Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An increase in the serum copper (Cu++) level has been described as a sensitive index of disease activity in several hematologic and nonhematologic malignancies. In order to explore the diagnostic value of Cu++ compared to other hematochemical parameters frequently abnormal in malignancies, Cu++, serum alpha2 globulin (alpha2), plasmatic fibrinogen (Fibr), the erythrocyte sedimentation rate (ESR), and serum iron (Fe++) have been detected and evaluated in 267 patients affected with the following diseases: Hodgkin's lymphoma (HL), non-Hodgkin's Lymphomas (NHL), Acute Leukemias (AL), Chronic Myeloid Leukemia (CML), Chronic Lymphocytic Leukemia (CLL), Myeloma (MM), and Breast Cancer (BC). The best correlation between Cu++ increase and disease activity has been found in HL, NHL, AL, and BC. In these diseases, when the considered parameters were compared, Cu++ and ESR showed a similar pattern, i.e., a high frequency of abnormalities in active disease. It is concluded that Cu++ represents a good complement to some other aspecific parameters in evaluating the activity and diffusion of neoplasias and the therapeutic results, particularly in HL, NHL, AL and BC.
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PMID:The diagnostic value of serum copper levels and other hematochemical parameters in malignancies. 7 79

Review of the coagulation laboratory records and medical records at Memorial Sloan-Kettering Cancer Center over a three year period (1971--1974) revealed 89 patients with disseminated intravascular coagulation (DIC). The diagnosis of DIC was made if laboratory studies showed evidence of quantitative and qualitative changes in fibrinogen and significant thrombocytopenia. The patients included 19 with leukemia (17 acute), 3 with multiple myeloma, 15 with lymphoma, 46 with metastatic solid tumors, (10 lung, 9 breast, 8 gastrointestinal, 12 genitourinary, 7 miscellaneous) 4 with vascular tumors, and 3 without tumor. Other conditions which might have precipitated or initiated DIC such as gram-negative sepsis, liver impairment, or mucin secreting tumors were present in the majority of patients. Bleeding occurred in 75% of the patients and was fatal in 36%. Thromboembolism occurred in 22.5%. Thirteen percent were asymptomatic. Serum lactic dehydrogenase was elevated in over 75% of the patients at the time of, or subsequent to the occurrence of DIC. Treatment with heparin was helpful in only three of twenty patients. Eighty percent of the patients died within one to over 30 days of the onset of DIC. Post mortem evidence of DIC was present in 18 of 43 autopsies. Results of this study indicate that DIC is a frequent complication of a wide variety of tumors and that its occurrence causes morbidity and mortality in a significant number of patients. Treatment with heparin is of little help unless remission is induced and the precipitating factor(s) are reversed.
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PMID:Disseminated intravascular coagulation: experience in a major cancer center. 17 94

Platelets from patients with myeloid leukaemia showed reduced aggregation with collagen or thrombin. These platelets also had a lower capacity to bind thrombin. This lower thrombin binding is due to a decrease in the total quantity of receptors available and not because of a change in the affinity. In the presence of the patients' plasma, the aggregation behaviour of normal platelets induced by thrombin as well as the clotting time of fibrinogen remained unchanged. The results suggest that the platelet dysfunction in myeloid leukaemia is partially due to a membrane defect involving the thrombin receptors which leads to an impaired induction of the initial stimulation.
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PMID:Defective binding of thrombin to platelets in myeloid leukaemia. 27 56

The life-span of platelets and of fibrinogen was studied by the use of 75Se-selenomethionine and 51Cr in 28 cases of acute leukaemia (AL), and in 2 cases of chronic myelocytic leukaemia with blast-cell transformation. The patients were grouped on the basis of clinical remission or activity. In all groups, whether examined by means of 75Se or 51Cr, a reduction of variable degree was found in platelet life-span, and platelet turnover was reduced in the majority of the cases. The sequestration data were atypical. Simultaneous 75Se studies for platelet and fibrinogen life-span revealed a latent diffuse intravascular coagulation (DIC) in three cases, the process being still in progress in one case and in remission in two cases at the time of observation. Fibrinogen life-span was reduced in some of the cases. Thrombocytopenia in AL is attributed to a complex origin in which infiltration of the bone marrow, the destructive effect of antimetabolic therapy, abnormally increased consumption of storage of the functionally impaired platelets, possibly latent DIC or episodic excessive sequestration may be equally involved. Remission may be accompanied by normalization of both thrombopoiesis and platelet kinetics.
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PMID:Production and life-span of platelets and of fibrinogen in acute leukaemia. 75Se-selenomethionine- and 51Cr (Na-chromate)-studies. 28 51

Bleeding is common in acute myeloblastic leukemia (AML). At the time of diagnosis, the danger of bleeding cannot be predicted by laboratory means. However, the following factors represent increased risks: Promyeloblastic leukemia, high blast count, low fibrinogen, low plasminogen. From coagulation studies performed at the time of bleeding complications, the pathomechanism leading to bleeding complications usually cannot be detected. The question whether impairment of production, consumption coagulopathy, or primary fibrinolysis causes the bleeding complications can only be answered by controlling frequently clinical and hemostatic criteria, which include the thrombocytic stystem as well as plasmatic coagulation and fibrinolysis. At the present time, the therapy of bleeding complications in AML is symptomatic. It consists of transfusion with thrombocytes or fresh whole blood, respectively. Coagulation factor concentrates should only be given in combination with Heparin to prevent the deterioration of consumption coagulopathy.
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PMID:[Bleeding complications in acute myeloblastic leukemia (author's transl)]. 28 49

Three patients with acute lymphoblastic leukemia and one with lymphosarcoma cell leukemia developed transient hypofibrinogenemia during a course of treatment with vincristine and prednisone. There was no evidence of overt, disseminated intravascular coagulation or significant liver impairment. Fibrinogen survival using homologous-125-I-labelled fibrinogen was measured in two patients; it was moderately shortened in both, perhaps indicating subclinical intravascular coagulation. Rapid lysis of leukemic cells might have been responsible for activating coagulation and fibrinolysis in vivo. These four patients, however, were not different in any clinical or laboratory parameter from nine others with lymphoblastic leukemia similarly treated and investigated without observing any defect in their fibrinogen. There were no bleeding complications and the fibrinogen level became normal within 13 to 30 days.
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PMID:Hypofibrinogenemia associated with vincristine and prednisone therapy in lymphoblastic leukemia. 105 92

Fibrinogen survival using 125I-labelled homologous fibrinogen was studied in 17 adults with acute leukemia. Five patients in complete remission had normal fibrinogen survival and turnover rate. Five of 6 patients undergoing induction therapy and 4 of 6 in relapse had shortened fibrinogen survival; the turnover rate was increased in all 12 patients. Nine of 12 patients with active disease had elevated levels of fibrinogen degradation products in the serum. Serial coagulation studies did not support the diagnosis of overt disseminated intravascular coagulation. There was no correlation between the morphological type of leukemia, chemotherapy, the presence of fever and sepsis, or liver dysfunction and fibrinogen survival. Other possible causes of the accelerated fibrinogen turnover in patients with active disease are discussed.
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PMID:Fibrinogen survival and fibrinolysis in acute leukemia. 105 37

Immobilized asparaginase was prepared by embedding asparaginase (which is effective for remission in children with leukemia) into fibrin polymer formed by fibrinogen-fibrin conversion in the presence of thrombin. The immobilized asparaginase film did not dissolve in 6 mol/1 urea, suggesting that blood coagulation factor XIII participates in the cross-linking between fibrins and between fibrin and asparaginase.
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PMID:Immobilized L-asparginase embedded in fibrin polymer. 109 44

A consumption coagulopathy syndrome has frequently been reported in association with some cases of acute nonlymphoblastic leukemia (ANLL) and mainly in acute promyelocytic leukemia (M3). Eighteen cases of ANLL have been studied on admission, before chemotherapy was started. Levels of antithrombin III (AT-III), protein C (PC), protein S (PS), thrombin-antithrombin complex (T-AT-III), tissue plasminogen activator, plasminogen (Pg), alpha-2-antiplasmin (alpha-2-AP), D-dimer (DD) and fibrinogen (Fg) were determined. The results showed normal levels of AT-III and PS, decreased levels of PC, alpha-2-AP, Pg and Fg in some cases, and an elevation of DD and T-AT III complex in almost all patients. There was a continuous evolution of data from M1 cases in which only slight alterations were seen up to M3 cases where all those pathologic data were observed.
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PMID:A continuous spectrum of hypercoagulability exists in acute nonlymphoblastic leukemia. 128 98

In proliferative diseases of the homeopathic system before starting and at the end of treatment, the values of 8 acute phase factors were studied simultaneously, that is: seromucoid, sialic acid, alpha 1 acid glycoprotein, alpha 1 antitrypsin, haptoglobin, ceruloplasmin, transferrin, and fibrinogen. In chronic myeloid and lymphatic leukaemia no constant increase nor decrease of the concentration of any of the factors was found. In non-Hodgkin lymphoma the concentration of one factor -ceruloplasmin was constantly increased, and that of two factors--sialic acid and fibrinogen was decreased, while in plasmocytoma the concentration of two factors--haptoglobin and ceruloplasmin was constantly increased. At the end of treatment the concentration of certain factors was changing. In chronic myeloid leukaemia the concentration of ceruloplasmin, fibrinogen, and seromucoid was decreasing, while in non-Hodgkin lymphoma the concentration of haptoglobin and fibrinogen was increasing, in chronic lymphatic leukaemia the concentration of haptoglobin and increasing, in chronic lymphatic leukaemia the concentration of haptoglobin and transferrin was increasing, and in plasmocytoma the concentration was increasing of haptoglobin, sialic acid, and transferrin. The result of treatment in chronic myeloid leukaemia was good, in non-Hodgkin lymphoma and chronic lymphatic leukaemia--moderate, and in plasmocytoma it was least beneficial.
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PMID:[Factors of the "acute phase" in proliferative diseases of the hemopoietic system]. 129 50


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