Abstract
Elevated levels of lipoprotein(a) are causally related to premature atherosclerosis. It is therefore of interested to evaluate by which treatment modalities elevated lipoprotein(a) levels can be decreased. With the exception of niacin, currently available lipidmodifying drugs have only little effect on lipoprotein(a) levels. Niacin can decrease lipoprotein(a) concentration in a dose dependent fashion by approximately 20-30%. Similarly, acetylsalicylic acid and L-carnitine as well as some medications in development (mipomersen, eprotirome, Proprotein convertase subtilisin/kexin type 9 (PCSK-9) inhibitors, Cholesterol-ester-transfer protein (CETPinhibitors) can decrease elevated lipoprotein(a) concentrations. It is unclear whether this lipoprotein(a) reduction also translates into a decreased cardio-vascular morbidity or mortality. Estrogen (with or without progesterone) and tibolone but not tamoxifene or raloxifene can also decrease elevated lipoprotein(a) concentrations. The most dramatic change in lipoprotein(a) concentration can be achieved with regular lipid apheresis.
Keywords: Apoprotein(a), carnitine, ascorbic acid, mipomersen, statin, eprotirome, anacetrapib, dalcetrapib, apolipoprotein, plasminogen, stenosis, L-carnitine, methionine, Scandinavian, thyreo-mimetics, Lomitapide, Niacin, monotherapy, tamoxifene, gonadotropin
Current Pharmaceutical Design
Title: Lipoprotein(a): Medical Treatment Options for an Elusive Molecule
Volume: 17 Issue: 9
Author(s): Klaus G. Parhofer
Affiliation:
Keywords: Apoprotein(a), carnitine, ascorbic acid, mipomersen, statin, eprotirome, anacetrapib, dalcetrapib, apolipoprotein, plasminogen, stenosis, L-carnitine, methionine, Scandinavian, thyreo-mimetics, Lomitapide, Niacin, monotherapy, tamoxifene, gonadotropin
Abstract: Elevated levels of lipoprotein(a) are causally related to premature atherosclerosis. It is therefore of interested to evaluate by which treatment modalities elevated lipoprotein(a) levels can be decreased. With the exception of niacin, currently available lipidmodifying drugs have only little effect on lipoprotein(a) levels. Niacin can decrease lipoprotein(a) concentration in a dose dependent fashion by approximately 20-30%. Similarly, acetylsalicylic acid and L-carnitine as well as some medications in development (mipomersen, eprotirome, Proprotein convertase subtilisin/kexin type 9 (PCSK-9) inhibitors, Cholesterol-ester-transfer protein (CETPinhibitors) can decrease elevated lipoprotein(a) concentrations. It is unclear whether this lipoprotein(a) reduction also translates into a decreased cardio-vascular morbidity or mortality. Estrogen (with or without progesterone) and tibolone but not tamoxifene or raloxifene can also decrease elevated lipoprotein(a) concentrations. The most dramatic change in lipoprotein(a) concentration can be achieved with regular lipid apheresis.
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Cite this article as:
G. Parhofer Klaus, Lipoprotein(a): Medical Treatment Options for an Elusive Molecule, Current Pharmaceutical Design 2011; 17 (9) . https://dx.doi.org/10.2174/138161211795428777
DOI https://dx.doi.org/10.2174/138161211795428777 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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