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)

In patients with liver cirrhosis, especially in the advanced stage, the coexistence of low clotting factor levels, hypofibrinogenemia, thrombocytopenia and elevated fibrin(ogen) degradation product (FDP) and D-dimer levels may suggest the presence of disseminated intravascular coagulation (DIC). In this study we evaluated, in 21 patients with decompensated liver cirrhosis and elevated FDP and D-dimer levels, the time sequence of their coagulation data during a follow-up period of 15 days after the first observation; our aim was to clarify if these patients tend to develop during this time interval a severe consumption coagulopathy as an expression of overt DIC. We evaluated serum fibrinogen, platelet count, prothrombin activity, serum FDP and plasma D-dimer levels at days 1, 3, 6, 10 and 15. The coagulation data were fairly stable during the study period in all patients, even in the two patients who had upper digestive tract bleeding during the study time. Only two patients affected by infectious diseases showed a decrease of D-dimer and FDP levels after healing. Our data suggest that in decompensated liver cirrhosis the detection of elevated FDP and D-dimer levels is seldom related to the occurrence of an overt DIC, at least during a short time interval; in this condition heparin therapy seems therefore not advisable and even potentially dangerous.
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PMID:Time sequence of coagulation data in patients with decompensated liver cirrhosis and suspected disseminated intravascular coagulation. 186 73

Two populations of dogs with cutaneous hemangiomas and hemangiosarcomas were evaluated retrospectively. One population consisted of 96 dogs seen at the Veterinary Medical Teaching Hospital at the University of California, Davis. The second population consisted of 116 dogs that had skin biopsy specimens submitted to a private veterinary diagnostic laboratory for histologic diagnosis. Nine dogs from the teaching hospital and 2 dogs, from which samples had been submitted to the veterinary diagnostic laboratory, developed hemostatic defects in association with the tumors. Hemostatic defects included hemorrhage directly from the tumor, thrombocytopenia, hypofibrinogenemia, and findings associated with disseminated intravascular coagulation. Because bleeding during surgery can develop in animals with hemostatic defects, dogs with one or more tumors suspected of being vascular in origin should have platelet numbers and hemostatic analytes evaluated prior to surgery, especially if petechiae or ecchymoses are evident.
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PMID:Evaluation of hemostatic defects secondary to vascular tumors in dogs: 11 cases (1983-1988). 202 48

A 63-year-old woman was diagnosed as having blue rubber bleb nevus syndrome (BRBNS) with disseminated intravascular coagulation (DIC). Hematological data showed typical DIC: PT 13.2 sec, activated PTT 55.3 sec, fibrinogen 20 mg/100 ml, FDP-E 928 ng/ml, D-dimer 3,477 ng/ml, platelet count 25 x 10(3)/microliters. Although hypofibrinogenemia was successfully controlled by the continuous infusion of heparin, 10,000 units/day, thrombocytopenia has continued. Based on shortened platelet life span, high level of platelet associated IgG, and increased number of megakaryocyte in the bone marrow, the thrombocytopenia was thought to be due to antiplatelet antibody. Her platelet count returned to normal after intravenous infusion of high-dose gamma globulin (IVIg, Sandoz) at the dose of 400 mg/kg for 2-5 days, while corticosteroid, Gabexate mesilate, synthetic thrombin inhibitor MD-805, urinastatin and warfarin had no effect. Thus, DIC or thrombocytopenia may become a serious complication in some patients with BRBNS and IVIg may be useful for correcting thrombocytopenia in the patient.
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PMID:Blue rubber bleb nevus syndrome with disseminated intravascular coagulation and thrombocytopenia: successful treatment with high-dose intravenous gammaglobulin. 204 21

Three patients with consumption coagulopathy due to left atrial thrombosis associated with mitral valve disease are described. They had hypofibrinogenemia (0.7-1.7 g/L), mild thrombocytopenia (104-117 x 10(9)/L), and elevated fibrinos/fibrin degradation products (FDP) (20-64 micrograms/ml). Two patients had bleeding symptoms, and one of these also had two episodes of transient ischemic attack. One without bleeding symptoms had three episodes of transient ischemic attack and repeated retinal vein thrombosis. In two patients, preoperative anticoagulation with either heparin or nafamostat mesilate was followed by an increase in plasma fibrinogen level from 0.7 to 5.6 g/L and a decrease in FDP from 64 to 8 micrograms/ml in one patient, and fibrinogen from 1.0 to 2.8 g/L and FDP from 40 to 5 micrograms/mL in another patient. The mitral valve replacement and thrombectomy were performed uneventfully, and their coagulopathy disappeared thereafter. These three patients had a lower platelet count and a shorter platelet survival time than another three patients with mitral valve disease of a similar severity but without coagulopathy. Hemostatic evaluation should be performed in patients suspected of intracardiac thrombosis.
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PMID:Consumption coagulopathy associated with left atrial thrombosis. 205 Jun 2

Blood coagulation, fibrinolytic and unspecific proteolytic parameters were investigated in 34 patients with acute myeloid leukemia. An increased activity of the coagulation system, documented by elevated thrombin-antithrombin III-complex (TAT) plasma levels, was found in 91% of the patients; 50% had increased elastase plasma levels. Hyperfibrinolysis, as shown by elevated fibrin split-product D-Dimer plasma levels, was detected in 91% of AML patients. Activation of these enzyme systems was not associated with relevant defects in blood coagulation or fibrinolysis in the majority of the patients investigated. In selected cases of promyelocytic M3 and monoblastic M5 leukemia, however, hypofibrinogenemia and alpha 2-plasmininhibitor deficiency was found, most likely due to depletion of these proteins in the course of disseminated intravascular coagulation and secondary hyperfibrinolysis. Significant correlations were calculated between TAT and fibrinogen (r = -0.57, P less than 0.005), TAT and D-Dimer (r = 0.89, P less than 0.0005), and D-Dimer and alpha 2-plasmininhibitor (r = -0.77, P less than 0.0005) levels. Indications of a pathogenetic importance of primary hyperfibrinolysis or unspecific proteolysis for hypofibrinogenemia and alpha 2-PI deficiency were not found.
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PMID:Hemostatic and fibrinolytic parameters in patients with acute myeloid leukemia: activation of blood coagulation, fibrinolysis and unspecific proteolysis. 227 76

A female patient with intravitally diagnosed splenic angiosarcoma is described. Progress of the cancerous process was attended by the development of consumption coagulopathy with profound fibrinogenopenia and thrombocytopenia. In this case the DIC syndrome was characterized by the lack of systemic fibrinolysis activation. The rupture of the cavernous tumor of the spleen and profound disorders of hemostasis determined profuse intraperitoneal hemorrhage and the patient's death. Diagnostic criteria that contribute to early recognition of splenic angiosarcoma are suggested.
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PMID:[Angiosarcoma of the spleen with consumption coagulopathy]. 228 95

We examined fibrinolytic substances in homogenate of leukemic cells, normal granulocyte or mononuclear cells fraction. Plasminogen activators (PA) were significantly low in normal cells, but they were slightly increased in lymphoblastic leukemia cells and markedly increased in myeloblastic leukemia cells. In almost leukemic cells homogenate, the antigen ratio of tissue type PA (t-PA)/urokinase type PA (u-PA) was about 2.0. In especially AMMoL and AMoL, PA activity had discrepancy between euglobulin lysis time and amidolytic assay using chromogenic substrate. As PA inhibitor (PAI)-II was markedly increased in them. PAI might effect the PA assay. PA activity of leukemic cells homogenate was similar to that without t-PA stimulator and leukemic cells homogenate significantly stimulated t-PA. As both PA activity and antigen were statistically increased in leukemic cells homogenate of patient with disseminated intravascular coagulation (DIC), PA and PA stimulator in leukemic cell might play an important role in hypofibrinogenemia or DIC.
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PMID:[Plasminogen activator in leukemic cell homogenate]. 228 63

We described here a seventy-one year-old male, who had repeated disseminated intravascular coagulation related to atherosclerosis and aneurysm of the aorta, and was successfully treated with self-subcutaneous injection of heparin sodium. He developed gingival bleeding and purpura in 1977. He was first treated with prednisolone (30 mg/day) and ACTH-Z under the diagnosis of idiopathic thrombocytopenic purpura associated with chronic thyroiditis, since platelet count (0.2 x 10(4)/microliters) was markedly decreased and megakaryocytes in the bone marrow were increased. By the treatment, platelet count recovered to 16.7 x 10(4)/microliters, while fibrin-degradation product levels were increased and hypofibrinogenemia developed, suggesting disseminated intravascular coagulopathy. Additional treatment with heparin was effective, and the coagulation studies became normal. In 1980, he again developed the episode with thrombocytopenia. At this time, prednisolone did not improve the episode, but heparin was effective. Since 1983, an enlargement of abdominal aorta had been recognized and gradually progressed. In 1983, he developed lumbago and abdominal pain, and received an emergency operation using artificial Y-graft vessel under the diagnosis of rupture of the aneurysm. There was no evidence of consumption coagulopathy at that time. He had been well until 1987, when he developed the third episode of thrombocytopenia with gingival bleeding. Thrombocytopenia was controlled with the treatment of heparin, but needed a continuous treatment with heparin. Thereafter, he has been well managed with self-injection of the anticoagulant, heparin sodium.
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PMID:[Disseminated intravascular coagulation related to atherosclerosis and aneurysm of aorta: successful management with subcutaneous self injection of heparin sodium]. 259 49

A 71-year-old male with disseminated intravascular coagulation (DIC) caused by abdominal aortic aneurysm was successfully treated surgically. He had aortic regurgitation, an old myocardial infarction, and nephrotic syndrome. The infrarenal part of the inferior vena cava, which was on the left side of the aneurysm, was temporarily transected during the surgical procedure. Preoperative heparin therapy was insufficient, but infusion of blood components during the operation and minimal dissection of the aneurysm were effective in controlling intraoperative hemorrhage. Hypofibrinogenemia and thrombocytopenia were normalized immediately after operation, and hemorrhagic diathesis was completely cured. In this case, the definitive treatment of DIC caused by an abdominal aortic aneurysm war removal of the lesion and the infusion of coagulation factors during the operation was effective in minimizing blood loss.
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PMID:Disseminated intravascular coagulation caused by abdominal aortic aneurysm. 341 54

Forty children, aged 1/2-14 years, with serologically proven dengue haemorrhagic fever were daily studied for hemostatic tests. There were 4, 20 and 16 cases of grade I, II III respectively. Hemostatic derangements in DHF is a multifactorial mechanism. Vasculopathy, thrombocytopenia, platelet dysfunction were found in most cases. Mild to moderate degree of prothrombin complex deficiency was observed in 15% and 50% of grade II and grade III respectively while laboratory evidence of consumptive coagulopathy was noted in 30% of shock cases and 10% of non-shock cases. Hypofibrinogenemia and increased PTT are commonly seen in grade III reflect the presence of stimulation of intrinsic coagulation pathway probably from immunologic reaction. Frank DIC is very rarely observed. FDP is slightly increased but not as high as in classical DIC. Further study on the role of platelet-endothelial interaction should be elucidated including the efficient management to stop bleeding in severe shock cases.
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PMID:Hemostatic derangement in dengue haemorrhagic fever. 343 65


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