Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple and complex abnormalities of hemostasis are revealed by laboratory tests in such common diseases as cirrhosis and end-stage renal insufficiency. Because these abnormalities are associated with a bleeding tendency, a causal relationship is plausible. Accordingly, an array of transfusional and nontransfusional medications that improve or correct these abnormalities is used to prevent or stop hemorrhage. However, recent data indicate that the use of hemostatic drugs is scarcely justified mechanistically or clinically. In patients with uremia, the bleeding tendency (mainly expressed by gastrointestinal bleeding and hematoma formation at kidney biopsy) is reduced dramatically by the improvement of anemia obtained with the regular use of erythropoietin. In cirrhosis, the most severe and frequent hemorrhagic symptom (acute bleeding from esophageal varices) is not explained by abnormalities in such coagulation screening tests as the prothrombin and partial thromboplastin times, because formation of thrombin the final coagulation enzyme is rebalanced by low naturally occurring anticoagulant factors in plasma that compensate for the concomitant decrease of procoagulants. Rebalance also occurs for hyperfibrinolysis and platelet abnormalities. These findings are consistent with clinical observations that transfusional and nontransfusional hemostatic medications are of little value as adjuvants to control bleeding in advanced liver disease. Particularly in uremia, but also in cirrhosis, thrombosis is becoming a cogent problem.
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PMID:Hemostatic defects in liver and renal dysfunction. 2323 77

A 52-year-old woman was admitted to the hospital three times in a span of 5 years in hypovolemic shock because of spontaneous and massive bleeding in the pleural and abdominal cavity. Blood tests revealed a high number of blood cells, and bone marrow smears showed trilineage myeloproliferation. Serum erythropoietin level was decreased. Analysis revealed a V617F mutation in the JAK2 protein. Her activated partial thromboplastin time was slightly prolonged, the ratio between von Willebrand factor (vWF) propeptide and vWF antigen was in the normal range, but the ratio between vWF and ristocetin cofactor was decreased dramatically. Further investigation revealed the absence of large and intermediate vWF-multimers. She was diagnosed with polycythemia vera with acquired von Willebrand syndrome. The bleeding was stopped using a transfusion of freshly thawed plasma and cryoprecipitate.
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PMID:Acquired von Willebrand syndrome in a case of polycythemia vera resulting in recurrent and massive bleeding events in the pleural and abdominal cavity. 2521 16


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