Long-Term Effects of CS-514 on Serum Lipoprotein Lipid and Apolipoprotein Levels in Patients with Familial Hypercholesterolemia View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1987

AUTHORS

H. Mabuchi , N. Kamon , H. Fujita , I. Michishita , M. Takeda , K. Kajinami , H. Itoh , T. Wakasugi , R. Takeda

ABSTRACT

Familial hypercholesterolemia is an autosomal dominant disorder characterized by elevated levels of low-density lipoprotein (LDL) cholesterol, tendon xanthomas, and premature coronary artery disease (CAD) (1). The disorder results from a complete or partial defect of the LDL receptor (1) that normally controls the degradation of LDL. Reduction of LDL-cholesterol levels has proved to be effective in decreasing the incidence of CAD (2, 3). Compactin (4) and mevinolin (5), competitive inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, are effective in lowering cholesterol levels of patients with familial hypercholesterolemia. These drugs lower plasma LDL by decreasing the rate of LDL production and stimulating the production of LDL receptor in the liver (6) (Fig. 1). LDL receptor has a specific binding activity for apolipoproteins B and E (7). The apolipoprotein B is present in very low-density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and LDL (8), which are highly associated with CAD (9, 10). Apolipoproteins A-I and A-II are primary apolipo-proteins in high-density lipoprotein (HDL) (8), and apolipoprotein A-I in patients with CAD has been demonstrated to be decreased (11). More... »

PAGES

260-268

Book

TITLE

Drugs Affecting Lipid Metabolism

ISBN

978-3-642-71704-8
978-3-642-71702-4

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-642-71702-4_49

DOI

http://dx.doi.org/10.1007/978-3-642-71702-4_49

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1051880374


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