Biomedical subjects

I Pabinger-Fasching

Publications and source records attributed to I Pabinger-Fasching.

7 recordsLinked to original sources

PubMed1991

Disseminated intravascular coagulation and decrease in fibrinogen levels induced by vincristine/prednisolone therapy of lymphoid blast crisis of chronic myeloid leukemia.

Therapy with vincristine (2 mg i.v. weekly) and prednisolone (100 mg p.o. daily) caused a decrease in fibrinogen levels in nine patients treated for lymphoid blast crisis LBC) of chronic myeloid leukemia (CML). During the first days of treatment disseminated intravascular coagulation (DIC), evidence by a positive ethanol gelation test, markedly increased thrombin-antithrombin III complex and fibrin-split product D-dimer levels, and a rapid fall in fibrinogen levels was observed in two patients. The induction of DIC in these two patients caused profuse bleeding in one and necessitated substitution therapy with fibrinogen and platelet concentrates. The remaining seven patients revealed no signs of DIC; nevertheless, four of them showed a moderate increase in D-dimer levels after initiation of therapy. In these patients a well-known side effect of long-term steroid therapy, namely a decrease of fibrinogen levels, was observed within the first week of treatment. Fibrinogen levels did not fall below 150 mg/dl and increased after dose reduction from 100 mg/day to 50 mg/day. We conclude from our results that two types of disturbances in fibrinogen metabolism can be observed during vincristine/prednisolone therapy of LBC of CML: (a) a decrease of fibrinogen levels due to a steroid-mediated impairment of liver synthesis, and (b) a rapid fall in fibrinogen levels in the course of DIC, most likely induced by the release of procoagulants from deteriorating blast cells, leading to severe bleeding in selected cases.

Adult↗

PubMed1991

Anticardiolipin antibodies in patients with venous thrombosis.

The levels of anticardiolipin antibodies (ACA) and lupus anticoagulant (LAC) were measured in 266 consecutive unselected patients with a history of venous thrombosis. 19 (7.1%) had elevated levels of IgG- or IgM-ACA. The prevalence of LAC was 1 of 266 (0.4%) in the whole patient group and 1 of 19 (5.3%) in the ACA-positive group. Patients with elevated ACA levels did not differ from those with normal ACA with regard to age at the first thrombosis, risk of recurrence, presence of arterial thrombosis, and other clinical features. 8 out of 19 (42.1%) patients with elevated ACA levels also had elevated levels of antinuclear antibodies, but only 1 fulfilled the criteria of systemic lupus erythematosus. These data indicate that in some patients with elevated ACA, autoimmune processes may be present. The clinical significance of elevated ACA levels is uncertain.

Adolescent↗

PubMed1991

[Warfarin embryopathy in maternal coumarin therapy for protein S deficiency].

A case of Warfarin embryopathia is shown. The newborn, whose mother had been treated with Marcoumar (Phenprocoumon 3 mg/day) during the whole pregnancy because of a hereditary protein-S-deficiency showed the typical symptom of nasal hypoplasia. Coumarol derivates pass the placental membrane and are known as teratogenic. Recent retrospective and prospective studies show that the risk of fetal or embryonal teratogenic injury is about 25-30% if Coumarol derivates are given through the 6th to the 9th week of pregnancy. It is possible to nearly avoid those injuries when Heparin is used for anticoagulant therapy in this period and Coumarol itself is used in the lowest possible therapeutic dose.

Abnormalities, Drug-Induced↗

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↗

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↗