Lipoprotein(a): Medical Treatment Options for an Elusive Molecule

Klaus      G. Parhofer

doi:10.2174/138161211795428777

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