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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of tissue-plasminogen activator.plasminogen activator inhibitor (t-PA.PAI) complex and active PAI were assayed in 58 cases of disseminated intravascular coagulation (DIC). A significant elevation of both parameters was observed in most cases of DIC, especially in patients with non-Hodgkin lymphoma, sepsis, or some patients with acute leukemia, but no such elevation was observed in patients with acute promyelocytic leukemia (APL). The levels of both parameters were higher in cases of DIC with multiple organ failure (MOF) than in those without MOF. Since no elevation of t-PA.PAI complex was observed in most cases of APL, t-PA did not seem to play an important role in the activation of fibrinolytic system in APL. Active PAI, which reflects the inhibitory regulation in fibrinolytic system, was considered to play a role in the progression of MOF. Plasma levels of active PAI were low in the cases of APL, which had no complication of MOF.
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PMID:Changes in plasma levels of tissue-plasminogen activator/inhibitor complex and active plasminogen activator inhibitor in patients with disseminated intravascular coagulation. 130 60

To evaluate the clinical usefulness of D-dimer, various effects on the measurement of D-dimer were examined. Although both fibrinolytic and fibrinogenolytic products were detected by the measurement of FDP, only fibrinolytic products were detected by the measurement of D-dimer. In patients with DIC and other thrombo-embolic diseases, plasma D-dimer levels were significantly higher than in normal persons. A significant positive correlation between plasma D-dimer and serum FDP was found in DIC patients. In patients with DIC associated with acute promyelocytic leukemia, which is thought to be an increased fibrinogenolysis state, serum FDP was higher than the plasma D-dimer which suggests that increased fibrinogenolysis affects the result of serum FDP measurement. Plasma D-dimer significantly increased 5 minutes after endoscopic embolization with thrombin in the patients with esophageal varices. However serum FDP increased 30 minutes after the treatment, which suggests that the D-dimer is more useful for rapid detection of coagulo-fibrinolytic change than serum FDP. Plasma D-dimer was significantly higher in patients with cerebral infarction and increased with age. These finding suggest the usefulness of plasma D-dimer measurement for the specific and rapid evaluation of coagulo-fibrinolytic activation and thrombo-embolic state.
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PMID:[Clinical usefulness of the measurement of plasma D-dimer levels]. 192 Aug 61

The coagulation abnormalities in 20 cases of acute promyelocytic leukemia (APL) treated at a single institution were reviewed. A remarkably uniform picture of defibrination and increased FDPs with well-preserved levels of other coagulation factors including AT-III was seen. Our data, together with those available in the literature, do not support DIC as the underlying mechanism of bleeding but seem rather to point to increased proteolysis as the cause.
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PMID:Bleeding in acute promyelocytic leukemia (APL): fibrinolysis or defibrination? 194 23

We identified seven new recurring translocations among 483 cases of acute lymphoblastic leukemia (ALL) with adequate chromosome banding studies. Four were apparently balanced [t(1;3)(p34;p21), t(7;9)(p15;p23-p24), t(12;13)(p13;q14), t(17;19)(q22;p13)], while three were unbalanced with the formation of a dicentric chromosome [dic(7;9)(p13;p11), dic(7;12)(p11;p12), and dic(12;17)(p11;p11-p12)]. One translocation was observed in five cases, two in four cases, and the remaining four in two cases each. The modal chromosome numbers in these 21 cases were 45 (n = 11), 46 (n = 8), and 47 (n = 2). Eight of the 11 cases with a dicentric chromosome had a modal number of 45. Only a single translocation was found in 14 cases (67%), representing the sole structural abnormality in six cases. In three of the seven translocation subgroups, the blast cells were consistently of B lineage (pre-B, early pre-B, or both); in all others, they represented both the B and T lineages. The small size of these subgroups prevented definitive clinical correlations, although it may be important that two of the four cases with a t(17;19) and an early pre-B-cell immunophenotype had disseminated intravascular coagulation, an event usually observed in acute promyelocytic leukemia or T-cell ALL. These findings add substantially to the existing list of nonrandom chromosomal translocations in childhood ALL and may help to explain the genetic alterations leading to the loss of normal growth control mechanisms in this disease.
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PMID:New recurring chromosomal translocations in childhood acute lymphoblastic leukemia. 201 38

Hemostatic abnormalities are present in a majority of patients with metastatic cancer. These abnormalities can be categorized as 1) increased platelet aggregation and activation, 2) abnormal activation of coagulation cascade, 3) release of plasminogen activator, and 4) decreased hepatic synthesis of anticoagulant proteins like Protein C and antithrombin III. The abnormal activation of coagulation cascade is mediated through release of Tissue Factor, Factor X activators, and other miscellaneous procoagulants from the plasma membrane vesicles of tumor cells. Macrophages of a tumor-bearing host also produce increased amounts of Tissue Factor. Production of Factor X activators and macrophage Tissue Factor is decreased by warfarin. The ability of the tumor cells to produce platelet-aggregating activity and plasminogen activator parallels their metastatic potential in animal and experimental systems. These studies also show that antiplatelet agents and antibodies against plasminogen activator can suppress the metastatic process. One or more laboratory abnormalities of hemostasis can be shown in up to 95% of patients with metastatic cancer. These abnormalities, however, are unable to predict subsequent development of thromboembolic or hemorrhagic complications. Clinical complications occur in 9-15% of the patients in the form of thrombotic or hemorrhagic disorders. The therapy of tumor-related coagulopathy should be guided by its clinical expression. Subclinical DIC should not be treated. Coumadin is generally ineffective for therapy of thrombosis in cancer patients. There is no consensus regarding the use of heparin in acute promyelocytic leukemia (APL). The defibrination in APL may be from disseminated intravascular coagulation as well as systemic fibrinolysis, as shown by decreased alpha 2 antiplasmin levels. In such cases, epsilon aminocaproic acid plus heparin therapy may be of benefit.
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PMID:Hemostasis in malignancy. 174 46

Early diagnosis and immediate treatment of the disease responsible for DIC are most important for successful therapy of DIC. Furthermore, it is also necessary to use anticoagulant agents in most cases of DIC. The agents may be classified on the basis of their mode of anticoagulant action into three groups: ones with antithrombin effect, ones with anti-Xa effect or ones with both effect, and each agent is hoped to be chosen appropriately for development of DIC in near future. At present, such anticoagulant agents as standard heparin, antithrombin-III concentrate, gabexate mesilate, nafamostat mesilate, MD-805, low molecular weight heparin, heparan sulfate, activated protein C, are known as drugs for DIC, and each of them was effective for improvement from DIC in our experience. Antifibrinolytic agents, which have been considered to be contraindicated for therapy of DIC, may be good indication for selected cases of DIC with enhanced fibrinolysis such cases as acute promyelocytic leukemia. Antiplatelet agents may be available for some cases of chronic DIC.
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PMID:[Treatment of disseminated intravascular coagulation]. 221 66

From 1976 to 1989, 21 adult patients with previously untreated acute promyelocytic leukemia were seen at the University of Virginia Hospital. We reviewed their cases retrospectively to determine the impact of hemorrhagic complications and other factors on treatment outcome. We observed a complete remission rate of 35%; the median survival in complete responders was 15 months. Evidence of disseminated intravascular coagulation was found in 13 (62%) of the 21 cases at diagnosis. Fatal intracranial hemorrhage was the leading cause of death, occurring in eight (40%) of the 20 patients evaluated. Initial leukocyte count greater than 4.0 x 10(9)/L and platelet count less than 20 x 10(9)/L were significantly associated with an increased risk of intracranial hemorrhage. In patients with disseminated intravascular coagulation, the rate of intracranial hemorrhage was reduced by treatment with heparin. The high mortality of 40% (8/20) due to intracranial hemorrhage during induction was a major contributor to the low complete remission rate of 35% (7/20) in this series of consecutive unselected patients with newly diagnosed acute promyelocytic leukemia.
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PMID:Acute promyelocytic leukemia: impact of hemorrhagic complications on response to induction chemotherapy and survival. 221 55

Two cases of the acute disseminated intravascular coagulation (DIC) are presented. DIC in the first case was diagnosed in healthy pregnant woman without any obstetric pathology. This patient recovered completely. The acute DIC in another patient preceded the acute promyelocytic leukemia. The patient died despite a control of DIC. DIC therapy included antifibrinolytic agents and additionally corticoids in pregnant patient. Heparin was not administered because of post partum period and foreseen cytostatic therapy in the leukemic patient.
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PMID:[2 cases of acute disseminated intravascular coagulation in normal pregnancy and as the first symptom of acute promyelocytic leukemia]. 223 4

We measured blood concentrations of tumor necrosis factor (TNF), interleukin-1 beta (IL 1-beta), soluble interleukin 2 receptor (s-IL 2r), and interferon alpha (IFN alpha) in 30 patients with disseminated intravascular coagulation (DIC) and compared the results to those of 25 patients without DIC. Plasma levels of TNF, IL 1-beta, and s-IL 2r were higher in patients with DIC than in those without DIC. In one case of acute promyelocytic leukemia, plasma levels of TNF and IL-1 beta increased at the onset of DIC but decreased upon DIC improvement. These findings suggest that activation of the immune system is involved in the development of DIC. However, these concentrations were not markedly increased in patients with leukemia, although blood TNF and s-IL 2 r were markedly elevated in patients with solid cancers. Especially in patients with solid cancers, hyperactivation of the immune system may cause an increase in blood TNF and IL-1 beta and the development of DIC.
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PMID:[Elevated levels of cytokines in plasma from patients with disseminated intravascular coagulation]. 225 53

Disseminated intravascular coagulation (DIC) commonly occurs in patients with acute promyelocytic leukemia (APL, FAB-M3) but may also be seen in other subtypes of AML. DIC in patients with AML has been attributed to procoagulants released from granular fractions of leukemic blast cells. The present study was designed (i) to evaluate thrombin activity in patients with AML by measuring plasma levels of fibrinopeptide A (FPA) prior to chemotherapy, and (ii) to examine whether a relationship between FPA levels and the number of peripheral blast cells exists. Plasma levels of FPA were determined using a commercially available RIA kit. To remove fibrinogen and the majority of elastase-induced fibrinopeptides (A alpha 1-21) known to crossreact with the FPA (A alpha 1-16) antiserum used in this assay, plasma samples were treated with bentonite prior to further processing. The study was conducted on 5 patients with APL and on 22 patients with other subtypes of AML. Peripheral blast cell counts at initial diagnosis ranged from 2100 to 56,000/microliters in patients with APL and from 1900 to 151,000/microliters in patients with other AML subtypes. The mean (+/- 1 SEM) pretreatment plasma level of FPA was significantly higher (p = 0.021) in the 5 patients with APL (38.2 +/- 8.3 ng/ml) than in patients with other AML subtypes (8.1 +/- 0.7 ng/ml). No relationship was found between peripheral blast cell counts and the corresponding FPA levels in the total group of 27 patients. However, when considering the 5 patients with APL separately, a significant correlation was observed between peripheral blast cell number and FPA plasma levels (r = 0.88, p = 0.050). This study confirms that thrombin generation is considerably greater in patients with acute promyelocytic leukemia than in other subtypes of AML. We conclude that type and number of circulating blast cells and their related capacity to express procoagulant activities appear to be major determinants of excessive fibrinogen degradation in AML.
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PMID:Relationship of thrombin generation to peripheral blast cell count in patients with acute myeloblastic leukemia (AML). 236 38


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