Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute thrombocytopenia occurs commonly in hospitalized patients. For most, the etiology of an acutely declining platelet count is obvious and includes sepsis with disseminated intravascular coagulation, large-volume crystalloid infusion, or the administration of cytotoxic therapies, such as chemotherapeutic agents. For others, however, the etiology may be less apparent. In these cases, drug-induced thrombocytopenia (DIT), including heparin-induced thrombocytopenia (HIT), must be a diagnostic consideration. The approach to the hospitalized patient with thrombocytopenia, without an obvious cause, includes a careful medication history to identify potential culprits, such as glycoprotein IIb/IIIa inhibitors, vancomycin, linezolid, beta-lactam antibiotics, quinine, antiepileptic drugs, or heparin/low-molecular-weight heparin. Usually, discontinuation of the offending medication is all that is necessary for resolution of thrombocytopenia. Heparin-induced thrombocytopenia, however, is an exception to this general rule given its unique pathogenesis and propensity for thrombotic complications and death. Differentiating between HIT and DIT due to nonheparin medications may prove challenging. Through a careful clinical assessment, consideration of the pre-test probability for HIT, and the thoughtful application of laboratory testing, HIT can be accurately diagnosed. Because patients with HIT have a high risk of thrombosis and bleeding is uncommon, the prompt initiation of an alternative anticoagulant (e.g., a direct thrombin inhibitor) is warranted in these patients.
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PMID:Drug-induced thrombocytopenia for the hospitalist physician with a focus on heparin-induced thrombocytopenia. 2046 10

Although the pathophysiology of sepsis has been elucidated with the passage of time, sepsis may be regarded as an uncontrolled inflammatory and procoagulant response to infection. The hemostatic changes in sepsis range from subclinical activation of blood coagulation to acute disseminated intravascular coagulation (DIC). DIC is characterized by widespread microvascular thrombosis, which contributes to multiple organ dysfunction/failure, and subsequent consumption of platelets and coagulation factors, eventually causing bleeding manifestations. The diagnosis of DIC can be made using routinely available laboratory tests, scoring algorithms, and thromboelastography. In this cascade of events, the inhibition of coagulation activation and platelet function is conjectured as a useful tool for attenuating inflammatory response and improving outcomes in sepsis. A number of clinical trials of anticoagulants were performed, but none of them have been recognized as a standard therapy because recombinant activated protein C was withdrawn from the market owing to its insufficient efficacy in a randomized controlled trial. However, these subgroup analyses of activated protein C, antithrombin, and thrombomodulin trials show that overt coagulation activation is strongly associated with the best therapeutic effect of the inhibitor. In addition, antiplatelet drugs, including acetylsalicylic acid, P2Y12 inhibitors, and glycoprotein IIb/IIIa antagonists, may reduce organ failure and mortality in the experimental model of sepsis without a concomitant increased bleeding risk, which should be supported by solid clinical data. For a state-of-the-art treatment of sepsis, the efficacy of anticoagulant and antiplatelet agents needs to be proved in further large-scale prospective, interventional, randomized validation trials.
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PMID:Coagulation abnormalities in sepsis. 2554 51