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Biomedical subjects

G Sas

Publications and source records attributed to G Sas.

At least 37 records · Page 2Linked to original sources
PubMed1990

[Heparin cofactor II studies in thrombophilic patients].

The plasma concentration of heparin cofactor II was measured by "rocket" immunoelectrophoresis in healthy volunteers, patients taking Syncumar and thrombophiliacs. The values in healthy volunteers averaged 99% (+/- 16.5). In the group of Syncumar treated patients 100% (+/- 10.5) was measured. This did not differ from the control group. The average of heparin cofactor II level in thrombophiliacs was 92.5% (+/- 23). In this group three patients had low heparin cofactor II levels. In one case this was due to intestinal protein loss. In the two other cases the role of heparin cofactor II is uncertain in the pathogenesis of thrombophilia.

Acenocoumarol↗
PubMed1989

[Distribution of the causes of congenital thrombophilia].

In recent years there have been discovered more and more such connatal mostly hereditary coagulopathies, which can explain the thrombosis susceptibility of the given individual or/and the family. The International Thrombosis and Haemostasis Society made a survey to estimate the frequency of those defects causing thrombophilias. In this survey the authors analysed the cases of their patients according to the given points of view. In their work they discuss some theoretical and practical problems of the theme, which can have an importance in respect to the everyday medical practice.

Adult↗
PubMed1984

On the therapeutic effects of trivalent and divalent iron in iron deficiency anaemia.

The effectiveness of orally administered iron was investigated using three different iron preparations in a randomized study with 3 patient groups, each consisting of 20 subjects with iron deficiency anaemia. Group A received a ferric(III)-dextrin complex, group B Fe(II)-sulfate, and group C Fe(II)-fumarate with vitamins. For all three preparations the increase in the number of erythrocytes as well as hemoglobin and hematocrit values ran absolutely parallel for a period of 12 weeks. A relevant difference between the trivalent ferric-dextrin complex and the two bivalent iron preparations could not be detected on evaluation of the parameters measured except for a moderate increase in the transaminase values in the patients group who received the Fe(II)-sulfate preparation. No differences were found among the preparations with respect to tolerance. The results are discussed with respect to a possible overloading of the iron transport system by highly absorptive Fe(II)-preparations.

Adult↗
PubMed1984

Hereditary antithrombin III deficiency: biochemical aspects.

Since the description of the first thrombophilic family with congenital AT-III deficiency, increasing numbers of different types of the condition have become evident. Initially the anomaly seemed to be homogeneous and simple: the three main characteristics of AT-III (thrombin inactivating and heparin cofactor activity, antigen concentration) were decreased. This type of AT-III deficiency (type 1) was later divided into type 1a and 1b on the basis of the heparin affinity of the AT-III molecule. The first family with a different qualitative AT-III disorder (type 2) was described by our group in 1974. In the members of this family the AT-III antigen concentration was normal, but the molecule had no functional activity (AT-III Budapest). In the last few years some new variants of type 2 hereditary AT-III disorders have been observed; they are characterized by a loss of one or more functional properties of the AT-III molecule.

Antigens↗