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Biomedical subjects

G Witzke

Publications and source records attributed to G Witzke.

12 recordsLinked to original sources
PubMed1989

Long-term prophylaxis with C1-inhibitor (C1 INH) concentrate in patients with recurrent angioedema caused by hereditary and acquired C1-inhibitor deficiency.

A case of hereditary angioedema (HAE) type I (inherited C1-inhibitor [C1 INH] deficiency) and a case of late-onset acquired C1 INH with angioedema is described. In both patients, long-term prophylaxis with C1 INH had become necessary because treatment with danazol and epsilon-aminocaproic acid was not effective or not tolerated. Consequently, both patients received a pasteurized concentrate of C1 INH continuously for a period of 1 year in a dosage that kept them free of symptoms. The patient with HAE was administered 500 units of C1 INH intravenously every 4 or 5 days, whereas the patient with acquired angioedema required 1000 units of C1 INH every 5 days. As a result of this long-term prophylaxis, both patients became free or nearly free from their episodes of cutaneous and internal edema. The low plasma levels of C1 INH, C4, and C2, rose. In the patient with acquired C1 INH deficiency, the swellings increasingly reappeared after 10 months, although the patient's antibody titer did not rise during treatment. No side effects were recorded during therapy. In particular, both patients remained HIV and hepatitis B antibody negative.

Angioedema↗
PubMed1984

Coagulation factors and proteinase inhibitors in the plasma of children with acute lymphoblastic leukoses. Behaviour before and during treatment according to Protocol I of the Cooperative Leukaemia Study COALL-80.

The thrombocyte count, the factor XIII (F XIII) activity, the concentration of fibrinogen (F I), prothrombin (F II), fibronectin (CIG), albumin and the proteinase inhibitors antithrombin III (AT III), alpha 2-macroglobulin (A2M), alpha 1-antitrypsin (A1A) and Cl-esterase inactivator (Cl-INA) were determined in ten children with acute lymphoblastic leukaemia (ALL). Changes due to the disease and to therapy were observed. Before the start of treatment the patients had thrombocytopenia secondary to the disease, and the proteinase inhibitors--especially Cl-INA and A1A--were raised. During the induction phase the thrombocyte count rose but there was also a marked increase in the concentration of F II and CIG. During the consolidation phase there was a general fall in protein concentration under L-asparaginase medication. The cause was attributed to a disorder of protein synthesis. The concentration of the factors studied rose again during maintenance therapy.

Adolescent↗
PubMed1984

Interaction between C1-INA, coagulation, fibrinolysis and kinin system in hereditary angioneurotic edema (HANE) and urticaria.

The C1-inactivator plays an important role not only in the initial phases of the complement system, but also in those of the coagulation, fibrinolysis and kinin systems. The present study was concerned with the reciprocal influence of decreased C1-inactivator levels in patients with hereditary angioneurotic edema (HANE, HAE). In 13 HANE-I patients there were significantly increased levels of the coagulation factors XII, XI, V, of plasminogen and of alpha 2-antiplasmin, while the factors IX and VII were decreased. Conversely, it emerged that in patients with markedly raised prephase factor levels, angioneurotic edema occurred in the presence of normal or only slightly decreased C1-inactivator levels. However, the ratio between factor XI and C1-INA activity was significantly higher than in normal and urticaria patients. Factor XII, HMWK, XI, VIII and V levels were significantly raised in 10 patients with frank chronic urticaria, while factor VII was lowered. Numerous other factors and inhibitors of the coagulation, fibrinolysis and kinin systems were, however, normal or showed no significant differences.

Angioedema↗
PubMed1983

Hereditary angioneurotic oedema and blood-coagulation: interaction between C1-esterase-inhibitor and the activation factors of the proteolytic enzyme systems.

C-1-inactivator (C-1-INA) does not only exert its important inhibitory functions in the complement system but also in the first step in the activation of the coagulation, fibrinolytic and kallikrein system. We therefore determined in nine patients with hereditary angioneurotic oedema (HANE) with obvious quantitative or functional defects of C-1-INA, and one further patient with Quincke-type oedema of different origin, the coagulation factors of the initial phase such as Hageman factor, plasma thromboplastin antecedent (PTA) and high molecular weight kininogen (HMWK). These factors were further correlated with the concentration as well as functional activity of C-1-INA. Nine of ten patients showed a significant, sometimes even excessive, increase in the levels of factor XII (mean +/- SD = 146% +/- 63), HMWK (mean +/- SD = 126% +/- 56) and PTA (mean +/- SD = 289% +/- 294), and a decrease of C1-esterase inhibitor (C-1-inactivator), which was measured with a immunologic method (mean +/- SD = 9.6 mg/dl +/- 6.6) for its concentration as well as being measured for its activity (mean +/- SD = 30.4% +/- 24.9).

Angioedema↗
PubMed1981

[Haemostatic changes related to extracorporeal circulation (ECC) (author's transl)].

After-bleeding not due to surgery following extracorporeal circulation (ECC) in open heart surgery has its origin in disorders of platelet number and function as well as in changes of the haemostatic balance. Not only are the plasmatic factors of the coagulation and the fibrinolytic system of importance but also their inhibitors which tend to avoid dysfunctions and overshooting reactions. To detect early the danger of an excessive bleeding tendency assays of fibrinogen (factor I), prothrombin (factor II), antithrombin III (AT III) and of alpha 2-macroglobulin (A 2 M) are recommended. A substitution therapy can be oriented by the results of these coagulation parameters.

Aged↗
PubMed1979

[Recommendations for transfusion therapy. Volume substitution, raising oxygen transport capacity and replacement of clotting factors (author's transl)].

The principal aims of whole blood transfusion therapy are simultaneous volume substitution, raising the oxygen transport capacity and the replacement of clotting factors. The necessary control factors for volume substitution are described. It must be borne in mind that the blood undergoes changes during storage which among other things affects the ability of the blood to transport oxygen and the clotting potential. Not only the destruction of thrombocytes must be considered but also the loss of activity of the proaccelerin and the antihemophilic globulin A. For this reason for massive blood transfusions using older blood conserves it is recommended that the loss of activity be compensated by antihemophilic cryoprecipitate.

Biological Transport↗
PubMed1979

[Coagulation problems associated with massive blood transfusions. An experimental study (author's transl)].

During storage banked blood show changes as far as function and concentration of their corpuscular and plasmatic ingredients are concerned. Antihaemophilic globulin (factor VIII) and pro-accelerin (factor V) in particular lose their activities so quickly that only very few activities still remain after a storage period of 3-5 days. In connection with existing primary diseases but also in trauma and shock a dilution-coagulopathy caused by insufficient supply of factors VIII and V can develop during massive transfusion, and this especially with banked blood already stored over a longer period of time. Therapy of this disturbance of coagulation consists of substituting the missing coagulation factors under heparin protection.

Blood Coagulation Disorders↗