Search PubMed⌕ Search

Biomedical subjects

C Korninger

Publications and source records attributed to C Korninger.

At least 37 records · Page 2Linked to original sources
PubMed1987

Enhanced fibrinolysis caused by tissue plasminogen activator release in hemodialysis.

The effect of hemodialysis on components of the fibrinolytic system was measured in 22 patients. Plasma levels of t-PA antigen, t-PA activity, u-PA antigen and plasminogen activator inhibitor were determined by means of immunological and functional assays. During hemodialysis, 11 patients exhibited an increase in t-PA antigen within the first hour to about three times the starting values (P less than 0.05), followed by a decrease to about double of the initial values until the end of the treatment. Eleven patients showed a continuous increase up to 200% of the starting values until the end of hemodialysis. u-PA levels did not change significantly during the time of investigation (P greater than 0.5).

Adolescent↗
PubMed1987

Evaluation of fibrinolytic capacity by a combined assay system for tissue-type plasminogen activator antigen and function using monoclonal anti-tissue-type plasminogen activator antibodies.

An assay system has been developed that allows consecutive quantification of tissue-type plasminogen activator (t-PA) activity and t-PA antigen in the same plasma sample. In the first step t-PA is bound to an immobilized IgM monoclonal anti-t-PA antibody and functional activity of bound t-PA is quantified by its plasminogen-activating activity. In the second step the amount of bound t-PA antigen is determined by using a different peroxidase-labeled monoclonal anti-t-PA antibody. In this combined assay system t-PA functional activity was found to depend not only on the amount of t-PA antigen but also on the amount of plasminogen activator inhibitor (PAI), whereas in the t-PA antigen assay PAI did not affect the results. In plasma samples obtained from normal controls t-PA activity was detected only in post-venous occlusion plasma (3.7 +/- 2.5 IU/ml), whereas 2.7 +/- 0.5 ng/ml t-PA antigen was found before and 12.6 +/- 4.4 ng/ml after venous occlusion. Using this combined assay system to study plasma samples from patients who did not respond to venous occlusion with shortening of the euglobulin clot lysis time (ECLT), it was possible not only to confirm that in none of these patients could t-PA activity be detected in the postocclusion plasma samples but also to subdivide that group of patients into a group of about 39% not reacting with normal t-PA antigen release to venous occlusion and into a second group of about 61% that reacted with normal t-PA antigen release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Sandwich ELISA for t-PA antigen employing a monoclonal antibody.

A sandwich enzyme-linked immunosorbent assay (ELISA) for determination of tissue-type plasminogen activator (t-PA) was developed. 96-well flat-bottom polystyrene plates were coated with polyclonal (goat) anti t-PA IgG (10 micrograms/ml). After addition of samples monoclonal (murine) anti t-PA IgG (1.5 micrograms/ml) was added. Finally, peroxidase labelled anti-mouse IgG (goat) was used to quantify the bound second antibody. The assay can be used for determination of t-PA antigen in purified systems, in cell culture supernatants, and in human plasma, provided that EDTA (0.005 M) is present in the sample. In 78 healthy volunteers, t-PA antigen levels at rest were 0.4 - 15.2 ng/ml (4.3 +/- 2.7, means +/- S.D.); A significant positive correlation between t-PA antigen and age could be demonstrated.

Adult↗
PubMed1986

Increased risk of thrombosis due to abnormalities of the hemostatic system.

In recent years a number or hereditary or acquired abnormalities of the hemostatic system have been discovered which predispose to thrombosis. The type of this abnormality determines not only whether there is a tendency to venous or arterial thrombosis but also predisposes in some instances to thrombosis at a specific site. Such hemostatic abnormalities may be present in 10-30% of patients with a history of venous thrombosis. The detection of a thrombophilic state has important implications as regards the choice and the duration of antithrombotic treatment.

Blood Coagulation Disorders↗
PubMed1985

The prevalence of hereditary antithrombin-III deficiency in patients with a history of venous thromboembolism.

Antithrombin-III activity was determined in 752 patients with a history of venous thrombosis and/or pulmonary embolism. 54 patients (7.18%) had an antithrombin-III activity below the normal range. Among these were 13 patients (1.73%) with proven hereditary deficiency. 14 patients were judged to have probable hereditary antithrombin-III deficiency, because they had a positive family history, but antithrombin-III deficiency could not be verified in other members of the family. In the 27 remaining patients (most of them with only slight deficiency) hereditary antithrombin-III deficiency was unlikely. The prevalence of hereditary antithrombin-III deficiency was higher in patients with recurrent venous thrombosis.

Antithrombin III Deficiency↗
PubMed1985

[Plasminogen activator of tissue type. Physiology, pathophysiology and clinical value].

Tissue-type plasminogen activator (t-PA), the major physiological activator of fibrinolysis, is contained in most human organs, tissues and secretions. t-PA is synthesized by endothelial cells and is released, in response to various stimuli, into the blood stream. Activation of plasminogen by t-PA is greatly enhanced in the presence of fibrin, whereby the fibrinolytic process is confined to the immediate environment of a formed thrombus. The enzymatic activity of t-PA is controlled by a fast-acting plasminogen activator inhibitor. Methods are now available for the immunological and functional determination of t-PA in biological fluids. The major function of plasmatic t-PA is the lysis of intravascular fibrin deposits. A reduced capacity to liberate functionally active t-PA from the vessel wall may result in the development of a thrombotic tendency. Extravascular t-PA is involved in various processes associated with cell migration and tissue remodelling. Purified t-PA preparations have been shown to induce marked fibrinolysis and thrombolysis with negligible fibrinogenolysis, in vitro and in various animal models. At present, the efficacy of recombinant t-PA in the lysis of arterial and venous thrombi is being tested in man.

Animals↗
PubMed1985

Prevention of arterial and pulmonary embolism by oral anticoagulants in patients with dilated cardiomyopathy.

The incidence of arterial embolism (AE) and pulmonary embolism (PE) during treatment with oral anticoagulants (OA) or without OA therapy was studied in 38 patients with dilated cardiomyopathy (DCMP). AE/PE occurred in 17 patients (44.7%) before initiation of OA treatment. The severity of DCMP was a risk factor for AE/PE, but not the presence of atrial fibrillation or intracardial thrombi. No AE/PE episodes occurred during the period of OA therapy. No major bleeding complications were seen, probably due to the moderate intensity of OA therapy (therapeutic range 5-15% Thrombotest [TT], 2.1-4.8 International Normalized Ratio [INR], median TT value 11%, median INR 2.6). Recurrence of AE was observed in 4 of 5 patients in whom treatment with OA had been discontinued.

4-Hydroxycoumarins↗
PubMed1985

[Use of monoclonal antibodies in the diagnosis of fibrinolysis].

Monoclonal antibodies to tissue type plasminogen activator (t-PA), urokinase (u-PA) and alpha-2-antiplasmin were obtained by immunizing Balb C mice with the respective purified antigens and fusion of spleen cells with mouse myeloma cells (NSO). The selected monoclonal antibodies reacted exclusively with the respective antigens used for immunization. 3 out of 7 monoclonal antibodies directed against t-PA inhibited plasminogen activation by t-PA and 6 of 7 interfered with the fibrin potentiating effect. Only one out of 5 monoclonal antibodies directed against u-PA inhibited plasminogen activation by u-PA. None of the monoclonal antibodies directed against t-PA or u-PA inhibited the cleavage of low molecular weight paranitroanilide substrates by the respective plasminogen activators. Likewise, the 3 monoclonal antibodies to alpha-2-antiplasmin did not functionally inhibit alpha-2-antiplasmin. The selected monoclonal antibodies were used to develop sensitive test systems for the respective antigens. The lower detection limit for determination of t-PA was found to be 0.5 ng/ml, for determination of u-PA 0.05 ng/ml, and for determination of alpha-2-antiplasmin 5 ng/ml.

Animals↗
PubMed1985

Deficiency of fibrinogen and factor VII following treatment of severe aplastic anaemia with anti-thymocyte globulin and high-dose methylprednisolone.

In 4 patients with SAA treated with ATG and high-dose MP, an as yet unrecognized acquired deficiency of fibrinogen and factor VII was observed. The plasma level of fibrinogen fell to 39% (34-51%) and of factor VII:C to 50% (31-55%) of the pretreatment value. The nadirs were between days 10 and 35 (fibrinogen) and d 3 and 11 (factor VII) after the 1st dose of ATG/MP. From additional clotting studies it is concluded that disseminated intravascular coagulation, fibrinolysis, liver cell damage and synthesis of abnormal clotting factors are unlikely causes of these clotting abnormalities. The most probable explanation seems to be a selective inhibition of the synthesis of fibrinogen and factor VII by an as yet unknown mechanism. These clotting abnormalities might, to some extent, increase the bleeding tendency in these patients, which up to now had been solely attributed to thrombocytopenia.

Adult↗
PubMed1985

Treatment of severe chronic idiopathic thrombocytopenic purpura in adults with high-dose intravenous gammaglobulin.

12 patients with severe chronic idiopathic thrombocytopenic purpura (ITP) were treated with i.v. polyvalent intact immunoglobulin (0.14-0.4 g/kg body weight for 5 d) because of various bleeding episodes or prior to surgery. In 9 patients a significant rise in platelet counts was noted, starting on d 2 and reaching its maximum between d 4 and 11. Thereafter, platelet counts decreased slowly, approaching pre-treatment values after 20 d in most cases. Response to immunoglobulin was reproducible, when infusions were repeated. Response to high-dose immunoglobulin was independent of age of patients and duration of disease. Platelet-associated IgG decreased in all patients tested. A pepsin-treated immunoglobulin preparation was ineffective in 3 patients.

Adult↗
PubMed1985

Tissue plasminogen activator inhibitor in human plasma: development of a functional assay system and demonstration of a correlating Mr = 50,000 antiactivator.

An assay system for determination of the "fast"-acting inhibitor (antiactivator, AA) of tissue-type plasminogen activator (tPA) in human plasma was developed. The system is based on incubation of plasma samples with various amounts of vessel wall-derived tPA for 8 minutes at 25 degrees C, followed by acidification and determination of the residual tPA activity by an indirect spectrophotometric assay. One unit of AA was defined as the amount inhibiting 1 U of tPA. AA levels in normal controls (n = 26) were 1.4 to 17.4 U/ml (median 3.0 U/ml) and 0.9 to 17.5 U/ml (median 3.0 U/ml) in patients with a history of deep venous thrombosis (n = 26). When plasma was subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by reverse fibrin autography, AA activity appeared as an inhibitory band corresponding to a relative molecular mass of 50,000. In six samples the inhibitory activity of this band was directly correlated to the functional AA activity of the plasma samples.

Electrophoresis, Polyacrylamide Gel↗
PubMed1984

Impaired fibrinolytic capacity predisposes for recurrence of venous thrombosis.

The fibrinolytic capacity of 121 patients with a history of venous thrombosis and/or pulmonary embolism was studied by venous occlusion technique, at earliest 3 months after the last thromboembolic episode. After discontinuation of oral anticoagulation treatment the clinical course of the patients was followed and new thromboembolic episodes were noted. During the observation period of 56 +/- 18.8 months 45 of 121 patients experienced recurrence of thrombosis. The recurrence-rate was significantly lower in patients with a post-occlusion ELT shorter than 60 min (4.8%/year) than in patients with an ELT longer than 60 min (10.3%/year). It is concluded that the fibrinolytic capacity is a useful parameter for determining the risk of recurrence in patients with venous thrombosis.

Anticoagulants↗
PubMed1984

CRM+ severe Fletcher factor deficiency associated with Graves' disease.

A 59-year-old male patient with Graves' disease and severe hereditary Fletcher factor deficiency is described. PKK clotting activity as well as the activity by a chromogenic substrate method (Chromozym PK) was less then 0.01 U/ml. In contrast to functional tests, the immunological assay (Laurell method) showed a PKK antigen concentration of 0.25 U/ml, indicating the presence of an abnormal nonfunctional PKK molecule (CRM+ variant). An inhibitor was excluded since the patient plasma did not inactivate partially purified PKK. Investigation of 11 family members revealed a reduction of the PKK clotting activity in 9 relatives of the patient. Since Graves' disease is considered an autoimmune disease, our case represents an example of an association of a severe hereditary deficiency of a contact factor and an autoimmune disease.

Cross Reactions↗
PubMed1983

Protein C deficiency in two Austrian families.

Protein C antigen was determined by Laurell rocket immunoelectrophoresis in 225 patients with a history of venous thrombosis. Among these patients two females with protein C deficiency were detected. Additional studies in the families of the protein C deficient patients revealed further 7 family members with protein C deficiency. In 8 not anticoagulated patients with protein C deficiency the protein C ranged from 36 to 62% (median: 45%). In one patient on oral anticoagulant treatment protein C antigen concentration was less than 10%, F II and FX were 65 and 50%, respectively. The pattern of inheritance was consistent with autosomal dominant inheritance. 5 of the 9 protein C deficient patients had severe thrombotic tendency characterized by recurrent deep venous thrombosis (n = 4), pulmonary embolism (n = 1), probable mesenteric vein thrombosis (n = 1) and superficial thrombophlebitis (n = 2). All protein C deficient patients without thrombosis were less than 17 years old.

Adult↗
PubMed1983

1-Deamino-8-D-arginine-vasopressin--an alternative in the management of mild haemophilia A and von Willebrand's disease.

Intravenous administration of 0.4 micrograms DDAVP/kg body weight in 16 normal controls, 34 patients with haemophilia A and 30 patients with von Willebrand's disease (vWd) was followed by an increase in FVIII: C from 230 to 410%, in FVIIIR:Ag from 160 to 260% and FVIIIR:RC of from 160 to 320%. Additionally, in the patients with vWd, a shortening of the bleeding time and improvement in platelet retention was observed. In 7 haemophiliacs with pretreatment levels of FVIII: C ranging from between 11 and 43% dental extractions were performed successfully after DDAVP whereas in 2 patients with FVIII: C levels of 5 and 6%, respectively, severe bleeding necessitated administration of factor VIII concentrates. In 8 haemophiliacs (FVIII: C between 6.5 and 50%) and 2 patients with vWd (FVIII: C 18 and 36%, respectively) DDAVP enabled minor surgery and successful therapy of spontaneous or traumatic bleeding complications. However, severe postoperative bleeding after stomach surgery in 2 haemophiliacs (FVIII: C 23 and 40%, respectively) and severe menstrual bleeding in one patient with vWd (FVIII: C 15%) required administration of factor VIII concentrates. At present DDAVP therapy should be restricted to minor surgery and non-life-threatening, spontaneous or traumatic bleeding complications in patients with pretreatment FVIII: C levels higher than 10%.

Arginine Vasopressin↗
PubMed1983

T-cell alterations in hemophiliacs treated with commercial clotting factor concentrates.

Various immunological parameters were determined in 46 patients with severe hemophilia A and in 9 patients with severe hemophilia B. All patients were treated over many years with commercial factor VIII or IX concentrates. Patients with severe classic hemophilia had a significantly reduced relative and absolute number of T-helper cells and a significantly increased relative and absolute number of T-suppressor cells. About half of these patients had an inverse T-helper/suppressor cell ratio. Patients with moderate hemophilia A and severe hemophilia B did not show these abnormalities. Hemophiliacs with an inverse ratio had a significantly higher concentration of serum total protein, IgG and IgM. No relationship between the amount of factor VIII concentrate administered, the HLA-type of the patient, the presence or absence of CMV-antibodies, hepatitis markers, thrombocytopenia and abnormal liver function tests to the T-cell abnormalities could be established. Lymphadenopathy was frequently associated with an inverse ratio. Indirect evidence suggests that the alterations of the immune system began in 1979/80.

Acquired Immunodeficiency Syndrome↗