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Complement activation and depletion during LDL‐apheresis by heparin‐induced extracorporeal LDL‐precipitation (HELP)
Author(s) -
WÜRZNER R.,
SCHUFFWERNER P.,
FRANZKE A.,
NITZE R.,
OPPERMANN M.,
ARMSTRONG V.W.,
EISENHAUER T.,
SEIDEL D.,
GÖTZE O.
Publication year - 1991
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1991.tb01372.x
Subject(s) - complement system , apheresis , extracorporeal , immunoadsorption , extracorporeal circulation , heparin , chemistry , complement component 5 , chromatography , pharmacology , medicine , immunology , biochemistry , antibody , platelet
. The heparin‐induced extracorporeal elimination of low density lipoproteins (LDL) is a well‐established clinical procedure to markedly reduce cholesterol levels. The biocompatibility of this artificial filter system (HELP) was investigated by quantitation of representative complement proteins within the extracorporeal circuit using established ELISA procedures, based on monoclonal antibodies recognizing exclusively either native (C6, C7) or activated proteins (act.C3, C5a, TCC). HELP was found to be a self‐limiting extracorporeal system with respect to complement activation, since act.C3 and TCC, generated mainly at the plasma filter, were partially adsorbed to the following HELP specific filters to concentrations which were lower than those obtained before the plasma filter.C5a, which increased 14.5‐fold at the plasma filter was not eliminated by the following filters; however, elevated levels were not found in the patients at the end of apheresis and no leucocytopenia was observed.

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