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Biomedical subjects

M Domula

Publications and source records attributed to M Domula.

At least 37 records · Page 2Linked to original sources
PubMed1984

[Effect on hemostasis and thrombogenesis by septic processes especially in childhood].

In 284 children with sepsis coagulation analyses were carried out. In sepsis in the postnatal period number of thrombocytes, plasminogen, antithrombin III, alpha 2-macroglobulin and factor V were initially decreased on an average, but fibrinogen, alpha 2-antiplasmin, the factors II and X as well as the trypsin inhibitor capacity were increased. The initially on an average reduced parameters often still considerably decreased, in order to increase after this to the norm of age within one to two weeks. The thrombocytopenia longest persists, often to the third week. The components initially found increased on an average in most cases rapidly increase and beyond the norm of age. They behave as acute phase proteins. In sepsis beyond the neonatal period the quality of the acute phase protein is in numerous components still more distinct than in the postnatal period. Several parameters also showed a completely other dynamics: the thrombocytopenia is of lesser size and shorter duration and is very often changed by a thrombocytosis. Here alpha 2-macroglobulin also has the quality of an acute phase protein. From the dynamics observed is concluded that disseminated intravascular coagulation processes frequently accompany the initial phase of the sepsis. They cause an eminent over-production of coagulation components which is limited by their production capacity and partly compensates the defects. The diversity of the constellation is explained by different sizes of consumption and compensation. The parameters in their dynamics have diagnostic valency. As far as the difference from fibrinogen level and number of thrombocytes is concerned it could already proved by simple means.

Bacterial Infections↗
PubMed1984

[Elimination of inhibitors in children with hemophilia A].

In five hemophilic children an attempt was made to eradicate inhibitors by continuous treatment with low doses of cryoprecipitate. All patients were high responders with maximum titers of 25 and 600 U. In four patients the anamnestic response was prevented or diminished by simultaneous treatment with cyclophosphamide. In these patients the inhibitor did not return during the continuous replacement therapy, even not after cessation of cyclophosphamide administration and in three of them not after intensive substitution. In the other child the titer decreased continuously in the beginning, but only to values unsuitable for replacement effects. Attempts to exterminate the inhibitor should be occasionally made by continuous low dose substitution therapy. The importance of the combination with cyclophosphamide cannot be decided until now because of the small number of observations.

Child↗
PubMed1983

[Heparin and antiheparin in childhood. 3. Heparin level measurements and their importance in heparin monitoring].

Measurements of the heparin level were made under continuous anticoagulation in a total of 7 patients. For the purpose of monitoring heparin the coagulation time values were determined parallelly. Except a patient with a sepsis and a 7 days old newborn baby the desired prolongation for the partial thromboplastin time and the reaction time of thrombelastogram resulted from heparin titres lying within the range of 0.2-0.7 U/ml of plasma. Even after applying depot preparations there was a relatively good correspondance of heparin level curves and coagulation parameters. In childhood the partial thromboplastin time is primarily suitable for monitoring the heparin therapy. Heparin half-life times calculated during the transumbilical exchange transfusion in 7 children amounted to values ranging between 40-110 minutes. In addition to checking low dose heparinizing, measurements of the level are suitable for deriving dosage standards for neutralizing heparin effects by protamine sulfate.

Adolescent↗
PubMed1982

[Alpha 2-antiplasmin in childhood].

In 119 children, predominantly newborns and babies with sepsis, alpha 2-Antiplasmin was determined by the use of the chromogenic substrate S-2251. In healthy newborns, the inhibitor level averaged 65 per cent of the adult level. Already in the initial phase of sepsis, enhanced alpha 2-antiplasmin values were observed. During the further course, they increased markedly. Thus, alpha 2-antiplasmin proved to be an acute phase reactant together with fibrinogen, factors II and X, and alpha 1-antitrypsin measured as trypsin inhibitor capacity. The correlation analysis in all subgroups showed moderately tight binding to fibrin. In patients with shock or in those who decreased, lower levels were measured. The overproduction is assumed to be caused by disseminated intravascular coagulation processes. In other diseases such as respiratory distress, alpha 2-antiplasmin was reduced. In case of disseminated intravascular coagulation that was not caused by sepsis consumption of components dominated. In the probability paper, distribution of the values of the subgroups was found to differ markedly. Thus, the inhibitor proved to be of diagnostic value.

Blood Coagulation Factors↗
PubMed1982

[Heparin and antiheparin in childhood. 2. Clinical relevance of the phenomenon of heparin resistance].

Investigations of the content of platelet factor 4 in different thrombocyte lysates and platelet-rich plasma after induced release reaction were aimed at checking the efficiency of the own antiheparin measuring system. In this connection, the age dependent dynamics of platelet factor 4 could be first discovered. In platelet-poor plasma of healthy grown-up test persons there was an evidence of antiheparin titres which were five times higher as compared with those persons born maturely. All patients with disseminated intravascular coagulation processes of different aetiology, however, will have significantly increased values. As demonstrated in two children with hyperpyretic toxicosis, the liberated platelet factor 4 will only show a short plasma half decay period. From investigations made for refinding heparin in the plasma after in vitro addition the conclusion can be drawn that, in addition to platelet factor 4, even unspecific adhesions of heparin to certain plasma proteins may be responsible for increasing heparin resistance.

Adolescent↗
PubMed1982

[Heparin and antiheparin in young children. 1. Report: development of a method for determining heparin and antiheparin in the antithrombin-thrombin system].

A new method of determining the biological activity of heparin and antiheparin is described. The principle is based on measuring the coagulation time in the antithrombin-thrombin system. By using a partially purified antithrombin III preparation and after coagulating the plasma samples with small amounts of thrombin the measuring system proves to be mostly independent on the inhibitory content of the test plasmas to be investigated. Heat defibrinated plasma cannot be used because it has essential properties with a close affinity to heparin. Additions of sodium and calcium ions will make the system more sensitive. Criteria of reaction kinetics are used for standardizing the antithrombin-thrombin system. The heparin level of up to 0.01 U/ml and the antiheparin titre of up to 0.005 U/ml can be covered by the procedure presented. Thus, it has a high sensitivity. The quality controls which were performed give evidence of the high precision of this method.

Antithrombin III↗
PubMed1981

[Hemostasis disorders after transfusions].

Disturbances of haemostasis caused immunologically and non-immunologically were observed after transfusion of blood and blood derivatives. Transfusion of heparin blood increased the bleeding susceptibility only in case of pre-existing high-degree defects of haemostasis or if they were performed as massive or exchange transfusions. Massive transfusions with blood stored for a long time will induce complex defects. Under intensive substitution therapy of haemophilia A the so-called paradoxical bleeding will occur in spite of a high factor VIII level. These bleedings are supposed to be disturbances of the thrombocyte function and are caused by fibrin(ogen) derivatives. Post-transfusional thrombocytopenias may be brought to remission by repeated plasmapheresis. Factor specific inhibitory bodies will appear after substitution in a small percentage of haemophilic patients. 5 to 7 days after the onset of therapy an anamnestic reaction can be observed as a titre increase by leaps. Usually, the inhibitory titre will decrease to a mostly low basal value in the course of three to five months. The therapy with cyclophosphamide simultaneously started with the substitution will more frequently prevent the anamnestic reaction or reduce it. Titres with more than 5 units cannot be overcome at the beginning even by higher concentrations of preparations. The substitution therapy should be preceded by exchange transfusions or plasmapheresis of up to 25 units. With still higher titres only procedures of inhibitor-bypassing are possible with factor VIII preparations of animal origin or better with activated prothrombin complex preparations, such as FEIBA. Recent reports give evidence that permanent substitution with factor VIII concentrates at a highest dosage can eliminate the production of inhibitors completely.

Blood Coagulation Disorders↗
PubMed1979

[The protease inhibitor potential in newborns with respiratory distress syndrome].

In 70 newborns with respiratory distress syndrome (RDS) and in roughly the same number of eutrophic mature newborns the total antiplasmin, progressive antithrombin and alpha 2-macroglobulin was determined, the latter in an enzymatical as well as immunochemical way. In healthy mature newborns the progressive antithrombin was somewhat below the level of adults, alpha 2-macroglobulin was above it in both methods and total antiplasmin within it. All parameters of protease inhibitory capacity were significantly lowered in newborns with RDS. Smaller values could be found in patients with bleedings and in those who died later on. Even in those patients with a birth weight under 2,000 g there was a tendency to lower values which can only be partially due to the specificity of development of inhibitors. Progressive antithrombin, total antiplasmin and alpha 2-macroglobulin determined enzymatically are correlated in newborns with RDS jointly and with numerous other parameters of the coagulation system. These relations point to the fact that all components are included in the same consumption process, viz. in the process of disseminated intravascular coagulation. Alpha 2-macroglobulin values determined immunochemically do not correlate with coagulation parameters determined enzymatically as well as with other parameters. They lay partially above or below those determined enzymatically. This behaviour can only be explained by a partial enzyme complex binding of alpha 2-macroglobulin in newborns with RDS.

Antithrombins↗
PubMed1978

[An inhibitor in the Willebrand-Jürgens syndrome and its effect on the factor VIII molecule properties].

In a patient with a clinically serious Willebrand-Jürgen's syndrome an inhibitor appeared at the age of 1 1/2 years, which, contrary to inhibitors in haemophilia A, was directed against all properties of factor VIII molecule. In a quantitative test the height of the inhibitor level to factor VIIIag was determined. Administrations of plasma concentrate resulted in a titre increase which could not be suppressed even by an immunosuppressive therapy with cyclophosphamide. After a long break in the substitution a severe bleeding could be successfully treated and the substitution effect for factor VIIIc, factor VIIIag and Ristocetin co-factor could be identified for several days.

Antigens↗
PubMed1977

[Effect of drug therapy during pregnancy on the clotting potential of the newborn].

Drug therapy in mothers may lead to various disturbances of the hemostasis of the newborn. Some authors reported on severe hemorrhages in newborn after coumarin treatment of the mothers, others had not or only seldom observed such events. Our examination did not reveal any significant clotting disorders in 4 newborns whose mothers had received Athrombom. Perhaps the indandion derivative does not significantly penetrate the placental barrier. However, therapy with anticoagulants of the vitamin K antagonist type may be instituted during pregnancy only in cases where it is strictly indicated. Streptokinase and heparin will certainly not enter the fetal circulation, therefore they may be used without risk for the child. Furthermore the clinican must known severe bleeding conditions of the vitamin K deficiency type in newborns of mothers with anticonvulsive therapy. Preventive administration of vitamin K to pregnant women and newborns or, in the presence of bleedings, instantaneous and exact substitution may bring under control the critical situation. Acetylsalicylic acid given during the last weeks of pregnancy causes an inhibition of the aggregation of thrombocytes of the newborn. Bleedings occur only seldom. Other drugs administered during pregnancy may induce neonatal thrombocytopenia through immunological or toxic mechanisms, such for instance quinine, quinidine, tolbutamide and thiazides.

Aspirin↗