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Biomedical subjects

M Udvardy

Publications and source records attributed to M Udvardy.

At least 73 records · Page 4Linked to original sources
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

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↗
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↗
PubMed1990

[Fatal thrombotic microangiopathy in the mother and fetus].

The appearance of thrombotic microangiopathy (thrombotic thrombocytopenic purpura, haemolytic uraemic syndrome) could have been documented in a 23 years old pregnant woman, who had been treated previously for immune-thrombocytolytic purpura. The disturbing anamnestic data caused significant delay in correct diagnosis and in starting of fresh-frozen plasma therapy, so the woman and her fetus (in utero) had been died. The specific histological microangiopathic lesions could have been well documented by the autopsy of the mother, however no such alterations could have been detected in the fetus and placenta. This latter intriguing observation might be remarkable in the evaluation of several concepts dealing with the aetiopathogenesis of thrombotic microangiopathy. The short review of literature of thrombotic microangiopathy in pregnancy and puerperial period is also given.

Female↗
PubMed1990

The use of polybrene for heparin neutralization in protein C activity assay.

The protein C activity assay of Francis and Patch (Thromb Res 1983; 32: 605-613) is based on the prolongation of the activated partial thromboplastin time in the presence of activated protein C isolated from the test samples. The assay was modified and standardized by Rapaport et al. (Am J Clin Pathol 1987; 87: 491-497), but could still only be used in patients on heparin therapy after chromatographic removal of the heparin. In this study we attempted to eliminate the heparin separation step without losing the advantages of the modified (Rapaport) method. Heparin was added to the isolated protein C to obtain a rapid and complete antithrombin effect after the thrombin activation step and polybrene was subsequently used to neutralize the excess heparin. Using this modified assay protein C activity ranged from 67 to 133% in the normal population, and from 9 to 25% in coumarin-treated patients. Precision of the modified method was acceptable in both normal and pathological PC ranges: within- and between-batch variations were 5.6 and 3.6%, and 8 and 14%, respectively. The assay correlated well (r = 0.84) with the ELISA technique in both healthy donors and non-coumarin-treated patients.

Biological Assay↗
PubMed1989

[Thrombotic microangiography (thrombotic thrombocytopenic purpura and hemolytic uremia syndrome)].

Thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome have quite uniform or identical histopathological features and share very similar clinical characteristics, so thrombotic microangiopathy may be used as a common descriptive term of the two syndromes. During the past one and a half year five patients with thrombotic microangiopathy, receiving plasma therapy were observed by the authors. Owing to the early, correct diagnosis and plasma administration four patients had been recovered from the disease. The evaluation of clinical signs and symptoms, altogether with some simple laboratory data (megakaryocytic thrombocytopenia, nonimmune acquired haemolytic anaemia, renal insufficiency, neurologic alterations, etc.) remained essential in the recognition and treatment of thrombotic microangiopathy. After giving a short review of the literature the authors deal with the results of some more specific examinations (prostanoids, beta-thromboglobulin, the quantitative and qualitative analysis of Willebrand factor, etc.) which may give further data to the complex aetiopathogenesis of thrombotic microangiopathy.

Adolescent↗
PubMed1989

[Connection between plasma thromboxane and prostacyclin levels in the metabolic control of diabetic children].

Platelet poor plasma thromboxane and prostacyclin levels and the quantity of metabolic control, altogether with vascular complications were evaluated in 55 children diabetes mellitus. The control group consisted of 33 healthy children of the similar age. Thromboxane levels remained unchanged in diabetics, while prostacyclin proved to be significantly decreased, which resulted in greater thromboxane/prostacyclin ratio. No meaningful differences were found according to the presence or absence of vascular complications in this group of diabetics. A positive correlation could have been detected between glycosylated haemoglobin and thromboxane levels, while a negative one between glycosylated haemoglobin and prostacyclin levels. The alterations of prostaglandin metabolism may be regarded as a consequence of diabetic metabolic changes, rather than of vascular complications. Disturbed prostaglandin metabolism in diabetic children might have a role in the pathogenesis of vascular complications.

Blood Glucose↗
PubMed1987

Plasma thromboxane and prostacyclin metabolite ratio in atherosclerosis and diabetes mellitus.

Thromboxane and prostacyclin metabolite determinations (radioimmunoassay) were performed in obliterative atherosclerosis and in diabetes mellitus with microangiopathy. The shift of these metabolites to the thromboxane side could have been documented in both diseases. This phenomenon calls attention to an increased platelet activation and endothelial cell damage. In a third group patients received aspirin (500 mg on alternative days) which caused a marked inhibition of both thromboxane and prostacyclin production, measured this way. The possible role of altered balance of these two prostanoids in atherogenesis and diabetic angiopathy is discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Glucose intolerance and insulin resistance with aging--studies on insulin receptors and post-receptor events.

The oral glucose tolerance test and immune reactive insulin level determination were performed on 100 non-obese healthy elderly and 40 young and middle-aged non-obese healthy subjects. In about 60% of the elderly an altered glucose tolerance test was found, but the insulin level was increased in the whole group of elderly subjects. This means an insulin-resistant state with aging. Further investigations were carried out to determine some possible causes of this insulin resistance. The chromium level in sera and granulocytes of elderly was significantly decreased as well as the insulin receptor numbers and the affinity to erythrocytes. In contrast, when the cyclic nucleotide levels were investigated in granulocytes under in vitro stimulation, an age-dependent increase of cAMP level was found and an unresponsiveness of cGMP, which ranged between mild and severe degrees. Concomitantly, all these changes found could contribute to the insulin resistance at the receptor and post-receptor levels with aging.

Adult↗
PubMed1986

Platelet function studies in myeloproliferative disorders.

Platelet functions were studied in 64 patients with various myeloproliferative diseases. The characteristic alterations were prolonged bleeding time, decreased platelet aggregation (but normal results induced by ristomycin), elevated level of BTG, high production of MDA, increased level of TXB2 with almost normal level of 6-keto-PGF1. However, considering the bleeding time and the amount of BTG in relation to the whole blood platelet count, no differences could be detected.

6-Ketoprostaglandin F1 alpha↗