G Lippi1, G Targher. 1. U.O. Diagnostica Ematochimica, Dipartimento di Patologia e Medicina di Laboratorio, Azienda Ospedaliero-Universitaria di Parma, Parma, Italy. glippi@ao.pr.it
Abstract
WHAT IS KNOWN AND OBJECTIVE: There is a growing body of experimental and clinical evidence for the atherogenic and pro-thrombotic potential of Lipoprotein(a) [Lp(a)], as well as for its causative role in coronary heart disease and stroke. We comment on novel strategies for reducing Lp(a) levels. COMMENT: Irrespective of the underlying biological mechanisms explaining the athero-thrombotic potential of this lipoprotein, most work has focused on the identification of suitable therapies for hyperlipoproteinemia(a). These include apheresis techniques, nicotinic acid and statins. None of these strategies have been shown to be definitely effective or convenient for the patient and new strategies are being attempted. Promising results are emerging with therapeutic interventions targeting the 'inflammatory pathways' by inhibition of Interleukin-6 (IL-6) signalling with natural compounds (e.g., Ginko biloba) or the IL-6 receptor antibody Tocilizumab. These may both lower Lp(a) and cardiovascular risk of the patients. Besides inhibiting platelet function, antiplatelet therapy with aspirin may also decrease the plasma concentration of Lp(a) and modulate its influence on platelets. WHAT IS NEW AND CONCLUSION: We highlight the inadequacy of current approaches for lowering Lp(a) and draw attention to novel insights that may lead to better treatment.
WHAT IS KNOWN AND OBJECTIVE: There is a growing body of experimental and clinical evidence for the atherogenic and pro-thrombotic potential of Lipoprotein(a) [Lp(a)], as well as for its causative role in coronary heart disease and stroke. We comment on novel strategies for reducing Lp(a) levels. COMMENT: Irrespective of the underlying biological mechanisms explaining the athero-thrombotic potential of this lipoprotein, most work has focused on the identification of suitable therapies for hyperlipoproteinemia(a). These include apheresis techniques, nicotinic acid and statins. None of these strategies have been shown to be definitely effective or convenient for the patient and new strategies are being attempted. Promising results are emerging with therapeutic interventions targeting the 'inflammatory pathways' by inhibition of Interleukin-6 (IL-6) signalling with natural compounds (e.g., Ginko biloba) or the IL-6 receptor antibody Tocilizumab. These may both lower Lp(a) and cardiovascular risk of the patients. Besides inhibiting platelet function, antiplatelet therapy with aspirin may also decrease the plasma concentration of Lp(a) and modulate its influence on platelets. WHAT IS NEW AND CONCLUSION: We highlight the inadequacy of current approaches for lowering Lp(a) and draw attention to novel insights that may lead to better treatment.
Authors: Indumathi Chennamsetty; Karam M Kostner; Thierry Claudel; Manjula Vinod; Sasa Frank; Thomas S Weiss; Michael Trauner; Gerhard M Kostner Journal: J Lipid Res Date: 2012-08-28 Impact factor: 5.922
Authors: Nike Müller; Dominik M Schulte; Kathrin Türk; Sandra Freitag-Wolf; Jochen Hampe; Rainald Zeuner; Johann O Schröder; Ioanna Gouni-Berthold; Heiner K Berthold; Wilhelm Krone; Stefan Rose-John; Stefan Schreiber; Matthias Laudes Journal: J Lipid Res Date: 2015-02-21 Impact factor: 5.922
Authors: Maria-Corina Serban; Amirhossein Sahebkar; Dimitri P Mikhailidis; Peter P Toth; Steven R Jones; Paul Muntner; Michael J Blaha; Florina Andrica; Seth S Martin; Claudia Borza; Gregory Y H Lip; Kausik K Ray; Jacek Rysz; Stanley L Hazen; Maciej Banach Journal: Sci Rep Date: 2016-01-12 Impact factor: 4.379