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

The association of acute leukemia (AL) and disseminated intravascular coagulation (DIC) in 89 patients with a de novo diagnosis of AL made in our center during the last 8 years was retrospectively evaluated. DIC was demonstrated in 14 patients (15.7%) (7 AML-M3, 1 AML-M3, 1 AML-M2, 1 AML-M4, 2 AML-M5, and 2 ALL-L1). In 5 of them ICD was diagnosed after the beginning of chemotherapy. The factors predisposing to the development of DIC were: 1) the type of AL (p less than 0.01), as 70% of AML-M3 had DIC; 2) the intensity of granulation in leukemia cells (p less than 0.004); 3) the presence of Auer's rods and/or splinters in these cells, and 4) the presence of hemorrhagic diathesis (p less than 0.007). Eight of the 14 patients with DIC received heparin at a prophylactic dosage. No significant differences in the clinical course were in the group of patients with DIC who received heparin and in those who did not, excepting that in the former the platelet requirements were higher (p less than 0.005). Mortality rate during the first month was higher in the group of AL with DIC than in AL without DIC (p less than 0.025). Long term mortality was similar in both groups. The control of hemostasis is fundamental in AL, even in those patients without DIC at the time of diagnosis. The administration of blood derivatives has a high priority in AL with DIC. The role of heparin is still controversial.
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PMID:[Association of acute leukemia with disseminated intravascular coagulation in adults. Analysis of 14 cases]. 260 8

Bone marrow necrosis is a rare and ominous complication of hematologic malignancy which is often associated with bone pain in the lower back and extremities. Widespread marrow necrosis makes a definitive diagnosis through bone marrow biopsy difficult. An accurate diagnosis is imperative in patients with promyelocytic leukemia (FAB-M3) because disseminated intravascular coagulation and hemorrhage secondary to release of tissue thromboplastins from the malignant cell population requires prompt and anticipatory therapy. The following case report describes a patient with acute leukemia and massive bone marrow necrosis which obscured the correct diagnosis of promyelocytic leukemia.
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PMID:Bone marrow necrosis obscuring the diagnosis of acute promyelocytic leukemia. 263 85

During a 10-year period, 621 episodes of Escherichia coli bacteremia occurred in 575 cancer patients. The infection was most common in patients with acute leukemia and genitourinary and gastrointestinal malignancies. Most of the patients acquired their infection while in the hospital, and 38 percent had received antibiotics during the preceding 10 days. Fever occurred in 96 percent of patients, and afebrile patients had an especially poor prognosis. Only 4.5 percent of the patients had disseminated intravascular coagulation, although hemorrhage contributed to the death of 15 percent of the patients. The overall response rate was 66 percent, but it increased from 48 percent in 1972 to 76 percent in 1981. Patients without pulmonary infection had a response rate of 78 percent, whereas patients with pulmonary infection had a response rate of only 41 percent. Patients who had positive blood culture results while receiving appropriate antibiotic therapy had a poor prognosis. There was no correlation between the patients' initial neutrophil counts and response, but patients whose neutrophil count increased during therapy had a response rate of 75 percent, compared with a 47 percent response rate for patients whose neutrophil count decreased. The response rate was 71 percent for patients who received appropriate antibiotics, 38 percent for patients who received inappropriate antibiotics, and 8 percent for patients who received no antibiotics. A single appropriate antibiotic was as effective as a combination.
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PMID:Escherichia coli bacteremia in cancer patients. 352 83

A 70-year-old woman with newly diagnosed acute nonlymphocytic leukemia (FAB M5) underwent therapeutic leukapheresis because of a white cell count (WBC) of 144 X 10(9) per I and clinical evidence of leukostasis. A peripheral blood film taken immediately after leukapheresis showed numerous cytoplasmic and nuclear fragments. The patient's clinical course thereafter was significantly compromised by disseminated intravascular coagulation with a severe bleeding diathesis, renal failure, and respiratory failure that led to her death. This case illustrates that therapeutic leukapheresis for elevated WBC in patients with acute leukemia may result in leukocyte fragmentation and possible intravascular coagulation.
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PMID:White cell fragmentation after therapeutic leukapheresis for acute leukemia. 360 66

We quantified coagulation parameters in vitro using standard automated methods in 12 adult patients with acute leukemia who also had Hickman catheters (HC). Test results from simultaneously obtained HC blood and control peripheral venous blood (PB) samples were compared in the respective patients. Heparin solutions (100 U/mL, US Pharmacopoela) used to prevent the formation of clots within the HC appeared to cause, to a significant degree, spuriously elevated levels of fibrin degradation products (FDP), decreased levels of fibrinogen (FBG), and prolongations of the prothrombin time (PT) and activated partial thromboplastin time (PTT) in the first 10 mL of HC blood. The second 10 mL sample from the HC showed that FBG levels were comparable with those demonstrable in PB samples, as were levels of FDP in eight of 12 cases. Both PT and PTT times, however, remained significantly prolonged. An alternative maneuver for obtaining HC blood studied in four patients showed significant prolongation of PTT values in the second 10-mL sample despite levels of FDP, FBG, and PT similar to those in the PB. Because heparin contamination of HC blood can mimic the laboratory findings of disseminated intravascular coagulation or other coagulopathies in patients with acute leukemia, we suggest that only values obtained from PB be used for interpretation of coagulopathy in these patients.
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PMID:Coagulation testing of Hickman catheter blood in patients with acute leukemia. 377 45

Acute leukemias with high white blood count have a poor immediate prognosis and the treatment must be started within the first hours following diagnosis. It is necessary to prevent and to treat the severe metabolic disorders observed during induction treatment of acute lymphoblastic leukemia with WBC greater than or equal to 100,000/mm3. We analysed all the metabolic disorders in a retrospective study of 45 patients in order to determine their adequate prevention and treatment. Prevention of hyperuricemia and of secondary renal failure is now possible with urate oxidase, allowing an aggressive and rapid induction. Hyperkalemia can be prevented by urinary alkalinization and hyperphosphoremia with hypocalcemia by high dose intravenous calcium therapy. Renal failure is often transitory and functional. Disseminated intravascular coagulation is treated by heparin and platelets infusion and severe hyperglycemia requires insulin therapy.
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PMID:[Acute hyperleukocytic lymphoblastic leukemia (greater than or equal to 100,000 leukocytes/mm3). Metabolic changes during induction treatment. Study, prevention and treatment]. 385 53

During a 4-year period, 26 children with systemic malignancies suffered cerebrovascular accidents. These occurred in 17 patients with lymphoreticular malignancy and nine patients with solid tumors. They were the presenting signs of malignancy in three patients and were the direct cause of death in six. Cerebrovascular accidents were directly related to disseminated intravascular coagulation in eight patients, to chemotherapy in eight patients, to metastatic tumor in three patients, to thrombocytopenia in three patients, and to fungal meningitis in one patient. All patients with disseminated intravascular coagulation had leukemia and at times, cerebrovascular thrombosis predated systemic or laboratory evidence of disseminated intravascular coagulation. This review indicates that four major syndromes are apparent in children with cancer: vascular thrombosis associated with disseminated intravascular coagulation, acute arterial or sagittal sinus thrombosis secondary to L-asparaginase in children with leukemia, acute neurologic dysfunction in patients with osteogenic sarcoma treated with high-dose methotrexate, and obtundation, seizures, and focal neurologic deficits in patients with neuroblastoma metastatic to the torcular region. Although elevated WBC counts and thrombocytopenia occur frequently in children with cancer, in themselves they uncommonly result in strokes. It is concluded that cerebrovascular accidents are a relatively frequent cause of acute neurologic compromise in children with cancer and that certain types of malignancies and their treatment predispose patients to this complication.
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PMID:Cerebrovascular accidents in children with cancer. 386 Jul 96

The authors reviewed the case records of 1419 children with acute leukemia and other types of malignant disease involving the bone marrow to define the clinical and laboratory features associated with marrow necrosis as well as the prognostic significance of this complication. Only seven patients were found to have this abnormality: four with newly diagnosed acute lymphoblastic leukemia (ALL), one with relapsed ALL, and two with disseminated neuroblastoma. All patients presented with severe bone pain, bone tenderness, and fever. Levels of serum lactic dehydrogenase were uniformly increased, being especially high in patients with ALL. There was no evidence of severe infection or disseminated intravascular coagulation, complications that have been causally related to marrow necrosis. Four of the five children with ALL remain in complete remission for 10+ to 48+ months. Both patients with neuroblastoma are off therapy, in remission, for 9+ to 15+ months. In contrast to earlier reports, bone marrow necrosis does not appear to confer a poor prognosis in children with malignancy.
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PMID:Bone marrow necrosis in children with malignant disease. 386 Dec 29

We studied the clinical, morphological, and immunologic characteristics of 11 patients with 11q translocation-associated acute leukemia. There were three patients with t(9;11)(p22;q23), one with a variant of the t(9;11), three with t(11;19)(q23;p13), two with t(1;11)(p32;q23), one with t(10;11)(p15;q22or23), and one with t(11;17) (q23;q25). The breakpoints in chromosome 11 clustered in band q23. The morphological feature was FAB-M5 in two patients, FAB-M2 in one, FAB-L1 in six, and lymphoblastic lymphoma in one. The remaining patient underwent morphological changes from FAB-L1 seen at the time of diagnosis to M5b at relapse. Immunologic marker studies in ten patients revealed that one had T cell type; another pre-B cell type; three CALLA- Ia- non-T, non-B type; two CAL-LA- Ia+ non-T, non-B type; two monocytic type (positive Fc-receptor); and the remaining one underwent phenotypic changes from CALLA+ Ia+ non-T, non-B type to monocytic type. The patients were usually young; five were under 1 year and two were 9 and 13 years. Hyperleukocytosis was observed in eight of the ten patients with acute leukemia, and two of the eight died of intracranial hemorrhage within two days of admission, associated with disseminated intravascular coagulation. These findings indicate that leukemia with the 11q23 translocation share certain characteristics in common, irrespective of the recipient chromosome, even though the latter may have some influence on the morphological and immunologic phenotype. Our data provide a hypothesis that multipotent stem cells are involved in the genesis of the 11q translocation-associated leukemia.
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PMID:Clinical and hematologic characteristics in acute leukemia with 11q23 translocations. 394 33

The biologic activity of Factor XIII was measured in four groups of patients: 20 with liver cirrhosis, ten with acute DIC, 30 with acute leukemia with DIC, and 20 with acute leukemia without DIC. In all groups, the plasma Factor XIII transamidating activity was reduced, but this deficiency was more evident in patients with DIC alone or with leukemia and DIC. The immunologic determination of the a and b subunits of Factor XIII was also performed. Both subunits were below the normal range in the groups of patients studied, except for subunit b, which was normal in patients with leukemia without coagulopathy. Acute DIC patients showed an equally reduced level of both subunits, whereas in patients with leukemia, even in the presence of a complicating coagulopathy, a lesser decrease of subunit b than subunit a was found. Both subunits were equally reduced in patients with cirrhosis, suggesting an impaired synthesis of these proteins. In conclusion, our findings do not support the use of Factor XIII subunit measurements in distinguishing between thrombin- or protease-mediated consumption coagulopathy, and they seem to suggest that the deficiency pattern of the subunits is not accounted for by a simple pathogenetic mechanism.
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PMID:A contribution to the pathology of acquired plasma factor XIII deficiency. 407 Oct 61


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