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)

In 56 patients with Hodgkin's disease, the following bloodtests were carried out: erythrocyte sedimentation rate (ESR), fibrinogen, alpha2-globuline, serium iron concentrations and alkaline phosphatase activity. In some patients we additionally measured alkaline leucocyte phosphatase and serum ribonuclease activity. In our series ESR, serum iron and alpha2-globuline concentrations were the most sensitive metabolic parameters. A rise in fibrinogen concentration, alkaline phosphatase and serum ribonclease activity seems to indicate extensive disease. It is not possible, however, to discern between a state of remission and stage I by means of these parameters. ESR, serum iron and alpha2-globuline concentrations might be either elevated or normal in both instances. These parameters seem important in order to distinguish between a remission or stage I on the one hand and extensive disease in stage III and IV on the other hand. Concomitant findings of ESR above 40 mmh, elevated concentrations of fibrinogen and alpha2-globuline, as well as elevated alkaline phosphatase and serum and serum ribonuclease activity mostly indicate stage III or IV.
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PMID:[Significance of metabolic parameters in Hodgkin's disease (author's transl)]. 5 79

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

We studied Reed-Sternberg cells from 14 patients with Hodgkin's disease to learn whether they had monoclonal immunoglobulin synthesized by the cell or polyclonal immunoglobulin of external origin. Double-label immunofluorescence with F(ab')2 anti-serums to human light chains showed that cytoplasmic immunoglobulin of individual Reed-Sternberg cells is always polyclonal and usually associated with membrane-bound immunoglobulin of the same type. The predominant immunoglobulin was IgG; in one case IgM was also present. In vitro studies confirmed the internalization of exogenous IgG and phagocytosis of immune complexes by viable Reed-Sternberg cells. Their exclusion of trypan blue dye and lack of albumin and fibrinogen suggests relatively specific uptake of immunoglobulin, mediated by the Fc receptor or antigen (or antigens) associated with Hodgkin's disease at the cell membrane. Our studies support other recent evidence that the Reed-Sternberg cell is derived from a macrophage.
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PMID:Exogenous immunoglobulin and the macrophage origin of Reed-Sternberg cells in Hodgkin's disease. 10 41

Total serum haemolytic complement activity, plasma fibrinogen, erythrocyte sedimentation rate and other biological values in forty-three patients with Hodgkin's disease were correlated with results of staging. A highly significant increase (P=10(-5)) of the mean total serum haemolytic complement activity was found in stages IIIA and IVA and in all stages with systemic symptoms. The complement activity in patients with less extensive disease without systemic symptoms (stages IA and IIA) did not show a significant increase over the controls. The best initial parameters correlating well with disease activity were complement activity, ESR and fibrinogen level. It is concluded that total serum haemolytic complement activity gives additional information and can be helpful in differentiating between favourable and unfavourable forms of Hodgkin's disease.
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PMID:Total serum haemolytic complement activity, erythrocyte sedimentation rate and plasma fibrinogen as indicators of the stage in Hodgkin's disease. 40 50

The responses of the coagulation and fibrinolytic systems in nine patients with Hodgkin's disease undergoing splenectomy and lymph node mapping have been compared with those in nine patients undergoing elective upper abdominal operation for benign conditions. Differences have been noted in base line levels of fibrinogen, prothrombin, partial thromboplastin time and euglobulin lysis time. Platelet count increases were exaggerated following splenectomy, but other parameters of coagulation activity behaved similarly in the two groups. There is no evidence from this study to support the suggestion that blood coagulability is increased more markedly following splenectomy than it is after other upper abdominal operations.
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PMID:The coagulation and fibrinolytic response to splenectomy. 126 14

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

Nonmalignant lymphoid tissue and tissue from patients with nodular sclerosis, Hodgkin's disease, and large cell lymphocytic lymphoma was examined by immunohistochemical techniques for the occurrence in situ of components of coagulation and fibrinolysis reaction pathways. Staining for material interpreted as fibrinogen was observed in abundance in both malignant and reactive lymphoid tissue. Fibrin also occurred to a variable extent but focally in all tissues. Components of coagulation pathways, including tissue factor, factor VII, factor X, and factor XIII ("a" subunit), were restricted to tissue macrophages. Double-labeling techniques revealed fibrin in direct apposition to tissue macrophages. We conclude that fibrinogen and fibrin occur in both benign and malignant lymphoid tissue and that the transformation of fibrinogen to fibrin is attributable to macrophage-initiated thrombin formation. We postulate that both systemic and local hypercoagulability associated with these disorders may be attributable to macrophage activation resulting in expression of procoagulant activity.
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PMID:Fibrinogen deposition and macrophage-associated fibrin formation in malignant and nonmalignant lymphoid tissue. 174 Jun 24

To investigate the possibility that a hypercoagulable state develops during autologous bone marrow transplantation (BMT), we measured levels of circulating natural anticoagulants and fibrinolytic proteins before and weekly during the hospital course of 18 patients undergoing autologous BMT for Hodgkin's and non-Hodgkin's lymphoma. Patients received either weekly (standard dose group) or daily (high dose group) vitamin K supplements with their total parenteral nutrition. By day 14 there had been a significant drop in protein C activity (mean of 95% of normal to 52%), protein C antigen (mean of 105% of normal to 70%), and antithrombin 3 activity (111% of normal to 83%), and an increase in fibrinogen (471-621 mg/dl) and tissue plasminogen activator (6.9-13.8 ng/ml). No changes were seen in free or total protein S, plasminogen activator inhibitor, prothrombin time or partial thromboplastin time. The decreases in protein C and antithrombin 3 persisted through day 28 after transplantation. The drop in protein C correlated strongly with decrease in serum albumin, suggesting impaired synthesis of these proteins by the liver. No differences were seen in any of these parameters between the standard and high dose groups. Deficiencies in anticoagulant proteins antithrombin 3 and protein C and a rise in fibrinogen without a concomitant improvement in fibrinolytic variables create a potentially hypercoagulable state which may contribute to the thrombotic complications of autologous BMT.
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PMID:High frequency of antithrombin 3 and protein C deficiency following autologous bone marrow transplantation for lymphoma. 179 Apr 30

The purpose of this report is to document and compare the presenting clinical and laboratory findings of 38 patients, all intravenous drug abusers, with pathologically documented persistent generalized lymphadenopathy (PGL), and of 50 patients with AIDS-unrelated malignant lymphoma (30 with Hodgkin's disease and 20 with non-Hodgkin's lymphoma). All patients, aged 40 years or less, consecutively seen since May 1984 in a single institution in Italy, have prospectively undergone a similar clinico-pathologic approach. In addition to a history of intravenous drug abuse and HIV serology, the results indicate that a history of infection in the previous year, night sweats, weight loss, generalized lymphadenopathy, beta 2 microglobuline, transaminase, T4/T8 ratio less than 1, and polyclonal hypergamma-globulinemia significantly increased among PGL patients compared with patients with AIDS-unrelated malignant lymphoma. In contrast, patients with malignant lymphoma had a significant increase in mediastinal lymph nodes, sedimentation rate, LDH, fibrinogen and anemia. Therefore, at this time of an AIDS epidemic, after histologic diagnosis of reactive lymphadenopathy has been performed in young patients presenting with generalized lymphadenopathy, a request for a second biopsy and other invasive procedures may be avoided if clinical and laboratory data suggest a PGL syndrome. If not already performed, HIV antibody detection should be carried out in this setting.
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PMID:Persistent generalized lymphadenopathy syndrome vs "AIDS"--unrelated malignant lymphoma: comparison of presenting clinical and laboratory findings in 88 patients. AIDS and Related Syndromes Study Group. 277 74

Factor VIII molecular complex is included in the proteins of "acute inflammation", being changed not only in the congenital diseases - hemophilia A and Willebrand disease but also in a series of acquired diseases as various inflammatory processes, hypercoagulability, DIC syndrome, neoplasms. The studies carried out on Hodgkin's disease and non-Hodgkin lymphomas reveal that the changes in its separate activities (factor VIIIK and Willebrand antigen) are not unidirectional with the changes of fibrinogen level and cannot serve as an index of the activity of the process.
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PMID:[Changes in the factor VIII molecular complex in Hodgkin's disease and non-Hodgkin's lymphoma]. 311 78


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