Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperlipidemia may be one of the risk factors in the development of atherosclerotic disease in renal transplant recipients. In the present study, 24 kidney recipients with hyperlipidemia were treated with an HMG-CoA reductase inhibitor, pravastatin (10 mg/day). All recipients had been treated with cyclosporine (CsA), azathioprine (Az), and prednisolone (Pred). The mean total cholesterol (T-chol) level decreased from 323 +/- 7.4 to 261 +/- 7.9 mg/dl at one month after starting treatment (P less than 0.01) and this level did not change during treatment for further 6 months. The mean LDL cholesterol level was also decreased from 205.9 +/- 11.2 to 118.7 +/- 8.1 mg/dl at 3 months after starting treatment (P less than 0.01). On the other hand, pravastatin did not affect the levels of HDL-cholesterol and triglycerides. Pravastatin did not show any effects on the white blood cell, monocyte, and lymphocyte counts, or the hemoglobin concentration (NS). One patient displayed a slight elevation of aspartate aminotransferase and alanine aminotransferase levels, but this was not sufficient to cease treatment. Pravastatin did not adversely affect the renal function or creatinine phosphokinase (CPK) levels. Two recipients developed nausea and vomiting and their treatment was stopped. Pravastatin appears to be a safe and efficacious method of treating hyperlipidemia in renal transplant recipients.
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PMID:The effects of pravastatin on hyperlipidemia in renal transplant recipients. 173 92

The authors administered lovastatin (Mevacor, MSD) to 18 patients with primary hyperlipoproteinaemia (familial and non-familial) with a lipoprotein pattern type IIa and IIb. During treatment a marked reduction of atherogenic indicators of the lipid metabolism occurred, i.e. a decline of total cholesterol (-28.6%), LDL-cholesterol -39%), apolipoprotein B (-18.6%), the index of total cholesterol/HDL-cholesterol (-44.6%) and the index LDL-cholesterol/HDL-cholesterol (-48.2%). At the same time a favourable effect on indicators of the lipid metabolism to which a protective action is ascribed was recorded: a rise of HDL-cholesterol (+13.6%) and apolipoprotein AI (+13%) and AII (+13%). An excellent effect was observed also in four heterozygotes with familial hypercholesterolaemia which is usually rather resistant to other types of hypolipidaemic treatment. The drug was very well tolerated and subjective side-effects of treatment were minimal. Despite the fact that a number of laboratory indicators was followed up, the authors did not observe any undesirable side-effects, only a transient and marginal rise of ALT in one patient. Lovastatin is, due to its potent hypolipidaemic effect, a new hope in the treatment of hypercholesterolaemia. Its usefulness in the prevention of ischaemic heart disease, as well as its safety during prolonged administration are tested at present in long-term investigations.
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PMID:[Personal experience with lovastatin, a HMG-CoA reductase inhibitor (Mevacor, MSD) in the treatment of hypercholesterolemia]. 184 44

Seventy-seven hypercholesterolemic patients participated in a 26-week, multicenter, randomized, double-blind, placebo-controlled study that investigated the efficacy and safety of pravastatin therapy. All patients had primary moderate hypercholesterolemia (total cholesterol 200-300 mg/dl, at the end of a 6-week dietary run-in period) and two additional coronary risk factors. Pravastatin, 20-40 mg/day given at bedtime, reduced total cholesterol by 19-22%, LDL-cholesterol by 24-30%, triglycerides by 10-30% and increased HDL-cholesterol by 9-13%. The drug caused mild elevation in alanine aminotransferase and aspartate aminotransferase. Almost all these elevations were within normal limits and no patient was clinically symptomatic. No other significant differences were observed between the pravastatin and the placebo-treated groups with regard to other adverse effects and to patient compliance and withdrawal. It is concluded that pravastatin has a beneficial effect on the lipid profile and that the drug is safe and well tolerated.
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PMID:Efficacy and safety of pravastatin once daily in primary moderate hypercholesterolemia: the Israeli experience. 831 85

Heterozygous familial hypercholesterolemia (HeFH) is associated with elevated cholesterol levels and early-onset atherosclerosis. We assessed the efficacy and safety for up to 2 yr of pravastatin treatment in 19 girls and 11 boys (age range, 4.1-18.5 yr) with HeFH. Pravastatin was started at 10 mg/d, with a forced titration by 10 mg at 2, 4, 6, and 12 months until the target cholesterol level [< or =194 mg/dl (< or =5 mmol/liter)] was reached. By 2, 4, 6, 12, and 24 months of treatment, the total cholesterol levels had, respectively, decreased by 19, 20, 23, 27, and 26%, and the low-density lipoprotein cholesterol levels had decreased by 25, 27, 29, 33, and 32% compared with the dietary baseline values. Seventeen percent of patients had lipid deposits (carotid plaque, xanthomas, or corneal arcus) at baseline, and 27% had deposits at 1 yr. The side effects were mild, and no clinically significant elevations in alanine aminotransferase, creatine kinase, or creatinine were seen. Growth and pubertal maturation remained normal in all subjects. In conclusion, pravastatin treatment was safe and well tolerated. The efficacy in children with slight or moderate hypercholesterolemia was satisfactory, but in children with severe hypercholesterolemia, it was insufficient.
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PMID:Efficacy and safety of pravastatin in children and adolescents with heterozygous familial hypercholesterolemia: a prospective clinical follow-up study. 1565 70

Statin medications have been suggested for widespread use in patients with systemic lupus erythematosus (SLE). We studied the dose effectiveness and tolerability of pravastatin in SLE. We compared 41 SLE subjects in a two-month open-label dose-titration study of pravastatin to 22 SLE controls. Lipids, ALT, CPK, CRP, adverse effects were assessed. Linear mixed models assessed changes in lipids and CRP, comparing pravastatin subjects to controls. After 1 month of pravastatin 10 mg a day, total cholesterol decreased by 16% (+/-12.1%) and LDL by 24% (+/-17%), compared with 1.8% (+/-7.5%) and 2.6% (+/-8.6%) decreases in controls (P < 0.001). CRP did not decline. Glucocorticoids appeared to decrease pravastatin effectiveness. Serum CPK increased in one subject. Pravastatin reduced LDL and total cholesterol levels approximately the same degree observed in normal individuals, but the effect appeared blunted in those on modest doses of glucocorticoids and those with higher BMI.
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PMID:A pravastatin dose-escalation study in systemic lupus erythematosus. 1872 2