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Biomedical subjects

Z Boda

Publications and source records attributed to Z Boda.

At least 37 records · Page 2Linked to original sources
PubMed1996

Coumarin-induced skin necrosis following heparin-induced thrombocytopenia and thrombosis. A case report.

A severe thrombotic thrombocytopenic status, induced by heparin in a sixty-nine-year-old woman undergoing total hip joint arthroplasty, was treated by switching the anticoagulant therapy to coumarin, which induced skin necrosis. There appeared to be a possible causal relation between the severe immune reaction to heparin and the condition that predisposed to skin necrosis in the presence of coumarin. In patients who express a strong immune response to heparin, a different anticoagulant approach other than use of coumarin congeners appears to be justified.

Aged↗
PubMed1996

Promotion of the crosslinking of fibrin and alpha 2-antiplasmin by platelets.

Factor XIII (FXIII) is of high importance in the regulation of fibrinolysis. It crosslinks alpha 2-antiplasmin (alpha 2AP) and fibrin and by this way protects fibrin from the prompt elimination by plasmin. Although FXIII of platelets has been implicated in this protective mechanism, the role of platelets and platelet FXIII in the crosslinking process is far from being elucidated. As demonstrated by SDS PAGE and by immunoblotting for alpha 2AP, intact normal platelets resuspended in FXIII-free plasma or FXIII-free fibrinogen solution catalyzed the crosslinking of fibrin chains and also the crosslinking of alpha 2AP to fibrin alpha-chains. With FXIII-deficient platelets no crosslinking reaction could be observed indicating that the crosslinking with normal platelets was, indeed, due to platelet FXIII and not to another, putative platelet transglutaminase. However, the crosslinking of alpha 2AP to fibrin induced by the FXIII of intact platelets resuspended in FXIII-free plasma was considerably less extensive than the crosslinking carried out by the FXIII of normal plasma in the presence of FXIII-free platelets. Furthermore, the replacement of FXIII-free platelets by normal platelets in normal FXIII-containing plasma resulted in little, if any, difference in the crosslinking process. When crosslinking was induced by highly purified plasma FXIII the presence of intact FXIII-free platelets significantly accelerated the formation of alpha-chain polymers as well as the incorporation of alpha 2AP-fibrin alpha-chain hetero-dimer into these polymers. The results indicate that, in physiological conditions, platelet FXIII plays only a minor role in the crosslinking of alpha 2AP and fibrin; however, platelets, independently of their FXIII content, promote the crosslinking reaction by providing a catalytic surface on which the formation of highly crosslinked fibrin polymers is accelerated.

Blood Platelets↗
PubMed1995

[Syncumar-induced necrosis following heparin-induced thrombocytopenia and thrombosis].

The authors describe the combined occurrence of heparin-induced thrombocytopenia and cumarin-induced skin necrosis, a rare condition that has not yet been reported in Hungary. The 69-year-old woman had received prophylactic heparin treatment prior to total hip arthroplasty. The first complication that the anticoagulant therapy brought about was serious thrombocytopenia paradoxically associated not with bleeding but with deep vein thrombosis. The latter necessitated coumarin therapy which resulted in severe skin necrosis.

Acenocoumarol↗
PubMed1994

Cyclic relapses of thrombotic thrombocytopenic purpura.

A 24-year-old male patient was first observed with full-blown acute thrombotic thrombocytopenic purpura in 1991. Complete remission was achieved with plasma and plasmapheresis therapy, but in spite of continuous corticosteroid and aspirin administration, thrombocytopenic (megakaryocytic) relapses were observed every 26-30 days. Splenectomy and danazol failed to prevent the recurrence of the disease. Surprisingly, cyclosporin A (5 mg/kg/day) administration resulted in a complete transitional remission, but after dose reduction a less regular pattern of repeated milder recurrences was observed. Cryopreserved plasma, obtained from the patient during remission also proved to be effective in treating the last two thrombocytopenic episodes.

Adult↗
PubMed1993

Platelet factor XIII becomes active without the release of activation peptide during platelet activation.

The potentially active A subunit of factor XIII of blood coagulation has also been detected in platelets and monocytes/macrophages through the exact function of this cellular protransglutaminase has not yet been elucidated. In physiological conditions the first step in the activation of plasma factor XIII is the removal of an activation peptide from the N-terminal end of subunit A by thrombin. The A subunit then, in the presence of Ca2+, dissociates from the inhibitory B subunit and assumes an active conformation. Cellular factor XIII, which lacks B subunit, can be proteolytically activated in vitro by thrombin and the intracellular Ca2+ sensitive protease, calpain, in the same way as plasma factor XIII subunit A, and calpain has been suggested as the intracellular protease involved in the activation of cellular factor XIII in platelets. In the present experiments it was shown by SDS PAGE that during long-term stimulation of platelets with thrombin nondisulfide-crosslinked high M(r) protein polymers not penetrating the concentrating gel were formed. The lack of these polymers in thrombin-stimulated factor XIII deficient platelets clearly indicated that their formation in normal platelets was due to factor XIII that became active during platelet activation. However, no release of the activation peptide could be detected by Western blotting during this process. Similarly, no proteolytic cleavage of factor XIII was detectable when platelets were stimulated by Ca2+ ionophore through this stimulus activated calpain as it was clearly demonstrated by the breakdown of major intracellular calpain substrates.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1993

Endothelium releases more von Willebrand factor and tissue-type plasminogen activator upon venous occlusion in patients with liver cirrhosis than in normals.

Venous occlusion was used in 8 patients with liver cirrhosis and in 10 normals to investigate the pathomechanism of long-term elevation of plasma von Willebrand factor antigen (vWFAg) in liver cirrhosis. The following parameters were determined at baseline, and immediately, 60 min and 24 h after 10 min venous occlusion: vWFAg, ristocetin cofactor (RiCoF), in vitro platelet retention (Adeplat T), and tissue-type plasminogen activator (t-PA). Every baseline value in the liver cirrhosis group was significantly higher than in the controls. In both groups the 10-min values were significantly higher than their corresponding baseline results. Hence, comparing the two groups, in liver cirrhosis a significantly higher release of vWFAg and t-PA could be observed. These findings suggest on the one hand that the increased release contributes substantially to the sustained elevation of plasma vWF level in liver cirrhosis. On the other hand, the results indicate that not only the vascular surface of the diseased liver but most probably the total endothelium plays an important role in this phenomenon.

Adult↗
PubMed1992

[Successful electroconvulsive treatment of a schizophrenic patient suffering from severe hemophilia A].

Experiences obtained with the electroconvulsive treatment of a schizophrenic patient suffering from severe haemophilia A are reported. No haemorrhagic complications were observed. According to our experiences electroconvulsive therapy can be applied also in severe haemophilia A if satisfactory replacement therapy can be ensured. Similar case has not been found in the literature.

Adult↗
PubMed1991

[Primary hemostasis in mixed connective tissue disease].

Willebrand-factor antigen level and structure analysis, ristomycin-cofactor assay, beta-thromboglobulin and thromboxane metabolite estimations were performed in 22 patients with mixed connective tissue disease. High levels of Willebrand factor antigen and activity were detected in the presence of thrombocytopenia, previous thrombotic events, pulmonary vascular lesions and in the presence of circulating antiendothelial antibodies. Increased platelet activation was documented also in antibody positive cases and in thrombocytopenia. The alterations of endothelial and platelet functions may play important role in the development of vascular complications of mixed connective tissue disease.

Adult↗
PubMed1991

[Successful treatment of severe hemorrhage by using thrombocyte suspension with cryoprecipitate in type III Willebrand disease].

A 24-year-old woman with severe haemorrhagic complication due to type III von Willebrand's disease is reported, as the first such case in Hungary. Analysis of seven family members affected by the type III mutant gene was compatible with an autosomal recessive mode of inheritance. Severe, iatrogenic epistaxis of the patient was not improved by cryoprecipitate and DDAVP. Platelet suspension together with cryoprecipitate immediately stopped bleeding. Simultaneous application of cellulare (platelet suspension) and plasmatic (cryoprecipitate) Willebrand protein is suggested for patients with severe (type III) von Willebrand's disease.

Adult↗
PubMed1991

Alterations of primary haemostasis in mixed connective tissue disease (MCTD).

Willebrand-factor antigen level and structure analysis, ristomycin-cofactor assay, beta-thromboglobulin and thromboxane metabolite estimations were performed in 22 patients with mixed connective tissue disease to evaluate the incidence and the possible role of haemostatic alterations in the complications occurring during the course of the disease. High levels of Willebrand-factor antigen and ristomycin-cofactor activity were detected in patients with thrombocytopenia, previous thrombotic event, pulmonary vascular lesions and usually in the presence of circulating anti-endothelial antibodies. Increased platelet activation could have been found in antibody positive cases and in patients with thrombocytopenia as well. The documented alterations of endothelial and platelet functions may play important role in the vascular complications of mixed connective tissue disease.

Adult↗
PubMed1991

[Successful cyclosporin therapy of acquired hemophilia caused by factor VIII (VIII:C) inhibiting antibody].

A 47-year-old woman is reported who had a life-threatening, subarachnoideal bleeding due to the spontaneous development of factor VIII:C inhibitor. Cyclosporin combined with prednisone allowed a full recovery and the elimination of antibody even when other therapeutic facilities failed to be effective. Actual problems of treatment of factor VIII inhibitors are briefly surveyed.

Antibodies↗
PubMed1991

Treatment of the severe bleeding episode in type III von Willebrand's disease by simultaneous administration of cryoprecipitate and platelet concentrate.

A severe, life-threatening bleeding episode in a 24-year-old woman suffering from type III von Willebrand's disease was treated by large doses of cryoprecipitate with unsatisfactory results. Bleeding ceased and the bleeding time normalized only after concomitant administration of platelet concentrates. In the treatment of von Willebrand's disease patients possessing platelets with absent or insufficient von Willebrand factor activity the administration of plasma concentrates together with platelets appears to be justified.

Adult↗
PubMed1990

[Thrombotic changes in hemostasis following streptokinase therapy in myocardial infarct].

Thrombolytic treatment of acute myocardial infarction proved to be able to restore infarct artery patency and to decrease hospital mortality. The number of bleeding complications have remained at an acceptably low level, however some thromboembolic complications occurring during the first week following thrombolytic therapy have been recently observed. Signs of increased in vivo platelet activation (by measuring beta-thromboglobulin and thromboxane metabolite levels) and endothelial damage (Willebrand-factor estimations) could have been detected in our patients treated with brief high dose intravenous streptokinase, altogether with diminished antithrombin III and protein C antigen levels and activity. Intravenous streptokinase treatment of acute myocardial infarction might be able to cause thrombotic haemostatic alterations, which require meticulous haemostasis monitoring and early, correct antithrombiotic therapy.

Blood Coagulation↗