title: The clinical significance of alpha 1-antitrypsin-elastase (alpha 1AT-ELP) and alpha 2-antiplasmin-plasmin (alpha 2AP-PL) complexes for the differentiation of coagulation protein turnover: indications for plasma protein substitution in patients with septicaemia.
abstract: In inflammation, particularly in septicaemia, complex coagulation disorders may lead to a dangerous haemorrhagic diathesis. The conventional concept for this syndrome called DIC implicates the occurrence of active thrombin in the circulation, which may be followed by hyperfibrinolysis due to plasmin formation. In this study data are presented suggesting an important role for a third proteolytic system, granulocytic elastase. The complexes of plasmin and elastase with their specific inhibitors, alpha 2-antiplasmin-plasmin (alpha 2AP-PI) and alpha 1-antitrypsin-elastase (alpha 1AT-ELP) were determined immunologically. The alpha 1AT-ELP appears mainly in gram-negative septicaemia, particularly in meningococcal disease. The estimation of alpha 2AP-PI and alpha 1AT-ELP, together with a method for the detection of the antithrombin III--thrombin complex which remains to be established, is a suitable tool for for the differential diagnosis of the consumption of coagulation proteins. The assumption that at least three proteolytic systems participate in the development of the haemorrhagic diathesis during inflammation leads to the concept of a broad, comprehensive substitution therapy with e.g. concentrates of AT III, PPSB, or fresh frozen plasma. The aim of this treatment is to replace not only the consumed procoagulatory factors, but also the lacking inhibitors in order to control this "abnormal proteolysis syndrome".
authors.forename: R
authors.initials: R
authors.lastname: Seitz
authors.forename: R
authors.initials: R
authors.lastname: Egbring
authors.forename: K P
authors.initials: KP
authors.lastname: Radtke
authors.forename: M
authors.initials: M
authors.lastname: Wolf
authors.forename: G
authors.initials: G
authors.lastname: Fuchs
authors.forename: J
authors.initials: J
authors.lastname: Fischer
authors.forename: L
authors.initials: L
authors.lastname: Lerch
authors.forename: H E
authors.initials: HE
authors.lastname: Karges
mesh_terms: D000328:Adult; D001779:Blood Coagulation Factors; D001798:Blood Proteins / Q000378:metabolism*; D001803:Blood Transfusion; D010450:Endopeptidases / Q000097:blood; D005260:Female; D005341:Fibrinolysin / Q000032:analysis*; D006098:Granulocytes / Q000201:enzymology; D006801:Humans; D007249:Inflammation; D046911:Macromolecular Substances; D008954:Models, Biological; D015260:Neprilysin; D010196:Pancreatic Elastase / Q000378:metabolism*; D017713:Platelet Transfusion; D018805:Sepsis / Q000097:blood* / Q000628:therapy; D000515:alpha 1-Antitrypsin / Q000032:analysis*; D000979:alpha-2-Antiplasmin / Q000378:metabolism*
chemical_list: D001779:Blood Coagulation Factors; D001798:Blood Proteins; D046911:Macromolecular Substances; D000515:alpha 1-Antitrypsin; D000979:alpha-2-Antiplasmin; D010450:Endopeptidases; D010196:Pancreatic Elastase; D005341:Fibrinolysin; D015260:Neprilysin