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)

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

The occurrance and significance of important carcinofetal antigens other than AFP and CEA are reported. These included the alpha 2 H-protein which is produced in the liver and increases in serum of patients with various tumors, the fetal sulphoglycoprotein antigen FSA from the gastric juice of patients with gastric cancer, the carcinoplacental alkaline phosphatase (REGAN-isoenzyme)which is found in the serum of patients suffering from e.g. bronchogenic, mammary, urogenital and gastrointestinal carcinomas, the beta-S-fetoprotein which is most likely to be identical with C-reactive protein, gamma-fetoprotein, the carcinofetal antigen in glial tumors (CFGA); ectopic production of placental hormones like human gonadotropin, placental lactogen, plasminogen-activators; leukemia-associated antigens. Furthermore, some other less known carcinofetal antigens are mentioned.
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PMID:[Carcinofetal antigens. III. Further carcinofetal antigens (author's transl)]. 115 52

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

Cytostatic therapy is known to aggravate tumor-induced coagulopathy. Therefore, we have studied the effect of different chemotherapeutic regimens on the activation of coagulation and fibrinolysis in patients with non-Hodgkin's lymphomas or acute leukemias. In non-Hodgkin's lymphoma patients treated with an aggressive protocol (COL-BLAM) and in leukemia patients (TAD-9) fibrinopeptide A, prothrombin fragment (F1 + 2) and thrombin antithrombin III complexes (TAT) increased (Tables 4 and 6), while D-dimer did not deviate significantly. The ratio D-dimer/TAT consequently showed a significant decrease, indicating increased formation of thrombin after release of procoagulant factors, which is not paralleled by an activation of fibrinolysis. Both these groups were also characterized by an increase in uric acid and in C-reactive protein and plasminogen-activator inhibitor, two acute-phase reactants. In contrast, patients with non-Hodgkin's lymphomas treated with a less aggressive protocol (COP) showed no significant changes in hemostatic variables, uric acid, or acute-phase reactants. The release of procoagulant factors relates to the cytostatic sensitivity of the tumor and to a high tumor-cell destruction. Our results further emphasize the need for large-scale studies on antithrombotic prophylaxis in patients undergoing cytostatic treatment.
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PMID:Influence of cytostatic treatment on the coagulation system and fibrinolysis in patients with non-Hodgkin's lymphomas and acute leukemias. 171 7

Disseminated intravascular coagulation (DIC) is a frequent complication of acute leukaemia, in particular acute promyelocytic leukaemia. Although procoagulant substances released from leukaemic blast cells may induce DIC by activating conventional coagulation pathways, there is increasing evidence to suggest that direct activation of fibrinogen by proteases released from blast cells may be the predominant mechanism by which DIC is initiated. Primary fibrinolysis has also been proposed as the cause of the haemorrhagic diathesis in some cases of acute leukaemia. Although plasminogen activators have been demonstrated in leukaemic blast cells supporting this view, cases of primary fibrinolysis would appear to be rare. A bleeding tendency attributed to primary fibrinolysis may more often be the result of an exaggerated fibrinolytic response secondary to DIC. The main strategies of treatment for leukaemia associated DIC are rapid initiation of chemotherapy and vigorous blood product support until the DIC resolves once the blast cells have been eradicated. The role of heparin in the management of leukaemia associated DIC remains controversial. There is recent evidence to suggest that heparin therapy does reduce the incidence of haemorrhagic death although it has been recommended that relatively low intravenous doses should be administered initially to reduce the risk of heparin induced haemorrhage.
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PMID:Haemostatic problems in acute leukaemia. 207 71

Treatment of acute lymphoblastic leukaemia (ALL) with L-asparaginase (L-asp) may be associated with thrombotic complications, but the pathogenetic mechanisms of thrombus formation and persistence remain unclear. We studied the procoagulant activity (PCA) of peripheral blood mononuclear cells and some components of the plasma fibrinolytic system in 10 children with ALL undergoing remission induction therapy which includes L-asp. Mononuclear cells obtained 14 days after starting L-asp treatment generated significantly higher amounts of PCA (identified as tissue factor) than cells isolated before the first dose of L-asp and 7 days after the cessation of L-asp administration (p less than 0.01). Augmented PCA coincided with an increase in the plasma D-dimer. The plasma levels of type 1 plasminogen activator inhibitor were found significantly elevated during L-asp therapy (p less than 0.05), whereas plasminogen levels were markedly decreased (p less than 0.05). These findings suggest that, during the course of L-asp treatment, the coagulation-fibrinolysis balance is shifted towards promotion of fibrin formation and deposition. Although it remains to be conclusively established whether L-asp per se or the concurrent administration of multiple chemotherapeutic agents is responsible for these changes, the latter could contribute to the thrombotic complications associated with remission induction therapy for ALL.
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PMID:Unbalanced coagulation-fibrinolysis potential during L-asparaginase therapy in children with acute lymphoblastic leukaemia. 227 27

The fibrinolytic system was studied in 46 patients with acute leukaemia at diagnosis. Untreated patients (with the sole exception of the M3 subgroup) showed an inhibition of fibrinolytic activity, measured by the euglobulin lysis time and area. This inhibition was accompanied by reduced t-PA antigen and t-PA inhibitor activity. No correlation was found between the above-mentioned fibrinolytic parameters and the biochemical haematological values considered, nor with clinical and/or laboratory features of DIC, fever, liver failure. The decrease in immunological plasminogen and functional alpha 2-antiplasmin, showed a significant correlation with the presence of clinical and/or laboratory signs of DIC, as diagnosed on the basis of concomitant increase in fibrin monomers, plasmatic fibrinopeptide A and serum FDP.
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PMID:Depressed fibrinolysis in patients with acute leukaemia. 244 34

We report a prospective study in nine consecutive adult patients with acute promyelocytic leukaemia (APL). The study objective was to assess the prevalence of activation of blood coagulation and/or activation of fibrinolysis in APL. Coagulation and fibrinolytic parameters relevant to the objective included antithrombin III, plasminogen, fibrin/fibrinogen degradation products and alpha-2 antiplasmin activity and antigen levels. The results of this study revealed consistently normal antithrombin III levels, both before and in the course of antileukaemic treatment. Plasminogen levels were slightly decreased or normal. However, a distinct alpha-2 antiplasmin activity deficiency in all patients was observed with levels even reaching zero in three patients, during chemotherapy. Alpha-2 antiplasmin activity levels were consistently lower than the alpha-2 antiplasmin antigen levels. The in vitro binding of alpha-2 antiplasmin activity to fibrin clots was severely reduced which appeared to be due to the reduced alpha-2 antiplasmin plasma levels. Upon crossed-immunoelectrophoresis against alpha-2 antiplasmin antiserum two alpha-2 antiplasmin antigen peaks were observed in the plasma of all nine patients. All abnormalities were reversible 4 d after completion of chemotherapy. In a second series of 12 consecutive APL patients we confirmed the consistency of the alpha-2 antiplasmin activity deficiency and normal antithrombin III plasma levels. In addition Protein C activity and antigen levels were normal or near normal in 10 and reduced in two patients. Thrombin-antithrombin III complexes were increased in 10 and normal in two patients. We conclude that some activation of blood coagulation is present in APL (increased thrombin-antithrombin III complex levels) but its contribution to the coagulopathy seems to be minor (normal antithrombin III and only slightly reduced protein C levels). The observed reduced alpha-2 antiplasmin content of the fibrin clot in vitro may result in vivo in a fibrin clot that is highly susceptible to fibrin degradation, thus aggravating the coagulopathy in APL.
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PMID:Acquired alpha-2-antiplasmin deficiency in acute promyelocytic leukaemia. 246 Jan 26

In 64 patients affected with acute leukaemia (51 patients with acute non-lymphatic leukaemia and 13 patients with acute lymphatic leukaemia) extensive investigations of blood coagulation were made during cytostatic therapy. The following conspicuous changes of haemostatasis could be observed in making the diagnosis: Lowered quick value and shortened PTT, increased fibrinogen, fibrinopeptide, A, alpha 1-antitrypsin and alpha 2-macroglobulin, diminished plasminogen and plasma fibrininectin. According to TAD (VP) protocol the induction therapy leads to hypercoagulability which can be recognized by an increase of fibrinopeptide A, coagulating factors and shortening of PTT. During the therapy with L-asparaginasis procoagulatoric as well as thromboprotective coagulating proteins are diminished. A dense laboratory control enables those disturbances of haemotasis caused by disease or therapy to be separated and contributes to preventing complications during the cytostatic induction therapy.
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PMID:[Blood coagulation factors and proteinase inhibitors in cytostatic therapy of acute leukemia]. 246 58

The levels of alpha-2-antiplasmin (alpha 2-AP), antithrombin III (At III) and plasminogen were studied in 21 patients with acute nonlymphoblastic leukemia (ANLL) before and after induction chemotherapy and during bone marrow cellularity recovery after the postchemotherapy aplastic phase. In the patients with M2, M3 or M4 leukemia who had clinical and laboratory evidence of DIC, the alpha 2-AP levels were very low in the initial phase of the disease but improved significantly during recovery of marrow cellularity. At III and plasminogen values were in the normal range at disease onset and showed no significant modification during the course of leukemia. Proteolytic cleavage of alpha 2-AP by granulocyte proteases, rather than hyperfibrinolysis, may be responsible for the low levels of the inhibitor in the proliferative phase of ANLL. This alpha 2-AP deficiency may well contribute to hemorrhagic diathesis in ANLL independently of the presence or absence of hyperfibrinolysis or DIC. Moreover, the lower alpha 2-AP levels observed during the proliferative phase of ANLL may relate to disease activity.
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PMID:Alpha-2 antiplasmin in acute nonlymphoblastic leukemia. 246 77


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