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Biomedical subjects

I Pabinger-Fasching

Publications and source records attributed to I Pabinger-Fasching.

35 records · Page 2Linked to original sources
PubMed1991

[Blood coagulation disorders in leukemia].

Bleeding and septicemia are the most common causes of death in patients with acute leukemia. Additionally to thrombopenia, which is present in most patients, in part of the patients severe coagulation abnormalities are observed. The prevalence of severe coagulation abnormalities in patients with acute myeloid leukemia including all FAB types is around 12%, in patients with promyelocytic leukemia the prevalence is more than 50%. The etiology of this coagulation abnormality remains unclear. There are 3 mechanisms currently under discussion: activation of coagulation, activation of fibrinolysis and an increased activity of specific leucocyte proteases. In particular, in promyelocytic leukemia the risk of cerebral bleeding is high (10 to 15% of early deaths). The most important therapeutic consequence is an intensified thrombocyte replacement regimen. Additional therapeutic efforts, like administration of heparin or antifibrinolytic drugs, have failed to improve the prognosis of patients with severe coagulation abnormalities.

Disseminated Intravascular Coagulation↗
PubMed1990

Hemostatic and fibrinolytic parameters in patients with acute myeloid leukemia: activation of blood coagulation, fibrinolysis and unspecific proteolysis.

Blood coagulation, fibrinolytic and unspecific proteolytic parameters were investigated in 34 patients with acute myeloid leukemia. An increased activity of the coagulation system, documented by elevated thrombin-antithrombin III-complex (TAT) plasma levels, was found in 91% of the patients; 50% had increased elastase plasma levels. Hyperfibrinolysis, as shown by elevated fibrin split-product D-Dimer plasma levels, was detected in 91% of AML patients. Activation of these enzyme systems was not associated with relevant defects in blood coagulation or fibrinolysis in the majority of the patients investigated. In selected cases of promyelocytic M3 and monoblastic M5 leukemia, however, hypofibrinogenemia and alpha 2-plasmininhibitor deficiency was found, most likely due to depletion of these proteins in the course of disseminated intravascular coagulation and secondary hyperfibrinolysis. Significant correlations were calculated between TAT and fibrinogen (r = -0.57, P less than 0.005), TAT and D-Dimer (r = 0.89, P less than 0.0005), and D-Dimer and alpha 2-plasmininhibitor (r = -0.77, P less than 0.0005) levels. Indications of a pathogenetic importance of primary hyperfibrinolysis or unspecific proteolysis for hypofibrinogenemia and alpha 2-PI deficiency were not found.

Acute Disease↗
PubMed1989

High risk of acquired immune deficiency syndrome (AIDS) and of AIDS related complex (ARC) in hemophiliacs seropositive for more than 5 years.

A group of 90 hemophiliacs who had been regularly treated with non virus-inactivated factor VIII or IX concentrates were studied in 1983. At that time 50 patients were HIV-1-antibody positive, 6 additional seroconversions occurred until 1985. 26 of the 50 patients seropositive in 1983 are currently asymptomatic. 4 patients have developed the lymphadenopathy syndrome, 9 patients AIDS and 11 patients ARC (CDC IV C 2). 6/9 cases of AIDS and 10/11 cases of ARC have occurred only after 1985. Patients, who subsequently became symptomatic, had significantly higher IgG levels in 1983, otherwise no predictive laboratory tests were identified. Patients with T4 counts above 500/microliters became symptomatic later, but after 5 years the incidence of AIDS was comparable in patients with original T4 counts of more than or below 500/microliters.

AIDS-Related Complex↗
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

HTLV-I antibody status in hemophilia patients treated with factor concentrates prepared from U.S. plasma sources and in hemophilia patients with AIDS.

Serum samples from 85 Austrian hemophilia patients treated with lyophilized factor concentrates prepared from U.S. plasma sources, 24 hemophilia patients from Georgia on a home therapy program with factor concentrates, and 10 U.S. hemophilia patients with acquired immunodeficiency syndrome (AIDS) were analyzed by two different methods for the presence of antibodies to the major internal antigen of human T-cell leukemia virus I (HTLV-I) p24. All but one, a Georgia sample, were negative. The absence of antibody to HTLV-I p24 in the serum of European hemophilia patients, of U.S. hemophilia patients with no symptoms of AIDS, and of U.S. hemophilia patients with AIDS is interpreted as an indication of the lack of ready transmissibility of HTLV-I in lyophilized factor concentrates.

Acquired Immunodeficiency Syndrome↗
PubMed1985

High levels of plasma protein C in nephrotic syndrome.

In patients with severe nephrotic syndrome determinations of plasma protein C: Ag levels (8 patients: 5 adults, 3 children) and protein C activity (3 out of 8 patients) revealed significantly elevated plasma protein C concentrations. Furthermore we observed a significant inverse correlation of protein C: Ag to AT III: Ag levels. No protein C: Ag could be detected in the urine of two patients studied. We conclude from our data, that changes of plasma protein C do not contribute to the high thrombotic tendency in nephrotic syndrome.

Adolescent↗
PubMed1985

Lupus anticoagulants and thrombosis. A study of 25 cases and review of the literature.

25 patients with lupus anticoagulant (LA) and a history of thrombosis are described and the cases reported in the literature with this association are reviewed. From the combined data it is concluded that the prevalence of thrombosis in patients with LA is about 30%, the thrombosis sites are the leg veins in about 66%, the cerebral arteries in 25% and the peripheral arteries in 10% of the patients. High anticardiolipin levels are associated with a higher risk, while age of less than 10 years, low prothrombin activity and a platelet count of less than 50,000/microliter is associated with a lower risk of thrombosis. Heparin and oral anticoagulants are effective in the treatment and prevention of thrombosis without untoward risk of bleeding.

Adolescent↗
PubMed1985

Lymphocytes of haemophilia patients treated with clotting factor concentrates display activation-linked cell-surface antigens.

Peripheral blood lymphocytes from 30 patients with haemophilia A were investigated for the expression of six activation-linked cell surface antigens as well as with regard to the relative proportions and total numbers of Leu-3a and Leu-2a positive cells. Twenty-nine of the haemophilia patients showed no clinical symptoms of immunodeficiency or infection whereas one patient presented the typical symptomatology of the acquired immunodeficiency syndrome (AIDS). The proportions and total numbers of circulating lymphocytes displaying Ia antigens, the p45 protein and/or the two recently defined surface antigens VIP-4 and VIP-5 were significantly increased in haemophilia patients when compared to healthy individuals of the same age group. No such increases could be observed for transferrin receptor and IL-2 receptor expression. After the observation of depressed helper/suppressor T-cell ratios in many haemophiliacs, the expression of activation linked surface antigens represents a further lymphocyte abnormality which resembles the findings in AIDS and its prodromal stages and can also be found in certain viral and parasitic diseases.

Acquired Immunodeficiency Syndrome↗
PubMed1984

[Sonography and scintigraphy in the differential diagnosis of diffuse liver parenchymal diseases].

70 patients with established diffuse liver disease (steatosis, fibrosis, cirrhosis) were investigated by sonography and scintigraphy. Sonographic parenchymal morphology and scintigraphic activity pattern were correlated with the histological diagnosis. Scintigraphy as a functional diagnostic technique revealed early fibrotic changes of the liver not seen by ultrasound. Cirrhosis could be demonstrated equally by both methods. The two major advances of ultrasound were: high accuracy in steatosis and ability of simultaneous analysis of the other abdominal organs.

Celiac Disease↗
PubMed1984

Efficacy of the M-2 protocol in previously untreated patients with advanced multiple myeloma.

37 consecutive, previously untreated patients with advanced multiple myeloma (16 patients Stage II, 21 patients Stage III) were treated with a five drug regimen consisting of carmustine, melphalan, vincristine, cyclophosphamide and prednisolone (M-2-protocol) in a prospective manner. Remission was achieved in 24 patients (65%). The median time to remission was 10 weeks, the median duration of remission 15,3 months. Median survival time from the onset of treatment was 24 months for all patients. Responding patients have a projected 65% three year survival. Median survival in non-responders was 10 months. 8 patients died during the first year of treatment. These results do not confirm the favourable results with this drug combination obtained in a previous trial. The discrepancy may be explained by a higher proportion of poor risk patients in the present study.

Aged↗
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↗