scholarly journals A Quantitative Immunoassay for the Lysine-Binding Function of Lipoprotein(a)

1996 ◽  
Vol 16 (5) ◽  
pp. 656-664 ◽  
Author(s):  
Jane L. Hoover-Plow ◽  
Nataya Boonmark ◽  
Pamela Skocir ◽  
Richard Lawn ◽  
Edward F. Plow
Keyword(s):  
Lipoprotein A ◽  
Binding Function ◽  
Quantitative Immunoassay

A quantitative immunoassay for the lysine binding function of lipoprotein(a) in plasma

1994 ◽  
Vol 8 ◽  
pp. 124
Author(s):  
J. Hoover-Plow ◽  
P. Skocir ◽  
J. Hinman ◽  
G.M. Fless ◽  
A.M. Scanu ◽  
...  
Keyword(s):  
Lipoprotein A ◽  
Binding Function ◽  
Quantitative Immunoassay

Structural and functional polymorphism of lipoprotein(a): biological and clinical implications

1995 ◽  
Vol 41 (1) ◽  
pp. 170-172 ◽  
Author(s):  
A M Scanu
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
The Other ◽  
Clinical Implications ◽  
Low Density ◽  
Functional Polymorphism ◽  
Lipoprotein A ◽  
Apolipoprotein A ◽  
Binding Function

Abstract Lipoprotein(a) [Lp(a)], a variant of low-density lipoprotein, is heterogeneous in density because of variability in the content and composition of its core lipids and size polymorphism of its specific glycoprotein component, apolipoprotein(a) [apo(a)]. In some individuals, density polymorphism may also derive from the fact that Lp(a) contains 2 mol of apo(a) per mole of apoB100, contrary to the more common 1:1 molar stoichiometry. Moreover, the size of apo(a) is polymorphic because of variations in the number of kringle 4 type 2 repeats. Another type of apo(a) polymorphism is related to sequence mutations at the kringle level. Two mutations can occur in kringle 4 type 10: one, Trp72-->Arg, is affiliated with an Lp(a) that is lysine-binding defective; the other, Met66-->Thr, with a normal lysine-binding function. Thus, Lp(a) is structurally and functionally polymorphic, a notion that must be considered in assessing the cardiovascular pathogenicity of this lipoprotein variant and in immunoquantification assays.

Lp(a): der akzeptierte unabhängige Risikofaktor

2019 ◽  
Vol 23 (09) ◽  
pp. 388-391
Author(s):  
Volker Schettler
Keyword(s):  
Lipoprotein A ◽  
Apolipoprotein A ◽  
Apolipoprotein B100

Lipoprotein(a) (Lp(a)) besteht aus einem LDL-Partikel, an dem über das Apolipoprotein B100 des Partikels eine Disulfidbrücke zu einem Apolipoprotein(a) besteht ( Abb. 1 ). Obwohl Lp(a) bereits 1963 von Berg et al. erstmals als „lipoprotein associated antigen“ entdeckt 1 und schon früh ein Zusammenhang mit kardiovaskulären Ereignissen diskutiert wurde 2, konnten diese Annahmen der klinischen Eigenschaften erst deutlich später im Rahmen von epidemiologischen Evaluationen bestätigt werden 3, 4. Ab einer Lp(a)-Konzentration von über 30 mg/dl (> 75 nmol/l) besteht ein nahezu linearer Zusammenhang zwischen dem Anstieg der Lp(a)-Konzentration und kardiovaskulären Ereignissen wie Myokardinfarkt und das Risiko für eine Aortenklappenstenose 3, 4.

Plasma Levels of Lipoprotein(a) Are Elevated in Patients with the Antiphospholipid Antibody Syndrome

1994 ◽  
Vol 71 (04) ◽  
pp. 424-427 ◽  
Author(s):  
Masahide Yamazaki ◽  
Hidesaku Asakura ◽  
Hiroshi Jokaji ◽  
Masanori Saito ◽  
Chika Uotani ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Active Form ◽  
Plasminogen Activator Inhibitor ◽  
Arterial System ◽  
Control Group ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Lipoprotein A ◽  
Soluble Thrombomodulin ◽  
Relationship Of

SummaryThe mechanisms underlying clinical abnormalities associated with the antiphospholipid antibody syndrome (APAS) have not been elucidated. We measured plasma levels of lipoprotein(a) [Lp(a)], the active form of plasminogen activator inhibitor (active PAI), thrombin-antithrombin III complex (TAT) and soluble thrombomodulin (TM), to investigate the relationship of these factors to thrombotic events in APAS. Mean plasma levels of Lp(a), TAT, active PAI and TM were all significantly higher in patients with aPL than in a control group of subjects. Plasma levels of Lp(a) and active PAI were significantly higher in patients with aPL and arterial thromboses than in patients with aPL but only venous thromboses. There was a significant correlation between plasma levels of Lp(a) and active PAI in patients with aPL. These findings suggest that patients with aPL are in hypercoagulable state. High levels of Lp(a) in plasma may impair the fibrinolytic system resulting in thromboses, especially in the arterial system.

Lipoprotein(a), Plasmin Modulation, and Atherogenesis

1995 ◽  
Vol 74 (01) ◽  
pp. 382-386 ◽  
Author(s):  
Peter C Harpel ◽  
Anita Hermann ◽  
Xiaoxia Zhang ◽  
Iris Ostfeld ◽  
Wolfgang Borth
Keyword(s):  
Lipoprotein A
Sign in / Sign up

Export Citation Format

Share Document