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)

Bleeding occurs in approximately 10% of patients with cancer: supportive transfusion therapy with Platelets Concentrates (PC), Fresh Frozen Plasma (FFP) and plasma-derived or recombinant concentrates is often required for the cessation and prevention of the bleeding episodes. The most frequent causes of bleeding in cancer is thrombocytopenia followed by liver insufficiency with or without vitamin K deficiency, disseminated intravascular coagulation (DIC) and the inappropriate or excessive use of anticoagulants. Other acquired hemostatic defects such as acquired hemophilia (AHA) and acquired von Willebrand syndrome (AVWS) are rare but they can be life-threatening. Thrombocytopenia in cancer patients may be the consequence of marrow invasion, chemotherapy or platelet auto-antibodies; patients with severe hypoproliferative thrombocytopenia, must be treated with PC and carefully followed to assess refractoriness to PC. The management of the other acquired defects of hemostasis usually requires the use of FFP and specific plasma-derived or recombinant concentrates. PC, FFP and plasma-derived concentrates can induce complications and/or adverse events in cancer patients: these include mainly allergic (ALR) or anaphylactic reactions (ANR), Transfusion-Associated Graft-Versus-Host Disease (TA-GVHD), Trasfusion-transmitted bacteriemia (TTB), Transfusion-Related Acute Lung Injury (TRALI), Acute Hemolytic Transfusion Reactions (AHTR), Febrile Non Hemolytic Transfusion Reactions (FNHTR). Therefore, modifications such as leukocyte-reduction and irradiation of the blood components to be transfused in cancer patients are recommended to reduce the risk of these complications.
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PMID:Supportive transfusion therapy in cancer patients with acquired defects of hemostasis. 2486 47

Severe protein C (PC) deficiency leads to purpura fulminans and stroke in newborns. However, the clinical impact of plasma PC activity on the development of neonatal cerebral disease remains elusive. We report a case of hemorrhagic stroke associated with neonatal asphyxia and severe PC deficiency. Plasma PC and protein S activity 7 days after birth was 12% and 43%, respectively. No PROC mutation was found. PC levels did not exceed 20% until 2 months of age, even in the absence of consumption coagulopathy or vitamin K deficiency. Neither thromboembolic nor hemorrhagic events occurred during the infusion of activated PC concentrate (twice weekly, up to 68 days after birth). The PC activity levels gradually increased to the standard value for age by 9 months of age. The present case showed that neonatal PC deficiency without a PROC mutation caused an intracranial hemorrhage before a slow increase in PC activity.
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PMID:Slow Elevation in Protein C Activity without a PROC Mutation in a Neonate with Intracranial Hemorrhage. 2965 98

Acquired factor VII (FVII) deficiency in the absence of vitamin K deficiency, oral, synthetic liver dysfunction, or DIC is rare, with only a handful of cases published in literature. Congenital deficiency of FVII is well known but, little is known about secondary FVII deficiency and its management. The knowledge of this syndrome should avoid false diagnosis of congenital factor VII deficiency. Here, we present the report of a young woman who presented with pyelonephritis, anaemia, prolonged prothrombin time and normal activated partial prothrombin time (aPTT). She was diagnosed to have acquired FVII deficiency and this was the first such case with pyelonephritis.
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PMID:Acquired Factor VII Deficiency in Association with Pyelonephritis. 3047 72

The activated partial thromboplastin time (APTT) assay is a very common coagulation test, used for several reasons. The test is conventionally used for assessing the contact factor (intrinsic) pathway of blood coagulation, and thus for screening deficiencies in this pathway, most typically factors VIII, IX, and XI. The APTT is also sensitive to contact factor deficiencies, including factor XII, prekallikrein, and high-molecular-weight kininogen. The APTT may also be elevated in a variety of conditions, including liver disease, vitamin K deficiency, and disseminated intravascular coagulation. The APTT can also be used for monitoring unfractionated heparin (UFH) therapy, as well as for screening lupus anticoagulant (LA) or for assessing thrombosis risk. Which of these separate uses is important to a given laboratory or clinician depends on the laboratory and the clinical context. For example, UFH sensitivity is important in hospital-based laboratories, where UFH therapy is used, but not in hospital-based laboratories where low-molecular-weight heparin (LMWH) is largely employed or where UFH may be assessed by anti-factor Xa testing, or in private/community laboratories not associated with a hospital system. High sensitivity to (low levels of) factors VIII, IX, and XI is generally preferred, as their deficiencies are clinically significant. Also preferred, but not usually achieved, is low sensitivity to factor XII and other contact factors, as these deficiencies are usually asymptomatic. Nevertheless, a good knowledge of factor sensitivity is usually needed, if only to help explain the reasons for a prolonged APTT in a given patient, or whether factor testing or other investigation is required. A good working knowledge of reagents sensitivity to LA is also advisable, especially when the reagent is used as part of a LA test panel, or else as a "general-purpose screening reagent." The current report is aimed at providing some guidance around these questions, and is intended as a kind of "how to" guide, that will enable laboratories to assess APTT reagents in regard to their sensitivity to heparin, LA, and clotting factors. The report also provides some advice on generation of normal reference ranges, as well as solutions for troubleshooting prolonged APTTs, when performing factor testing or searching for inhibitors.
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PMID:How to Optimize Activated Partial Thromboplastin Time (APTT) Testing: Solutions to Establishing and Verifying Normal Reference Intervals and Assessing APTT Reagents for Sensitivity to Heparin, Lupus Anticoagulant, and Clotting Factors. 3063 Feb 6

Coagulopathy in the nephrotic syndrome (NS) is very rare. Simultaneous prolongation of both prothrombin time and activated partial thromboplastin time suggests common coagulation pathway abnormality such as liver dysfunction, Vitamin K deficiency, disseminated intravascular coagulation, or primary fibrinolysis. This results in difficulty in proceeding with renal biopsy and tissue diagnosis. We report one such case of NS with coagulopathy and refractoriness to correction with blood products, which led us to make a diagnosis of AL amyloidosis, which was confirmed with abdominal fat pad biopsy and other work-up.
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PMID:Coagulopathy in the nephrotic syndrome. 3239 33


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