[Individualized "minimal invasive" anticoagulation controlled with D-dimer-antigen testing - a concept]. / Individualisierte "minimal invasive" Antikoagulation unter Kontrolle von D-Dimer-Antigen-Bestimmungen. Ein Konzept.

The aim of the proposed concept is to use anticoagulant therapy in prophylaxis and therapy of thromboembolic events only to an extent that the coagulation activation is just not any longer detectable. It results an individualized anticoagulation tailored to the coagulation activation of the patient (individualized "minimal invasive" anticoagulation). Intensity and control of efficiency are to be monitored by measurement of in vivo coagulation activation, e.g. by D-dimer-antigen measurement. Especially with the use of the new oral anticoagulants such a saver anticoagulant therapy - as far as possible from bleeding risk - could open up new indications, which so far are not used because of safety reasons. More patients at risk could be prevented from thromboembolic events. The proposed concept is based on pathophysiological considerations and own clinical experience. It should be evaluated for efficiency in clinical studies.

[Heparin-associated thrombocytopenia caused by low-molecular-weight heparin]. / Heparin-assoziierte Thrombozytopenie durch niedermolekulare Heparine.

Recent studies have shown that low-molecular-weight heparins (LMWH) are not suitable for treating patients with heparin-associated thrombopenia (HAT) type 2, as they can cause the same complications as unfractionated heparin UFH. The case described ist that of concerns as female patient who died after developing HAT type 2 following LMWH given perioperatively to prevent thromboembolism. This case indicates again that LMWH can trigger HAT type 2 even if administered only once a day. For HAT to be successfully treated it is essential that the condition is diagnosed early enough by means of routine regular laboratory checks of the number of thrombocytes during any heparin treatment in order to detect the disease before clinical symptoms become apparent.

[Portal hypertension due to thromboses of the portal, splenic and mesenteric veins in congenital protein c deficiency]. / Portale Hypertension durch Thrombosen der Pfortader, Milzvene und Mesenterialvene bei angeborenem Protein-C-Mangel.

In a 39-year-old man there occurred, over a period of four years, mesenteric vein thrombosis with haemorrhagic infarction of the intestines, as well as multiple bleedings from oesophageal varices due to portal hypertension caused by portal vein thrombosis. Search for the cause of the thrombosis tendency revealed congenital protein C deficiency. Splenectomy and a disconnection operation were performed, followed by administration of anticoagulants. Since then the patient has been free of symptoms, and there have been no further variceal bleedings or thromboses.