[Clinical trial of immunoregulation using the TFX Polfa preparation in non-Hodgkin's lymphoma].
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Biomedical subjects
Publications and source records attributed to M Kicińska.
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Hypoxia-ischemia produces brain damage by processes that continue for many hours after reoxygenation/reperfusion. This provides a window of opportunity for therapy aimed at preventing further loss of brain cells. Sulfate magnesium can prevent posthypoxic brain injury by blocking glutamate receptors within the calcium (Ca++) ion channel. We used sulfate magnesium in nine newborn infant after perinatal hypoxia. We investigated the brain damage, by ultrasound examination, on third day, in first, second and third week, and third, sixth month of life. We have estimated the neurological development in the first week of life and third and twelfth month of life. We did not find deviations in ultrasound examination. We did not observe convulsions. We did not observe any side effect of this therapy. The examination at 1 of year of life in all of children was correct.
In 11 patients with III A stage multiple myeloma in every week before new course of cytostatics started, three times plasmapheresis therapy had been performed. There was no difference in reducing of plasma cell mass, plasma immunoglobulins concentration and proteinuria or disappearance of osteolytic bone lesions between the group of patients treated with combination chemotherapy and plasmapheresis and chemotherapy alone. However there was visible disparity in the disappearance of bony pains: rapidly in the plasmapheresis group. One serious complication after plasmapheresis therapy was notified: gastric haemorrhage. The remaining plasmapheresis complications: tetany, nausea, vomiting, chills and bradycardia were related to citrate toxicity.
In 17 patients with idiopathic thrombocytopenic purpura unresponsive to treatment with steroids, immunosuppression or splenectomy, allogenic vincristine-loaded platelets were used. In 9 of them an increase of platelet number and regression of bleeding tendency was achieved. Among 13 patients with ITP who have been treated with danazol only in one case an increase of platelet number was observed. Under the rise of plasma transaminases and bilirubin level in majority of "danazol" patients we have discontinued the treatment. In none of 4 patients with chronic thrombocytopenic purpura treated with high doses of intravenous immunoglobulin an increase of platelet number was observed, however in all cases the regression of bleeding was achieved.
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