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Biomedical subjects

E Seifried

Publications and source records attributed to E Seifried.

116 records · Page 7Linked to original sources
PubMed1984

Treatment of refractory chronic idiopathic thrombocytopenic purpura with high dose intravenous immunoglobulin.

Three patients with a history of chronic idiopathic thrombocytopenic purpura stretching back over 20 years are reported. Despite splenectomy and immunosuppressive therapy satisfactory control of their disease has not been achieved. They had remained refractory to all therapeutic manoeuvres with corticosteroids and immunosuppressives for years with thrombocyte counts between 5,000 and 25,000/microliters and the concommitant risk of bleeding. This report describes the treatment of bleeding complications in these patients with high dose intravenous immunoglobulin; the peripheral blood thrombocyte count increased in all three patients from subnormal towards normal, but 2 to 4 weeks later returned to its initial low value. During the therapeutically induced raised thrombocyte count a normal bleeding time and only a moderate inhibition of thrombocyte adhesion and aggregation was observed resulting in reasonable haemostasis. High dose intravenous immunoglobulin is therefore a practical method for the control of bleeding complications in patients with refractory chronic idiopathic thrombocytopenic purpura. A clear explanation for its mode of action has not been found - the lymphocyte subpopulations remained unchanged and immunoglobulin production in vitro during the course of treatment was only minimally decreased.

Antibody Formation↗
PubMed1984

The treatment of haemophilia A inhibitor with high dose intravenous immunoglobulin.

In patients with Haemophilia A, the development of inhibitor is a life-threatening complication of treatment. These patients are at high risk for dangerous bleeding as a result of this acquired resistance to human Factor VIII concentrate. Although treatment of bleeding complications has been improved with the introduction of an activated prothrombin complex preparation, therapy remains unsatisfactory. Two patients with Haemophilia A inhibitor were treated with high dose intravenous immunoglobulin in the expectation of an immunosuppressive effect. A rise in the antibody titre at the same time as the administration of factor VIII concentrate showed that this treatment was ineffective in patients with Haemophilia A inhibitor.

Adolescent↗
PubMed1984

Impaired natural killer cell function in hemophiliacs with or without continuous substitution.

In the present study, 28 hemophiliacs substituted continuously and 5 hemophiliacs who had received almost no blood products were investigated. Cells of OKT 3+, OKT 4+, and OKT 8+ subsets were counted. Percoll separated fractions of peripheral blood mononuclear cells were examined by morphological criteria and were tested for NK cell activity. We found that the NK cell activity of both groups of hemophiliacs was decreased on testing Ficoll separated cells or low density Percoll separated cells. Normal NK cell activity was found in medium density cells of hemophiliacs. Two possible explanations are discussed: first, the NK cell activity may be suppressed in hemophiliacs and secondly, there may be a block in maturation of NK cell activity. It is unlikely that chronic substitution by blood products counts for these alterations. The possible role of chronic infections is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1982

[Blood clotting factor XIII substitution in acute leukaemia: result of a randomized and controlled study].

A randomized and controlled study was undertaken to test whether substitution with factor XIII concentrates influences the clinical course in patients with acute leukaemia and acquired factor XIII deficiency (less than or equal to 60%). A control group of 31 patients was compared with a factor XIII-treated group of 29 patients. Partial factor XIII deficiency was successfully corrected by substitution. On the other hand, there was no statistically significant difference between the two patient groups in the frequency and severity of bleeding complications, transfusion requirements, and the number of remissions. Undesirable side-effects as a result of substitution treatment were not observed.

Acute Disease↗
PubMedDate not supplied

Ex vivo expansion of highly purified NK cells for immunotherapy after haploidentical stem cell transplantation in children.

BACKGROUND: Allogeneic natural killer (NK) cells are known to show medium to high cytotoxic activity against HLA-nonidentical leukemia or tumor cells. For a possible benefit of post transplant treatment with NK cells after haploidentical stem cell transplantation (haplo-SCT) we developed a clinical scale procedure for NK cell processing observing Good Manufacturing Practice (GMP). METHODS: Allogeneic donor NK cells were selected from 15 unstimulated leukaphereses using two rounds of immunomagnetic T cell depletion, followed by an NK cell enrichment step. CD56 (+)CD3 (-) NK cells were stimulated and expanded in vitro according to GMP. Quality control of NK cell purity, residual T cells and cytotoxic activity was done by multi-coloured flow cytometric analyses. RESULTS: Purification led to an absolute number of 234-1 237 x 10 (6) CD56 (+)CD3 (-) NK cells from leukapheresis harvests with a median purity of 95 % and a 4 to 6(1/2) log depletion of T cells. After two weeks stimulation with IL-2 a five-fold expansion of NK cells with a T cell contamination below 0.1 % was reached. Median cell viability was 95 % after purification and 99 % after expansion. The IL-2 stimulated NK cells showed a highly increased lytic activity against the MHC-I deficient K562 cells compared to freshly isolated NK cells and a medium cytotoxicity against patients' leukemic cells. CONCLUSIONS: Clinical scale enrichment and activation of allogeneic donor NK cells is feasible. High dose NK cell application may be a new treatment option for pediatric patients with leukemia or solid tumors in case of minimal residual disease or unbalanced chimerism post haplo-SCT as we could show for the first three patients .

Antigens, CD19↗
PubMedDate not supplied

Analysis of glycoprotein Ia, Ib, IIb and IV RNA in platelets: quantitative determination using fluorescence-based polymerase chain reaction.

The aim of this study was to analyze the RNA level of glycoprotein (GP) receptors in platelets. We have therefore established a quantitative fluorescence-based polymerase chain reaction (PCR) to analyze GP Ia, Ib, IIb, and IV RNA. Isolation of platelet RNA was performed by guanidium isothiocyanate/phenol chloroform extraction. An internal standard consisting of cRNA copies from plasmid pAW109 was included before reverse transcription in each RNA sample and PCR amplification was performed using fluorescence-labeled primers. Subsequently, PCR fragments were separated by gel electrophoresis and quantitation of the GP-specific fragments was done by measuring the fluorescence intensities in comparison to the internal standard. Relative amount of GP RNA/platelet were calculated taking into account the number of platelets used for isolation of platelet RNA and the platelet size as determined by flow-cytometric analysis. Using this method we analyzed the GPIa, Ib, IIb and IV RNA content of platelets in healthy blood donors. In parallel experiments the number of GP cell surface receptors was measured by flow-cytometric analysis and correlated with the GP-specific RNA content. This method may be useful to study the GP-specific RNA content in platelets as well as in other tissues, such as megakaryocytes, especially in patients with congenital or acquired platelet function disorders.

Antigens, CD↗
PubMedDate not supplied

[The fibrinolytic system and its activators].

The human fibrinolysis system is a proteolytic enzymatic process in the blood. Its purpose is to locally limit intravascular thrombotic processes and to reopen vessels closed by thrombosis. The main enzyme of the fibrinolysis system is the active protease plasmin produced by activation of the inactive first step plasminogen by means of plasminogen activators via limited proteolysis. Thrombolytic therapy with plasminogen mimics and enhances physiological fibrinolysis. The following substances are presently available for clinical use: the non-physiological thrombolytics streptokinase and APSAC (acylated plasminogen-streptokinase activator complex), as well as the physiological plasminogen activators urokinase and tissue plasminogen activator (t-PA). Whereas the first three systemically activate the fibrinolysis system, t-PA possesses relative fibrin selectivity. The fibrin-selective active prourokinase and a recombinant mutant of t-PA with prolonged in vivo half-life have not yet been officially approved for the treatment of thromboembolytic diseases but are being clinically tested. In the development stage are mutants, hybrid enzymes and conjugates aiming at further improvement of this therapeutic concept by means of changing the half-life, thrombus affinity and thrombolytic activity. The development of highly effective antithrombotics will help to further improve the results of thrombolytic therapy.

Animals↗