Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to compare the cost effectiveness of micronised fenofibrate 200 mg and simvastatin 20 mg in the treatment of type IIa and IIb hyperlipidaemia. In a retrospective analysis, data from 2 randomised controlled clinical trials were evaluated. The results show that micronised fenofibrate has a better short term cost effectiveness than simvastatin. The costs per successfully treated patient with hyperlipidaemia over a 12-week period were [in Deutschmarks (DM); DMI = $US0.66, April 1995] DM537 for fenofibrate and DM809 for simvastatin. When the data were analysed according to type of hyperlipidaemia (classification of Frederickson), there were only small differences between both test drugs (DM450 for fenofibrate, DM517 for simvastatin) in patients with type IIa because simvastatin had higher response rates which, in part, compensated for the higher acquisition cost. However, response rates in patients with type IIb hyperlipidaemia were higher for fenofibrate, which led to a substantial cost advantage for this agent (DM768 for fenofibrate, DM2080 for simvastatin). These results were confirmed by various sensitivity analyses, including the assessment of drug monitoring programmes (postmarketing surveillance) to validate response rates and the total costs of the therapy. In this study, we evaluated the total costs of a 12-week period of therapy, not the costs per day. The results are based on actual clinical data and not just on theoretical models. The study underlines the necessity to differentiate between the types of hyperlipidaemia when performing a pharmacoeconomic analysis of lipid-lowering treatments.
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PMID:Cost effectiveness of micronised fenofibrate and simvastatin in the short-term treatment of type IIa and type IIb hyperlipidaemia. 1017 26

Oxidative modification of lipoproteins in vessel walls plays a key role in atherogenesis. Patients with glycogen storage disease type Ia (GSD Ia) do not develop premature atherosclerosis despite severe hyperlipidemia. We analyzed antioxidative defense and oxidative stress in plasma and serum of patients with GSD Ia (n = 17) compared to patients with type I diabetes mellitus (DMI, n = 17), familial hypercholesterolemia (FH, n = 18), and healthy controls (n = 20). We measured the total radical-trapping antioxidant parameter (TRAP), single antioxidants (sulfhydryl groups, uric acid, vitamin C, alpha-tocopherol, coenzyme Q10), malondialdehyde, oxidized low density lipoprotein (LDL) antibodies, lipid profile [cholesterol, triglyceride, lipoprotein (a)], homocysteine, and hemoglobin (Hb)A(1C). TRAP levels were elevated in the GSD Ia group (p <.01) and correlated with elevated uric acid levels (r = 0.72, p =.001). None of the other plasma antioxidants correlated with TRAP levels. DMI patients showed decreased sulfhydryl groups (p <.01) and a reduced ubiquinol-10 fraction (p <.01). Malondialdehyde (p <.001) and oxidized LDL autoantibodies (p <.05) were increased in the diabetic group. In FH patients, parameters of oxidative stress and TRAP did not differ from controls. We conclude that in GSD Ia an increased antioxidative defense in plasma may protect against lipid peroxidation and thus against premature atherosclerosis. Furthermore, we demonstrated that in DMI increased oxidative mechanisms are already present in childhood.
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PMID:Plasma antioxidants in pediatric patients with glycogen storage disease, diabetes mellitus, and hypercholesterolemia. 1208 88