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)

It is well-known that SFD babies are born of the mothers who had toxemia of pregnancy in many cases. Recently we examined the relation of hemocoagulatological changes in mothers with toxemia to the birth weight of their babies with the intention of investigating the cause of development of SFD babies and obtained some information as follows: 1. The pregnant women with toxemia were significantly lower (p less than 0.01) in platelet count, fibrinogen content, and serum factor XIII value, significantly longer (p less than 0.01) in bleeding time, and significantly higher (p less than 0.01) in serum-urine FDP, platelet ADP aggregation and platelet spreadability than the normal pregnant women. 2. As for the relation of these changes to the birth weight, the value obtained in the SFD baby and that obtained in the AFD baby group were 5.8 +/- 1.5 and 4.5 +/- 1.3 in bleeding time (min), 20.4 +/- 3.17 and 23.4 +/- 4.21 in platelet count x 10(4)/mm3), 296.5 +/- 58.5 and 346.8 +/- 50.4 in fibrinogen content (mg/dl), 1.3 +/- 0.80 and 0.6 +/- 0.63 in urine FDP (microgram/ml), respectively, and the difference between both groups was significant (p less than 0.05) in each of these parameters. The results stated above suggested that toxemia of pregnancy assumed as aspect of chronic DIC and this tendency was stronger in the SFD baby group. From these facts it is considered that a state of chronic DIC in toxemia of pregnancy may be a cause of disturbance in the development of the fetus.
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PMID:[Hemocoagulatological changes in toxemia of pregnancy--in reference to birth weight (author's transl)]. 727 47

A women with congenital cavernous hemangiomas and a bleeding diathesis since childhood was found to have a qualitative platelet defect characterized by the absence of a second-phase aggregation induced by epinephrine, adenosine diphosphate (ADP), and collagen, accompanied by decreased levels of adenosine triphosphate (ATP) and ADP, with a high ATP-ADP ratio consistent with the diagnosis of "storage pool disease" of the platelets. There was no evidence of disseminated intravascular coagulation or circulating antiplatelet antibodies. The bleeding tendency responded to platelet transfusion.
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PMID:'Storage pool disease' of platelets. Association with multiple congenital cavernous hemangiomas. 738 76

An 82-year-old man with a one-year history of spontaneous ecchymoses and posttraumatic bleeding was found on physical examination to have a pulsatile abdominal mass. Ultrasonography revealed a large abdominal aortic aneurysm with a freely moving 1.5--2-cm intraluminal thrombus. Laboratory data disclosed intravascular hemolysis, disseminated intravascular coagulation, and a prolonged bleeding time. Further investigation of platelet function demonstrated decreased glass bead retention (0-15%), and reduced or delayed aggregation responses to adenosine diphosphate, epinephrine, and collagen. Studies of platelet factor 3 availability, antiplatelet antibodies, and aggregation response to ristocetin were normal. Transfusion of ten units of normal platelets failed to shorten the patient's bleeding time, despite a marked rise in platelet count. Glass bead retention studies on normal and patient blood were not altered by mixture with patient and normal platelet-poor plasma, respectively. Platelet dysfunction in the presence of arterial aneurysm does not appear to have been reported previously.
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PMID:Platelet dysfunction associated with abdominal aortic aneurysm. 744 78

Abstract. Abnormal hemostasis in dengue hemorrhagic fever includes:- 1. Vasculopathy which occurs during the early febrile to pre-shock and shock phase. The evidences support are: 1.1 Increased anaphylatoxin, released by complement activation causing leakage of intravascular fluid in to serous space. 1.2 Positive tourniquet test, some of which occur preceeding thrombocytopenia in the acute phase of DHF. 1.3 Excessive increased in PGI2 which is the most potent vasodilator and platelet aggregation inhibitor. 2. Platelets: 2.1 Thrombocytopenia due to 2.1.1 The bone marrow hypocellularity with increased in all forms of megakaryocytes but the vacuolated and disintegrated ones. 2.1.2 Destruction by the liver and spleen. 2.1.3 Immune-mediated injury as demonstration of dengue antibody complexes on the platelet surface. 2.1.4 The in vitro spontaneous aggregation to vascular endothelial cell pre-infected by dengue virus inducing platelet aggregation, causing lysis and platelet destruction. 2.2 Dysfunction shown by 2.2.1 Increased release of betathromboglobulin (BTG), PF4 and PGI2. 2.2.2 In vitro hypoaggregation stimulated by ADP and defect in ADP-releasing ability. 3. Coagulopathy including: 3.1 Prothrombin complex deficiency due to liver damage. 3.2 Consumptive coagulopathy due to the activation by mononuclear phagocytes, PF3 released from platelet aggregation. DIC is seen in prolonged shock cases of DSS.
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PMID:Abnormal hemostasis in dengue hemorrhagic fever. 788 14

The effects of E. coli lipopolysaccharide (LPS) on washed platelets of the healthy volunteers were studied by measuring ADP induced aggregation and intracellular ionized calcium concentration ([Ca2+]i) by fluorescent calcium indicator, quin 2. Addition of LPS in platelets suspension in saline, caused an increased platelet aggregation. Adding LPS, however, in platelet suspension in Na(+)-citrated platelet poor plasma inhibited ADP aggregation. These trends were not affected by cyclooxygenase inhibitor, but partially antagonized by dibutyryl cyclic AMP, and verapamil. The intracellular calcium ion concentration ([Ca2+]i) was significantly increased (334 +/- 141 nM to 150 +/- 45 nM in control) on addition of LPS in platelet suspension containing ionized calcium. On the other hand, there was no significant difference observed with those suspended in calcium free solution (50 +/- 16 to 45 +/- 15 in control). These results indicate that changes of platelet aggregation by LPS were mediated by cyclic AMP and Ca2+, but not by arachidate derivatives. The author concludes that LPS changed the mechanism of Ca2+ influx of platelet membrane and elevated [Ca2+]i of platelets. These findings, however, probably are not the cause of aggregation of platelets during DIC.
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PMID:[Effects of E. coli LPS on human platelet aggregation]. 818 78

Thrombocytic, haemostatic and fibrinolytic quantities were investigated in 47 patients with cerebral infarction and 34 patients with cerebral haemorrhage. Sixteen of the infarction patients and ten patients of the haemorrhage group were on acetylsalicylic acid medication. Of the remaining 55 patients without acetylsalicylic medication 21/31 = 67.7% of the patients in the infarction group and 9/24 = 37.5% of the patients in the bleeding group had unphysiologically enhanced ADP-induced platelet aggregation. With regard to the coagulation and fibrinolysis markers no significant differences were found between the two groups. In both groups, coagulation activity markers (fibrin monomer and thrombin-antithrombin III), as well as D-dimers were significantly higher than in controls in a high proportion of cases. In 5/47 of the infarction patients and in 3/34 of the haemorrhage patients the fibrin monomer levels were elevated to such an extent, that it can be considered as low grade disseminated intravascular coagulation. In the cerebral haemorrhage group, 80.3% of the patients who subsequently died showed a significantly enhanced fibrin monomer concentration, compared with 28.6% of those who survived. The corresponding frequencies for D-dimer were 100% compared with 66.7%. In the cerebral infarction group, the only analytical quantity showing a significant difference between patients with a fatal outcome and those with a non-fatal outcome was ADP (2 mumol/l) induced platelet aggregation (83.3% in the fatal group, 40.0% in the non-fatal group).
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PMID:On the degree of platelet, coagulation and fibrinolysis activation after cerebral infarction and cerebral haemorrhage and the clinical outcome. 826 May 28

Collagen-related peptides, Gly-Pro-Arg and its analogues, were examined for their inhibitory effects on platelet aggregation induced by the addition of ADP. Human platelet aggregation was suppressed by more than 50% with each of Gly-Pro-Arg and such Gly-Pro-Arg-containing peptides as Gly-Pro-Arg-Gly, Gly-Pro-Arg-Gly-Pro, Gly-Pro-Arg-Pro-Pro, and Gly-Pro-Arg-Pro-Pro-Pro at a concentration of 0.3 mM. The inhibitory effects of these peptides were about 10 times higher in human PRP than in rat PRP. Other Gly-Pro-Arg analogues such as Sar-Pro-Arg, Gly-Pro-Lys, Gly-Ala-Arg, and Ala-Gly-Pro-Arg had no inhibitory effect at a concentration from 0.1 to 0.8 mM even in human PRP. Intravenous and oral administrations of Gly-Pro-Arg and enzymatic hydrolysates of collagen suppressed the decrease in platelet count for endotoxin-induced DIC in rats. Collagen itself has been regarded as a potent inducer of platelet aggregation, but these findings suggest that collagen-related peptides and enzymatic hydrolysates of collagen prevent platelet aggregation.
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PMID:In vitro and in vivo anti-platelet effects of enzymatic hydrolysates of collagen and collagen-related peptides. 917 51

Heparin-induced thrombocytopenia is an uncommon but potentially dangerous adverse effect of heparin therapy. Late onset thrombocytopenia is usually observed several days after initiating treatment and can be distinguished from early-onset benign thrombocytopenia which is more moderate and transitory and which results from a direct interaction between heparin and platelet membrane proteins which potentialize ADP-induced aggregation. Severe late-onset thrombocytopenia clearly results from an immunological mechanism due to the development of heparin-independent antiplatelet antibodies, often IgGs. These antibodies do not cause cell lysis but have a platelet-activating effect with release of the contents of the dense alpha granulations. This cell activation requires the formation of a heparin-dependent antibody-platelet complex. In most cases, platelet factor 4, an alpha granule protein, would be implicated. The antibody-platelet interaction has an activating effect following binding of the IgG Fc fragment to the Fc gamma RII receptor. The antibodies could also bind, favoring the development of thrombosis. The diagnosis of heparin-induced thrombocytopenia is evidenced by a platelet count under 100 Giga/l, usually from the 5th to 20th week of heparin therapy. Occasionally, the only sign is the low platelet count (drop of over 40% from pretreatment levels). Coagulation activation can lead to diffuse consumption coagulopathy in about 25% of the cases. Clinically, thrombosis is observed in about one half of the cases. Arterial thrombosis is the most characteristic and concerns the aorta and its branches as well as cerebral, coronary, mesenteric, renal and upper limb arteries. Venous thrombosis may be underestimated as they often occur as paradoxical recurrence after heparin therapy. Hemorrhage is much less frequent (less than 20% of cases) and often benign. To diagnose heparin-induced thrombocytopenia, one must eliminate other potential causes (infection, drug...), observe complete normalization of platelet count after heparin withdrawal, and demonstrate heparin-dependent antibodies in the plasma or serum. Different laboratory tests are quite helpful but have variable sensitivity. The incriminated heparin must be discontinued immediately. Use of low-molecular-weight heparins, even when cross-reactivity is not demonstrated in vitro, is not recommended. Other compound however, such as Orgaran 10,172 (or Lomoparan, appear to be the best choice. The action of antivitamin K agents is delayed and, due to the early dissociated drop in protein C at the beginning of treatment further raise the major risk of thrombosis. Classic antiplatelet agents such as aspirin are ineffective if used alone. More powerful compounds such as Ilomedine, are not available for this indication and are difficult to titrate. Part of the therapeutic problem with heparin-induced thrombocytopenia may be resolved with the advent of molecules with a direct antithrombin effect such as hirudine or its analogues. As suggested by a recent study, widespread use of low-molecular-weight heparin will undoubtedly have a highly significant effect on reducing the number of cases of severe thrombocytopenia.
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PMID:[Thrombopenia induced by heparin. From physiopathology to treatment]. 923 38

Regulation of cytoskeletal dynamics is essential for cell shape change and morphogenesis. Drosophila melanogaster embryos offer a well-defined system for observing alterations in the cytoskeleton during the process of cellularization, a specialized form of cytokinesis. During cellularization, the actomyosin cytoskeleton forms a hexagonal array and drives invagination of the plasma membrane between the nuclei located at the cortex of the syncytial blastoderm. Rho, Rac, and Cdc42 proteins are members of the Rho subfamily of Ras-related G proteins that are involved in the formation and maintenance of the actin cytoskeleton throughout phylogeny and in D. melanogaster. To investigate how Rho subfamily activity affects the cytoskeleton during cellularization stages, embryos were microinjected with C3 exoenzyme from Clostridium botulinum or with wild-type, constitutively active, or dominant negative versions of Rho, Rac, and Cdc42 proteins. C3 exoenzyme ADP-ribosylates and inactivates Rho with high specificity, whereas constitutively active dominant mutations remain in the activated GTP-bound state to activate downstream effectors. Dominant negative mutations likely inhibit endogenous small G protein activity by sequestering exchange factors. Of the 10 agents microinjected, C3 exoenzyme, constitutively active Cdc42, and dominant negative Rho have a specific and indistinguishable effect: the actomyosin cytoskeleton is disrupted, cellularization halts, and embryogenesis arrests. Time-lapse video records of DIC imaged embryos show that nuclei in injected regions move away from the cortex of the embryo, thereby phenocopying injections of cytochalasin or antimyosin. Rhodamine phalloidin staining reveals that the actin-based hexagonal array normally seen during cellularization is disrupted in a dose-dependent fashion. Additionally, DNA stain reveals that nuclei in the microinjected embryos aggregate in regions that correspond to actin disruption. These embryos halt in cellularization and do not proceed to gastrulation. We conclude that Rho activity and Cdc42 regulation are required for cytoskeletal function in actomyosin-driven furrow canal formation and nuclear positioning.
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PMID:Cellularization in Drosophila melanogaster is disrupted by the inhibition of rho activity and the activation of Cdc42 function. 985 49

Hemostasis is initiated by injury to the vascular wall, leading to the deposition of platelets adhering to components of the subendothelium. Platelet adhesion requires the presence of von Willebrand factor and platelet receptors (IIb/IIIa and Ib/IX). Additional platelets are recruited to the site of injury by release of platelet granular contents, including ADP. The "platelet plug" is stabilized by interaction with fibrinogen. In this review, I consider laboratory tests used to evaluate coagulation, including prothrombin time, activated partial thromboplastin time, thrombin time, and platelet count. I discuss hereditary disorders of platelets and/or coagulation proteins that lead to clinical bleeding as well as acquired disorders, including disseminated intravascular coagulation and acquired circulating anticoagulants.
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PMID:Coagulation and bleeding disorders: review and update. 1092 20


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