemia* ; Lovastatin* ; Male ; Oxidoreductases ; Triglycerides

No abstract available.
Animals ; Glomerulosclerosis, Focal Segmental* ; Lovastatin* ; Puromycin* ; Rats*

Adrenoleukodystrophy ; genetics ; therapy ; Humans ; Lovastatin ; pharmacology

Lovastatin is a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, which catalyzes the conversion of hydroxymethylglutaryl-coenzyme A to mevalonate, anearly and rate-limiting step in the synthesis of cholesterol. We studied the therapeutic effect and safety of lovastatin in 18 patients with nonfamilial primary hypercholesterolemia. Patients received 20mg/day lovastatin therapy as a single evening dose. If the total cholesterol level exceeded 200mg/dl after 2weeks of lovastatin therapy, the dosage of lovastatin was doubled. Mean percent total cholesterol level reductions from baseline were 26.4% and 31.9% after 4, and 8 weeks of lovastatin therapy respectively. Mean percent HDL-cholesterol level increase from baseline were 12% and 13% after 4, and 8 weeks of lovastatin therapy respectively. Adverse effects attributable to lovastatin were mild and temporary and no patient was withdrawn from therapy. We concluded that lovastatin was a well tolerated and effective agent for the treatment of nonfamilial primary hypercholesterolemia. Further studies are needed to establish the long-term safety and effectiveness of this drug.
Cholesterol ; Coenzyme A ; Humans ; Hypercholesterolemia* ; Lovastatin ; Mevalonic Acid ; Oxidoreductases

10 Patients with primary hypercholesterolemia were treated for 12 weeks with lovastation(20mg t.i.d). Lovastatin reduced mean total and low density lipoprotein cholesterol by 43% and 57% respectively(p<0.001). High density lipoprotein cholesterol and triglyceride levels were unchanged by the drug. Adverse effects attributable to lovastatin were not observed. Thus lovastatin is considered as an effective lipid lowering agent for the treatment of primary moderate hypercholesterolemia.
Cholesterol, HDL ; Cholesterol, LDL ; Humans ; Hypercholesterolemia* ; Lovastatin* ; Triglycerides

We evaluated the hypolipidemic effect and adverse reaction of Lovastatin, HMG-CoA reductase inhibitor 20 to 40mg once-daily in the evening, in 20 patients with primary hypercholesterolemia for 12 weeks and the following results were obtained. 1) Lovastatin significantly reduced the total cholesterol(from 264.8+/-12.9mg/dl to 195.3+/-31.3mg/dl) by 26.3%, TG(from 191.1+/-41.5mg/dl to 156.2+/-52.9mg/dl) by 18.3%, LDL-C(from 177.0+/-12.4mg/dl to 121.3+/-19.6mg/dl) by 31.5% and increased th HDL-C (from 39.8+/-4.2mg/dl to 41.6+/-5.0mg/dl) by 4.5% at the end of 12th week. 2) The adverse reaction during the period of study were limited to diarrhea and nausea in one patient, dryness of skin and itching in one patient, and no patients was withdrawn form therapy. In this study, Lovastatin was well toterated and effective agent for the treatment of hypercholesterolemia without serious side effects.
Diarrhea ; Humans ; Hypercholesterolemia* ; Lovastatin ; Nausea ; Oxidoreductases ; Pruritus ; Skin

This study pharmacokinetically examined the lovastatin sustained-release tablet and sustained-release capsule in Beagle dogs. An reversed-phase HPLC method was established for the determination of lovastatin in Beagle dog plasma. Pharmacokinetic findings were compared among three preparation(lovastatin sustained-release tablet, Tp; sustained-release capsule, TJ and conventional capsule). Our results showed that the pharmacokinetic parameters in 6 dogs after single-dose oral administration of three perparations were calculated. Tmax, Cmax and MRT revealed significant difference (P<0.05). Relative bioavailability was 111.5 +/- 16.9% (Tp) and 110.4% +/- 9.6% (Tj). The pharmacokinetic parameters in the 6 dogs after multiple-dose oral administration of three perparations, Tmax, Cmax MRT and DF had significant difference (P < 0.05); Cav, Cmin and AUC0-24 h displayed no significant difference (P>0.05). It is concluded that the lovastatin sustained-release tablet and sustained-release capsule are able to maintain a sustained-release for 24 h.
Anticholesteremic Agents/*pharmacokinetics ; Capsules ; Delayed-Action Preparations ; Lovastatin/*pharmacokinetics ; Tablets

To evaluate the efficacy and safety of lovastatin, new hypolipidemic agent of HMG-CoA reductase inhibitor, we administered lovastatin 40mg to 80mg once daily for 12 weeks in 20 patients(7 males, 13 females) with primary hypercholesterolemia, and observed the sequential chamges of the lipid profile every 4 weeks. The results are as follows ; 1) The seurm total cholesterol was reduced significantly by 31% from 321+/-36mg% to 210+/-26mg%(p<0.05). 2) The serum triglycerides was significantly reduced from 321+/-168mg% to 228+/-74mg% by 29%(p<0.05). 3) The low density lipoprotein cholesterol was reduced significantly from 177+/-36mg% to 120+/-22mg% by 32%(p<0.05). 4) The total lipid, high density lipoprotein cholesterol and very low density lipoprotein cholesterol were also reduced significantly. 5) The ratio between total cholesterol and high density lipoprotein cholesterol, low density lipoprotein cholesterol and high density lipoprotein cholesterol did not change after lovastatin therapy. 6) There was no adverse reaction due to lovastatin therapy during 12 weeks of therapy. These results suggested that lovastatin is a effective and safe now hypolipidemic agent and is a convenient HMG-CoA reductase inhibitor for clinical use.
Cholesterol ; Cholesterol, HDL ; Cholesterol, LDL ; Cholesterol, VLDL ; Humans ; Hypercholesterolemia* ; Lovastatin* ; Male ; Oxidoreductases ; Triglycerides