Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-two children with solid tumors (lymphangioma, fibrosarcoma, hepatocarcinoma, osteogenic sarcoma, rhabdomyosarcoma, lymphosarcoma, mesenchymoma, hepatoma, Ewing's sarcoma, reticulum cell sarcoma, neuroblastoma, Hodgkin's disease, and brain tumors) were studied for alterations in coagulation by means of platelet counts, platelet aggregation, thrombelastogram, procoagulant and antigenic factor VIII, fibrin split products, and antithrombin III level. Results indicated hypercoagulability as shown by abnormally short thrombelastograms and elevated factor VIII levels and platelet counts in approximately one-half of the group. With the exception of increased fibrin split products in a third of the patients, little laboratory or clinical evidence for disseminated intravascular coagulation was seen. Hypercoagulability, as noted in adult carcinoma patients, can also occur in childhood sarcoma patients.
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PMID:Hypercoagulability in childhood cancer. 120 73

Disturbances in hemostasis in cancer disease frequently occur. This clinical situation may contribute to the spread and metastasis of cancer. The determination of inhibitors controlling hemostasis especially during treatment may be of value for the evaluation of effectiveness of treatment and balancing of hemostasis. Twenty four patients diagnosed with Hodgkin's disease were introduced to our studies. The level of antithrombin III (AT-III) and alpha-2-antiplasmin (alpha-2-AP) in sera were determined before, during and after treatment with MOPP. We found decrease of AT-III concentration before treatment, and chemotherapy increased the level of this inhibitor but still below the level of control. Alpha-2-AP concentration was higher in patients and MOPP application decreased the level below the values found in controls. The determination of concentration of both inhibitors may be important for the evaluation of the effect of treatment in understanding how the disturbances of hemostasis may be equilibrated.
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PMID:Serum antithrombin III and alpha-2-antiplasmin concentrations in patients with Hodgkin's disease in the course of chemotherapy. 171 3

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

Forty-six patients with refractory malignant lymphoma (Hodgkin's and non-Hodgkin's) admitted for autologous marrow or peripheral blood stem cell transplantation (ASCT) were evaluated for the presence of hemostatic abnormalities known to be associated with a hypercoagulable state in other patient populations. All patients had received numerous chemotherapeutic agents in the past and often radiation therapy as well. Hemostatic abnormalities were found to be common in these patients. The most frequent finding was hyperfibrinogenemia, present in 35% of patients. Decreased protein C activity was present in 32% of patients. Protein C antigen was low in only one individual and protein S was normal or increased in all patients. Low levels of antithrombin III were present in 16%. Plasminogen activator inhibitor was elevated in 20%. Anticardiolipin antibodies were present in 29% of patients; other evidence of a lupus anticoagulant was present in only eight patients. The frequency of each hemostatic abnormality was similar for patients with Hodgkin's disease (HD) and those with non-Hodgkin's lymphoma (NHL) despite the fact that significantly more patients with HD had received irradiation and/or previous splenectomy than patients with NHL. We conclude that multiple prothrombotic abnormalities of hemostasis are present in patients with refractory lymphoma referred for ASCT. Whether these are the result of lymphoma or the result of therapy cannot be determined from this study.
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PMID:Prothrombotic hemostatic abnormalities in patients with refractory malignant lymphoma presenting for autologous stem cell transplantation. 187 94

Indicating activation of coagulation fibrinopeptide A (FPA) was elevated in 80.1% (mean = 10.5 ng/ml; P less than 0.01) and thrombin-antithrombin III complexes in 58.3% (TAT; mean = 5.3 ng/ml; p less than 0.05) in patients with adenocarcinomas (n = 57). In patients with non-Hodgkin's lymphomas (n = 30), however, elevation was observed only in 66.6% (FPA) and in 42.8% (TAT). Incidence of thrombosis is high only in the first group Local fibrinolysis explains elevated D-dimer in adenocarcinomas (1,818 ng/ml; p less than 0.01) and in non-Hodgkin's lymphomas (576 ng/ml; p less than 0.05). Significantly increased t-PA antigen was not committed by adequately increased t-PA activity in adenocarcinomas, because of high levels of the acute-phase protein, plasminogen activator inhibitor (mean = 25.3; p less than 0.01), indicating systemic hypofibrinolysis. Hemostatic disorder in patients with malignancy can be attributed to a combination of acute-phase reaction and an activation of coagulation.
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PMID:Investigations of coagulation system and fibrinolysis in patients with disseminated adenocarcinomas and non-Hodgkin's lymphomas. 221 92

Fourteen patients with hematologic neoplasia (11 acute myeloid leukemias, 2 non-Hodgkin's lymphomas and 1 blast crisis of chronic myeloid leukemia) who underwent high-dose cytosine arabinoside (HIDARAC) therapy with or without sequential asparaginase (ASNase) were investigated in order to evaluate liver toxicity and a possible decrease in antithrombin III (AT III) plasma level. AT III was found decreased only in patients who received ASNase, whereas HIDARAC alone did not influence AT III levels. It is pointed out that a single dose of ASNase seems to be sufficient to induce a decrease in AT III. A mild and transient liver toxicity due to HIDARAC therapy does not seem to be of any clinical relevance.
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PMID:Antithrombin III during high-dose cytosine arabinoside therapy with or without asparaginase. 309 Aug 30

The M(r) of the complexes formed when factor Xa reacts with antithrombin III (ATIII) in plasma were estimated by gel filtration and SDS-polyacrylamide electrophoresis. The predominant species of factor Xa-ATIII detected after plasma and plasma to which factor Xa had been added were gel filtered on Sephadex G-200 and Sepharose 4B had apparent M(r) > 200,000, in which factor Xa-ATIII was associated with vitronectin. Addition of factor Xa-ATIII to ATIII-depleted plasma also resulted in the formation of factor Xa-ATIII-vitronectin complexes with M(r) > 200,000. Using polyclonal antibodies to human factor Xa-ATIII and ATIII as the capture and detector antibodies, respectively, a sensitive and specific enzyme-linked immunosorbent assay was developed to quantify factor Xa-ATIII in plasma. The relationship between factor Xa-ATIII production and prothrombinase activity in vivo was investigated by quantifying factor Xa-ATIII and prothrombin fragment 1 + 2 endogenous to the plasmas of blood donors and patients with Hodgkin's and non-Hodgkin's lymphoma. Whereas the concentrations of prothrombin fragment 1 + 2 in the 84 normal plasmas increased with age, those of factor Xa-ATIII (mean +/- SD of 34.7 +/- 13.8 pM) did not, and no correlation existed between the concentrations of the two parameters in normal plasmas. In contrast, a highly significant correlation between the concentrations of these two parameters was found in the plasmas of the cancer patients which coincidentally also had higher concentrations of both factor Xa-ATIII and prothrombin fragment 1 + 2 than the normal plasmas. Thus, ATIII may differentially influence prothrombinase formation and activity in normal individuals and cancer patients.
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PMID:Measurement of factor Xa-antithrombin III in plasma: relationship to prothrombin activation in vivo. 764 8

Plasma levels of thrombin-antithrombin III complex (TAT), plasmin-alpha 2-plasmin inhibitor complex (PIC) and active plasminogen activator inhibitor (PAI) were assayed in 66 cases of disseminated intravascular coagulation (DIC). Significant elevation of both TAT and PIC was observed in all cases of DIC. Most elevated levels of TAT were seen in DIC with acute promyelocytic leukaemia (APL) and sepsis. The highest levels of PIC were seen in DIC with APL but were much lower in sepsis. A significant elevation in active PAI was observed in DIC due to acute leukaemia (apart from APL), chronic myeloid leukaemia and sepsis, but not in APL, non-Hodgkin lymphoma and cancer. Active PAI was higher in patients with multiple organ failure (MOF) than in those without MOF while PIC was lower in patients with this complication. Thus, the balance of coagulation and fibrinolysis varied according to the underlying cause of DIC; APL had more dominant activation of fibrinolysis, while sepsis had greater activation of coagulation. It is suggested that the inhibition of secondary fibrinolytic activation plays an important role in the progression of MOF by the disturbance of the microcirculation.
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PMID:Study of the balance between coagulation and fibrinolysis in disseminated intravascular coagulation using molecular markers. 786 91

Thromboembolic complications and decrease in protein C and S have been observed in patients while receiving combination chemotherapy for breast cancer. We investigated whether initial cytotoxic treatment of non-Hodgkin's lymphoma (NHL) and Hodgkin's disease (HD) is also associated with changes in these anticoagulant parameters. For this purpose 25 patients with intermediate to high grade NHL and seven with HD, undergoing primary treatment with cytotoxic drugs were evaluated at three time-points: pre-therapy, mid-therapy and post-therapy. In contrast to the breast cancer patients, no significant changes in protein C, protein S and antithrombin III levels were observed in the NHL patients during the various stages of therapy. However in HD patients, the mean protein C values had a tendency to be higher at mid-therapy compared to pre-therapy and protein S levels had a tendency to be higher at mid-therapy compared to post-therapy. In lymphoma patients receiving primary cytotoxic treatment we did not find changes in anticoagulant parameters that can explain a chemotherapy-induced hypercoagulable state, as has been reported in breast cancer patients.
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PMID:Levels of proteins C and S do not decline subsequent to first line chemotherapy in lymphoma patients. 960 Jan 11

BACKGROUND: Congenital thrombotic risk factors, oncological diseases and its therapies have been related to an increased occurrence of upper extremities deep venous thrombosis (UEDVT). PATIENTS AND METHODS: We studied seven patients bearing lymphoma (one Hodgkin's and six non-Hodgkin's) who developed UEDVT, one at diagnosis and six during chemotherapy (two of these six cases had implantation of a central venous catheter and four received Growth Colony Stimulating Factors in addition to chemotherapy). Patients were screened for: factor V G1691A (Leiden), prothrombin G20210A, methylene tetrahydrofolate reductase (MTHFR) C677T mutations and antithrombin III, proteins C and S plasma activity. RESULTS: All patients were wild-type homozygotes for G20210A. One was heterozygote for factor V G1691A, the other 6 were wild-type homozygotes. Three of the 7 patients were homozygotes and 2 heterozygotes for the MTHFR mutation; the remaining 2 were wild-type homozygotes. Clotting inhibitor levels were normal in all patients. CONCLUSIONS: UEDVT in patients bearing haematological malignancies can occur irrespective of congenital thrombophilic alterations. However, in a subgroup of patients UEDVT could also depend on congenital thrombophilic alterations. A screening for inherited thrombophilia can identify high risk patients that could be specifically treated to prevent thrombotic complications.
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PMID:Congenital and acquired thrombotic risk factors in lymphoma patients bearing upper extremities deep venous thrombosis: a preliminary report. 1503 64


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