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)

Thrombocytopenia is one of the most common laboratory manifestations of disseminated intravascular coagulation (DIC). To investigate whether thrombocytopenia in DIC is indeed due to platelet consumption, we measured the plasma levels of glycocalicin, a proteolytic fragment of the platelet membrane glycoprotein (GP) Ib alpha, a component of the GPIb/IX complex, in patients with solid tumors either with DIC(n=18) or without DIC (n=18). Patients with DIC had significantly elevated levels of glycocalicin(2.53 +/- 1.59 mg/1;n=18,p<0.05) compared to those without DIC (1.50 +/- 0.41 mg/1;n=18), indicating enhanced platelet consumption, or destruction, in patients with DIC. However, glycocalicin concentrations had a wide range (0.18-5.74 mg/1), and 3 DIC patients had levels lower than the normal lower limit. These findings suggest that, in patients with DIC, thrombocytopenia is not always due to increased platelet consumption, but it may be due to decreased production of platelets. Determination of plasma glycocalicin concentrations is an easy way to identify thrombocytopenia, due to bone marrow insufficiency in these patients.
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PMID:Increased but highly dispersed levels of plasma glycocalicin in patients with disseminated intravascular coagulation. 859 38

Important mechanisms underlying immediate xenograft loss by hyperacute rejection (HAR), in the pig-to-primate combination, have been recently delineated. There are now several proposed therapies that deal with the problem of complement activation and xenoreactive natural antibody (XNA) binding to the vasculature that have been shown to prevent HAR. However, vascularized xenografts are still lost, typically within days, by delayed xenograft rejection (DXR), alternatively known as acute vascular rejection (AVR). This process is characterized by endothelial cell (EC) perturbation, localization of XNA within the graft vasculature, host NK cell and monocyte activation with platelet sequestration and vascular thrombosis. Alternative immunosuppressive strategies, additive anti-complement therapies with the control of any resulting EC activation processes and induction of protective responses have been proposed to ameliorate this pathological process. In addition, several potentially important molecular incompatibilities between activated human coagulation factors and the natural anticoagulants expressed on porcine EC have been noted. Such incompatibilities may be analogous to cross-species alterations in the function of complement regulatory proteins important in HAR. Disordered thromboregulation is potentially relevant to the progression of inflammatory events in DXR and the disseminated intravascular coagulation seen in primate recipients of porcine renal xenografts. We have recently demonstrated the inability of porcine tissue factor pathway inhibitor (TFPI) to adequately neutralize human factor Xa (FXa), the aberrant activation of both human prothrombin and FXa by porcine EC and the failure of the porcine natural anticoagulant, thrombomodulin to bind human thrombin and hence activate human protein C. The enhanced potential of porcine von Willebrand factor to associate with human platelet GPIb has been demonstrated to be dependent upon the isolated A1 domain of von Willebrand factor. In addition, the loss of TFPI and vascular ATPDase/CD39 activity following EC activation responses would potentiate any procoagulant changes within the xenograft. These developments could exacerbate vascular damage from whatever cause and enhance the activation of platelets and coagulation pathways within xenografts resulting in graft infarction and loss. Analysis of these and the other putative factors underlying DXR should lead to the development and testing of genetic approaches that, in conjunction with selected pharmacological means, may further prolong xenograft survival to a clinically relevant extent.
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PMID:Factors in xenograft rejection. 1041 73

A 47-yr-old female with acute pancreatitis received four units of fresh frozen plasma because of subtle signs of disseminated intravascular coagulation (DIC). Seven days later, she developed severe thrombocytopenia. Serological studies demonstrated antibodies against HPA-1a together with pan-reactive antibodies against platelet glycoproteins (GPIIb-IIIa, GPIb-IX and GPIa-IIa), which was consistent with the diagnosis of PTP. The patient was treated with platelet transfusions, corticosteroids and intravenous immunoglobulin (IVIG) without permanent beneficial effect. After treatment with plasma exchange the platelet count increased to normal values.
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PMID:Post-transfusion purpura (PTP) and disseminated intravascular coagulation (DIC). 1280 1

Thrombocytopenia frequently appear in severe malaria. The reasons of low blood platelets count are different and its results of hypersplenism, subclinical course of intravascular coagulation (DIC). Thrombocytopenia from "consumption" is consequence of sequestration of blood platelets in blood vessels of lungs and cerebral. We examination 29 years old men, who was as forest worker in islands on Indonesia. He was treated with recurrent, poliethiological malaria (Plasmodium falciparum, Plasmodium vivar) and severe thrombocytopenia (17.0 G/L) without hepatosplenomegalia. Antiplatelet antibody was examined in blood serum by ELISA methods (GTI - PAKPLUS. In blood serum was detected IgG antibody agai nstglicoprotein receptors on surface of blood platelets GPIIb/IIIa, GPIV, GPIb/IX, GPV, GPIa/IIa. Chronic infections of Plasmodium may conduct to autoimmune destruction of blood platelets.
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PMID:[Autoimmune thrombocytopenia in recurrent polietiological malaria (Plasmodium falciparum, Plasmodium vivax)]. 1688 56