PubMed · 15587533
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Heather Curry. Bleeding disorder basics.. https://pubmed.ncbi.nlm.nih.gov/15587533/
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Hypothermia has long been known to be a potent putative neuroprotectant. Experimental evidence and clinical experience show that hypothermia protects the brain from cerebral injury. Recent insights into the mechanisms of cerebral ischemia and reperfusion suggest reasons why hypothermia may be an ideal modality for stroke therapy. Hypothermia protects brain tissue in multiple ways. It retards energy depletion, reduces intracellular acidosis, lessens the ischemia related accumulation of excitotoxic neurotransmitters, and attenuates the influx of intracellular calcium. Additionally, hypothermia suppresses the generation of oxygen free radicals involved in secondary damage associated with reperfusion. It also suppresses the mechanisms related to blood-brain barrier degeneration and postischemic remodeling. The clinical application of therapeutic hypothermia and its limitations will be summarized in this paper. Therapeutic hypothermia is likely to undergo phase III clinical trials in various clinical settings. Novel technologies are being developed to optimize the safety and efficacy of this promising approach.
The maintenance of the equilibrium between coagulation and fibrinolysis is crucial for normal haemostasis. In contrast, pathologic consequences of imbalance manifest tendencies of bleeding or thrombosis. Procarboxypeptidase U (proCPU, TAFI) is recognized as an important link between the coagulation system and fibrinolysis. Following activation by thrombin (IIa), carboxypeptidase U (CPU) exerts an antifibrinolytic effect by abolishing the cofactor function of partially degraded fibrin in plasminogen (Pg) activation. This review article focuses on the role of the proCPU/CPU system in the balance between fibrin deposition and removal. How a disturbed system can lead to a higher thrombotic tendency is discussed, while CPU inhibition as a new drug target for fibrinolytic therapy is extensively reviewed.
The pathogenesis of very severe thrombocytopenia in bacterial endocarditis is uncertain. We report a 50-year-old male with platelet counts < 10 x 10(9)/l and fragmentation hemolysis complicating Staphylococcus epidermidis pacemaker endocarditis with a giant vegetation. Antibiotics, corticosteroids, high-dose intravenous gammaglobulin, and plasmapheresis (for initially-suspected thrombotic thrombocytopenic purpura) failed to produce significant platelet count increase. However, therapeutic-dose heparin anticoagulation was associated with a platelet count increase from <10 to approximately 40 x 10(9)/l, with parallel reduction in thrombin-antithrombin complexes (from 8.9 to 3.5 microg/l), facilitating surgical intervention. The thrombocytopenia promptly resolved following surgical removal of the vegetation. Culture supernatant from S. epidermidis isolated from the patient's blood induced monocytes to express procoagulant activity (assessed by factor Xa generation) equivalent to lipopolysaccharide (1 microg/ml), with half-maximal activation seen with culture supernatant diluted to 1:12,800. These data are consistent with previous animal models of endocarditis demonstrating staphylococci-induced procoagulant changes in monocytes. This case demonstrates that heparin anticoagulation can be therapeutic in infective endocarditis-associated severe thrombocytopenia in a non-bleeding patient, and that such therapy may ameliorate the platelet count enough to permit surgical intervention.