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)

Plasmin-alpha 2-plasmin inhibitor (alpha 2PI) complex, an indicator of in vivo plasmin generation, was measured in the plasma of 48 patients with disseminated intravascular coagulation (DIC), by enzyme-linked immunosorbent assay (ELISA). Plasmin-alpha 2PI complex was markedly elevated to 7.9 +/- 4.26 mg/liter (mean +/- SD) in DIC at presentation, with normal values at less than 0.8 mg/liter. The concentration of plasmin-alpha 2PI complex changed in parallel with the course of DIC and decreased to 1.9 +/- 1.49 mg/liter (n = 28) in remission. Among various underlying disorders, DIC, in patients with acute promyelocytic leukemia, had the highest complex levels (mean 10.8 mg/liter), and septic patients had the lowest levels (mean 3.4 mg/liter). No significant correlation was found between FDP and plasmin-alpha 2PI complex. These results indicate that the quantitative assay of plasmin-alpha 2PI complex in plasma would be valuable in the assessment of hyperfibrinolysis in DIC.
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PMID:Plasmin-alpha 2-plasmin inhibitor complex in plasma of patients with disseminated intravascular coagulation. 245 7

Plasma samples from patients with disseminated intravascular coagulation (DIC) associated with acute promyelocytic leukemia (APL) exhibited higher levels of the D-fragment of fibrin and fibrinogen degradation products [FDP(D)], with relatively lower levels of cross-linked fibrin degradation products (XDP), than samples of DIC with non-APL. The difference between FDP(D) and XDP levels increased only when alpha 2-plasmin inhibitor (alpha 2-PI) fell below 60% of the normal level in APL patients. These findings suggest that fibrinogenolysis occurs in APL patients when the alpha 2-PI level has decreased significantly.
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PMID:Characterization of the fibrinolytic state by measuring stable cross-linked fibrin degradation products in disseminated intravascular coagulation associated with acute promyelocytic leukemia. 249 30

We performed a blood coagulation study during the course of disseminated intravascular coagulation (DIC) in 34 patients with hematological malignancies. Risk factors of DIC such as increasing tumor mass, anti-tumor therapy and severe infections were frequently observed at onset of DIC, and influenced the prognosis of DIC. Before the onset of DIC, the DIC score and FDP value were slightly elevated, and they were significantly increased after the onset of DIC. Before the onset of DIC, the level of fibrinogen was significantly increased but it was decreased after the onset of DIC. These hemostatic abnormalities continued for about 2 weeks. Patients with DIC showing prolonged APTT and PT had a poor prognosis. The abnormalities of PT, FDP, fibrinogen, DIC score, FDP-D-dimer and fibrinopeptide A were significantly greater in DIC than in Pre-DIC defined as the period one week before the onset of DIC. FDP-D-dimer was also higher in Pre-DIC patients than in those without DIC. Although protein S and C 4 b binding protein were not decreased in DIC or Pre-DIC, Protein C activity decreased during the course of DIC, suggesting that FDP-D-dimer and Protein C activity were useful for diagnosis of Pre-DIC and DIC.
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PMID:[Hemostatic changes before and after the onset of disseminated intravascular coagulation]. 259 41

Case 1: 75 years old male was admitted to our hospital with anterior chest subcutaneous bleeding. Coagulation study revealed that fibrinogen and alpha 2-PI decreased, and FDP, FPA, B beta 15 approximately 42 and D-dimer increased. Case 2: 78 years old male was admitted to Shingu City Hospital with a left hip subcutaneous hematoma. Coagulation study revealed that fibrinogen, ATIII and alpha 2-PI decreased, and FDP increased. US and CT showed abdominal true aneurysm in both cases. Either severe infection or malignancy was not found. Ticropidine and T-AMCHA were medicated for 8 days in case 1, and for 18 months in case 2. Symptom and coagulation study improved in these cases. Due to some side effects such as appetite loss and liver dysfunction in case 1, and diarrhea in both cases, we changed the therapy to mini-dose heparin therapy. This therapy also proved effective. It is concluded that anti-platelet and anti-fibrinolytic therapy are effective for chronic DIC with abdominal true aneurysm.
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PMID:[Chronic disseminated intravascular coagulation due to abdominal true aneurysm in two cases--effect of anti-platelet and anti-fibrinolytic therapy]. 262 2

Detection of the cross-linked fibrin degradation fragment, D-dimer, in patients at risk for disseminated intravascular coagulation (DIC) is strong evidence for the diagnosis. D-dimer confirms that both thrombin generation and plasmin generation have occurred. Patients at risk for DIC (58) and normal controls (7) were studied. Thirty-three patients had DIC--with fragment D-dimer identified in their serum by immunoblotting. Latex agglutination measurements of fibrin(ogen) degradation products (FDPs) and D-dimer were compared with immunoblotting in the detection of D-dimer. FDP measurement was extremely sensitive but not specific. D-dimer measurement was less sensitive but highly specific. Used in tandem, screening with FDP and confirming with D-dimer, sensitivity and specificity were maximized, rendering a predictive value of a confirmed FDP of 100% in this cohort. D-dimer is a valuable adjunct for the laboratory diagnosis of DIC but is most appropriately used as a confirmatory test for the very sensitive FDP test.
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PMID:Diagnosis of disseminated intravascular coagulation. Role of D-dimer. 264 5

Assessment of animals with a suspected hemorrhagic diathesis of unknown cause(s) should be methodical. Most acquired coagulopathies result from thrombocytopenia. A platelet estimate (from a blood smear) and/or a platelet count on a fresh blood sample therefore are useful first steps in case evaluation. If thrombocytopenia is present, the most likely causes are immune-mediated destruction of platelets, DIC, or megakaryocytic hypoplasia. These diagnoses can be pursued by further test, including antiplatelet antibody assays (for example, the platelet factor 3 tests or an ELISA test), measurement of FDP, and bone marrow biopsy, respectively. If the platelet count is normal, a buccal mucosa bleeding time test is a useful second step. If this is prolonged, most likely causes are vWD or a thrombocytopathy (functional platelet defect). von Willebrand's disease can be diagnosed by measurement of vWf concentration or activity. A normal bleeding time does not exclude a diagnosis of vWD, but suggests that the functional activity of vWf is not compromised markedly. If the bleeding time is normal, APTT and PT should be measured. A prolonged APTT with normal PT, in the clinical setting, implies a deficiency of factor XI, IX, or VIII. A prolonged PT with normal APTT indicates factor VII deficiency. Prolongation of both APTT and PT usually is caused by a deficiency of several factors and is seen most often in cases with vitamin K deficiency or antagonism. Obviously, if a particular cause is suspected from the case history or for other reasons, appropriate tests should be evaluated at the beginning. If these do not confirm the provisional diagnosis, the just-described protocol might be a useful one to follow.
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PMID:Laboratory evaluation of hemorrhagic coagulopathies in small animal practice. 267 37

We reported a female with vascular dementia due to chronic disseminated intravascular coagulation (DIC). The patient underwent operation for skin hemangiomas three times at age 18, 27, and 38. At age 43, she presented a slowly progressive dementia. She had bluish, compressive hemangiomas of skin and upper gastrointestinal tract, and she was suspected to have hemangiomas of brain, pleura, mediastinum, liver and pancreas. The hemangiomas were diagnosed blue-rubber-bleb-nevus syndrome (BRBNS). Laboratory data revealed persistent increase of serum FDP, FDP-D, FDP-E, and D-dimer. This condition was considered chronic DIC, therefore this case was the first case of combination of BRBNS and Kasabach-Merritt syndrome (chronic DIC). Brain MRI demonstrated bilateral lesions of paraventricular deep white matter and hemangioma of left temporal lobe. Because cerebral CT showed no contrast enhancement in paraventricular lesions, the lesions were considered multiple cerebral infarctions. Central nervous system (CNS)involvement in BRBNS is rare, and most cases of CNS involvement were associated with CNS angiomata. In this case it was suggested that brain was the target organ of DIC because thrombomodulin is absent or few in the human brain, therefore vascular dementia (multiple cerebral infarctions) developed due to chronic DIC.
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PMID:[Blue-rubber-bleb-nevus syndrome presented vascular dementia and chronic DIC--a case report]. 275 49

Fibrinopeptide A (FPA) was systematically investigated in 74 patients with acute leukaemia at different stages of the disease (50 with non-lymphocytic leukaemia, ANLL; 24 with lymphocytic leukaemia, ALL). At diagnosis, 75% of the cases had high FPA levels (86% in ANLL and 54% in ALL) with significantly higher levels in ANLL than in ALL (13.4 vs 4.4 ng/ml; p less than 0.001). Patients with DIC (20 cases in ANLL and 1 case in ALL) had significantly higher levels (p less than 0.001). FPA levels were neither correlated with fibrinogen or FDP levels nor with blast cell count. During chemotherapy, median FPA did not show significant changes whereas, at the end of therapy, a return toward normality was generally observed both in ALL and ANLL apart from the group of patients with acute promyelocytic leukaemia. Among the 24 patients who entered post-remission follow-up (13 ANLL and 11 ALL), 10 cases out of the 11 relapsing (6/6 with ANLL and 4/5 with ALL) had increased FPA 1 to 2 months before the ascertainment of the relapse. However, 16% and 9% of the samples obtained on different occasions, respectively from ANLL and ALL cases in maintained first remission, showed FPA above the normal limit. This study demonstrates that subclinical activation of blood coagulation, as indicated by high FPA level, is common both in lymphocytic and non-lymphocytic leukemia and suggests that this phenomenon is related to disease activity.
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PMID:Clinical significance of fibrinopeptide A in acute lymphocytic and non-lymphocytic leukaemia. 276 77

Fifty cirrhotic Japanese patients with oesophageal varices underwent sclerotherapy in a prospective randomized trial carried out to examine the effects of human thrombin given concomitantly with the sclerosant 5 per cent ethanolamine oleate. The two groups (25 patients each) were comparable with regard to size of the oesophageal varices, and the aetiology and severity of the liver disease. Twenty-five patients, 13 and 12 in the thrombin + and - groups, respectively, had at least one episode of variceal bleeding. The remaining 25 were given prophylactic injections. There was a significantly lower rate of occurrence of bleeding from injection sites when the injection needle was removed at the initial session of sclerotherapy in the thrombin + group, where human thrombin was injected (0.2-0.3 ml, 100-150 units per injection) just before removal of the injection needle. Endoscopy at 1 week after the initial session showed a significantly (P less than 0.05) higher rate of disappearance of red colour signs on varices in the thrombin + group (96 per cent) than in the thrombin - group (72 per cent). Fibrin degradation product E-fraction (FDP-E) values increased 1 h, 1 day and 6 days after the initial session of sclerotherapy in the two groups. The rate of increase in FDP-E values 1 h after sclerotherapy was significantly larger (P less than 0.001) in the thrombin + than in the thrombin - group. There was no clinical sign of disseminated intravascular coagulation. Administration of human thrombin plus a sclerosant seems to be useful and efficacious, especially for patients with huge oesophageal varices.
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PMID:Human thrombin plus 5 per cent ethanolamine oleate injected to sclerose oesophageal varices: a prospective randomized trial. 276 8

The clinical course of ten cases of head injury complicated with multiple systemic injuries were studied by comparing two groups divided according to the presence or absence of associated coagulative-fibrinolytic abnormality. All these cases had intracranial hemorrhagic lesions proven by the high density area in the initial CT scan. Five cases showed signs of disseminated intravascular coagulation (DIC) as evidenced by decreased counts of platelet, and/or elevated value of FDP at the time of admission. Four cases out of these five were in a state of hemorrhagic shock. All these five cases showed a subsequent enlargement of intracranial hematoma. Four cases died. Two of them, who had low initial Glasgow Coma Scale (G.C.S) died of uncontrollable increase of intracranial pressure. The other two, who had high initial G.C.S., died of acute renal failure and multiple organ failure. In contrast with these cases, five cases without signs of DIC intracranial hematomas did not enlarge in spite of the similar neurological conditions to the former group. In head injured patients with systemic injury, DIC frequently causes secondary hemorrhage in the intracranial lesions of minor severity.
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PMID:[Enlarging of intracranial hemorrhagic lesions and coagulative-fibrinolytic abnormalities in multiple-injury patients]. 277 Sep 70


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