Isolation of Lipoprotein (a) Using the Regenerate of a Dextran Sulfate Cellulose LDL Apheresis System

1994 ◽  
Vol 5 (2) ◽  
pp. 112-117 ◽  
Author(s):  
E. Gross ◽  
W. Marz ◽  
R. Siekmeier ◽  
I. Scharrer ◽  
W. Gross
1993 ◽  
Vol 100 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Junji Koizumi ◽  
Ichiro Koizumi ◽  
Yoshihide Uno ◽  
Akihiro Inazu ◽  
Kouvi Kajinami ◽  
...  

1997 ◽  
Vol 20 (3) ◽  
pp. 178-183 ◽  
Author(s):  
S. Kojima ◽  
M. Ogi ◽  
Y. Yoshitomi ◽  
M. Kuramochi ◽  
J. Ikeda ◽  
...  

The negative charges of dextran-sulfate (DS) used for low-density-lipoprotein (LDL) apheresis initiate the intrinsic coagulation pathway in which plasma kallikrein acts on the high-molecular-weight kininogen to produce large amounts of bradykinin. This study was undertaken to assess whether bradykinin generated during DS LDL apheresis has any physiologic effects in vivo. The plasma levels of bradykinin, prostaglandins and cyclic guanosine monophosphate (cGMP) were compared, when either of two anticoagulants, heparin or nafamostat mesilate (NM), was used during DS LDL apheresis. Although anticoagulative action by NM depends on the inhibition of thrombin activity, this substance also inhibits the activity of plasma kallikrein. During apheresis using heparin, the plasma levels of prostaglandin E2 (PGE2) increased significantly (5.6 ± 1.2 (mean ± SE, n=4) pg/ml before apheresis and 33.4 ± 13.2 after apheresis, p < 0.05) in association with an increase in bradykinin levels (17.9 ± 2.6 pg/ml before apheresis and 470 ± 135 after apheresis, p < 0.01). Interestingly, these changes were suppressed during apheresis using NM. There were no appreciable changes in cGMP during DS LDL apheresis with either of the anticoagulants. This finding suggests that bradykinin generated during apheresis has some pathophysiological effects via activation of the prostaglandin system. Our results support the view that in patients taking angiotensin-convertingenzyme inhibitors, the anaphylactoid reaction occurring during apheresis may be caused by an excessive rise in the bradykinin levels.


Author(s):  
Christoph Gruber ◽  
Klaus Swoboda ◽  
Johann Pidlich ◽  
Michael Gottsauner-Wolf ◽  
Gere Sunder-Plassmann ◽  
...  
Keyword(s):  

2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Rolf Bambauer ◽  
Carolin Bambauer ◽  
Boris Lehmann ◽  
Reinhard Latza ◽  
Ralf Schiel

The prognosis of patients suffering from severe hyperlipidemia, sometimes combined with elevated lipoprotein (a) levels, and coronary heart disease refractory to diet and lipid-lowering drugs is poor. For such patients, regular treatment with low-density lipoprotein (LDL) apheresis is the therapeutic option. Today, there are five different LDL-apheresis systems available: cascade filtration or lipid filtration, immunoadsorption, heparin-induced LDL precipitation, dextran sulfate LDL adsorption, and the LDL hemoperfusion. There is a strong correlation between hyperlipidemia and atherosclerosis. Besides the elimination of other risk factors, in severe hyperlipidemia therapeutic strategies should focus on a drastic reduction of serum lipoproteins. Despite maximum conventional therapy with a combination of different kinds of lipid-lowering drugs, sometimes the goal of therapy cannot be reached. Hence, in such patients, treatment with LDL-apheresis is indicated. Technical and clinical aspects of these five different LDL-apheresis methods are shown here. There were no significant differences with respect to or concerning all cholesterols, or triglycerides observed. With respect to elevated lipoprotein (a) levels, however, the immunoadsorption method seems to be most effective. The different published data clearly demonstrate that treatment with LDL-apheresis in patients suffering from severe hyperlipidemia refractory to maximum conservative therapy is effective and safe in long-term application.


1994 ◽  
Vol 109 (1-2) ◽  
pp. 160-161
Author(s):  
Y. Fuda ◽  
J. Suwa ◽  
Y. Ishii ◽  
T. Suzuki ◽  
H. Ando ◽  
...  

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