No abstract available.
Humans ; Hypercholesterolemia* ; Lovastatin*

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

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

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

Adrenoleukodystrophy ; genetics ; therapy ; Humans ; Lovastatin ; pharmacology

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were limited to diarrhea and nausea in one patient, dryness of skin and itching in one patient, and no patients was withdrawn form therapy.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

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

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

BACKGROUND AND OBJECTIVES: ovastatin, a HMG-CoA reductase inhibitor, is known to show antiproliferative effects on VSMC after vessel injury, but a large amount of the drug is needed orally for this purpose. This study investigated the effects of lovastatin given locally to injured carotid arteries of rats on reducing neointimal hyperplasia. MATERIALS AND METHOD: Lovastatin was given perivascularly to balloon-injured carotid arteries of 21 rats in 1 microM to the low-dose group, and 30 microM to the high-dose group. The control group was treated with pluronic gel only. Two weeks later, the lumen area, neointimal areas and the number of actively proliferating cells were obtained and compared. RESULTS: eointimal area was 0.113+/-0.032 mm2, 0.065+/-0.017 mm2, 0.072+/-0.017 mm2 in the control, low-dose and high-dose groups respectively. The area was significantly smaller in the treatment groups (p<0.05), but no significant difference was observed between the treatment groups. The number of actively proliferating cells per mm2 of neointimal area were 714.5+/-227.4, 688.4+/-333.7, and 1526.3+/-744.0 in the groups respectively, and the number was significantly high in the high-dose group (p<0.05). CONCLUSION: Local administration of lovastatin is effective in reducing neointimal hyperplasia after vascular injury, but extremely high doses are not needed locally for this purpose.
Animals ; Carotid Arteries* ; Carotid Artery Injuries* ; Hyperplasia* ; Lovastatin* ; Oxidoreductases ; Rats* ; Vascular System Injuries