The activity of serum acid phosphatase in bone marrow aspirates predicts response to steroids/splenectomy in acute/chronic immune thrombocytopenic purpura.
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Biomedical subjects
Publications and source records attributed to N Suvajdzić.
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The Belgrade laboratory (b/b) rat has a hereditary hypochromic microcytic anemia because of defective transmembrane iron transport into erythroblasts. The present study was prompted by our previous work in which we showed that the b/b rat has hypomegakaryocytic thrombocytopenia associated with increased megakaryocyte size. To define the basic mechanism underlying this abnormality in the b/b rat we have studied both megakaryocytopoiesis and granulopoiesis in anemic b/b rats, chronically transfused b/b rats, iron-treated b/b rats, and controls. We have found decreased concentrations of megakaryocyte and granulocyte progenitors in the marrow of b/b rats. Full correction of the severe anemia by chronic transfusion resulted in normalization of megakaryocyte progenitors, small acetylcholinesterase positive cells, megakaryocyte size, and platelet counts, along with granulocyte progenitors. In contrast, the partial correction of anemia obtained by iron treatment resulted in improvement, but not normalization, of these parameters. These findings indicate that abnormal megakaryocytopoiesis in the b/b rat can be best interpreted as a consequence of hypoxia because of the severe anemia. Because we have recently shown that the number of erythroid progenitors in b/b rats is also low, we propose that abnormal megakaryocytopoiesis in this animal is a reflection of an acquired stem cell disorder induced by the prolonged hypoxia resulting from the severe anemia.
The aim of this work was to investigate T cell subset composition of peripheral blood cells in patients with acute myeloid leukaemia, acute lymphoblastic and chronic lymphocytic leukaemia, by enumerating T cells positive for receptors for sheep erythrocytes (E-RFC, A-RFC) using the method of E-rosette, and for CD3, CD4 and CD8 antigens, by indirect immunofluorescence technique, using the monoclonal antibodies of the OK series. The study was performed on 57 patients without therapy and 46 healthy persons. The results of enumeration of T cells and their subsets obtained in the stage of the disease when the total leukocyte count was below 20 x 10(9)/L, were markedly decreased in all three types of leukaemias. The most significant decrease of relative count of T cells and their subpopulations was obtained in CLL patients. Analysis of T cells subsets and their ratio in CLL patient in the stage of disease when the total leukocyte count as higher than 20 x 10(9)/L, demonstrated the most pronounced decrease of total T lymphocytes and CD4+ cells. The relative count of the "active" (A-RFC)T cells and CD8+ cells did not change, and was the same as in the patients suffering from CLL with a lower leukocyte count.
It was recently proposed that prolonged hypoxia produces hypomegakaryocytic thrombocytopenia by reducing the pool of committed megakaryocyte progenitor cells at the expense of a greatly expanded erythroid progenitor pool. In order to test this hypothesis we have studied the relationship between megakaryocytopoiesis, erythropoiesis, and granulopoiesis at the level of progenitor cells (megakaryocyte colony-forming unit, CFU-Mk; erythroid CFU, CFU-E; erythroid burst-forming units; BFU-E; and granulocyte-macrophage CFU, CFU-GM) in the marrow of rats exposed for 4 weeks to normobaric hypoxia. We have found that hypomegakaryocytic thrombocytopenia was accompanied by decreased CFU-Mk, increased CFU-E, and a normal number of BFU-E and CFU-GM. These results support the hypothesis that prolonged hypoxia reduces the precursor cell commitment to differentiate into the megakaryocyte series by enhancing demand for differentiation into the erythroid cell line. However, the underlying mechanism needs further investigation.
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A patient with Ph1(Philadelphia chromosome) positive chronic granulocytic leukemia and extramedullary blast transformation (crisis) in lymph nodes of neck and axillae which appeared after 4-year of treatment with busulfan is presented. Biopsy of lymph node and histopathological examination showed lymphoblastic infiltration. The patient was treated with radiotherapy and chemotherapy with protocol COP. He survived 7 months and expired due to renal insufficiency.
Lymphomas are relatively rare in the orbit: only about 8-11% of all orbital tumours. The most common histological type is diffuse well-differentiated lymphocytic lymphoma (DWDLL--Rappaport's classification)--70%. Orbital lesions are always curable by radiotherapy, but in some 40% of these patients local recurrence or dissemination occur. The authors present two patients with diffuse well-differentiated lymphocytic lymphoma, and one patient with FCC lymphoma of centrocytic type (Kiel classification) localized in the orbit. Two of them were irradiated after an unsuccessful treatment by chemotherapy. In the third patient local radiotherapy is still in the course.
The paper deals with the progression of idiopathic refractory sideroblastic anaemia (IRSA) and its transformation to acute B lymphoblastic leukaemia (ALL). Attention is paid to haematological changes prior to leukaemia development. Acute leukaemia was best expressed in this patient by severe deterioration of dyserythropoiesis, leukopenia, and by an increase of blasts in the bone marrow over 5%. Our patient is an additional evidence to the hypothesis of the common lymphohematopoietic progenitor.
The authors present two patients with acute myeloid leukaemia and pulmonary-disseminated form of zygomycosis developed during the period of bone marrow aplasia. Diagnosis was established on necropsy on the basic of the patho-histological finding of wide, short and nonseptate hyphe with irregular branching. Hyphe were clearly recognized on Gomori methenamine Silver stained preparations. There were multiple haemorrhagic-necrotic infarcts of different organs due to the mycotic invasion of blood vessels. The authors discuss some some important diagnostic and therapeutic problems.
Acute intermittent porphyria is an inherited disease caused by genetic deficiency of enzyme prophobilinogen deaminase, which stopped heme synthesis. It is characterized by overproduction, accumulation and excretion of heme precursors. The authors present a young woman with clinical signs and symptoms of disease, treated successfully with heme-arginate, a newly synthetized drug in clinical use since 1985.
A patient with Ph1(Philadelphia chromosome) positive chronic granulocytic leukemia and extramedullary blast transformation (crisis) in lymph nodes of the neck and axillae which appeared after a 4-year treatment with busulfan, is presented. Biopsy of lymph node and histopathological examination showed lymphoblastic infiltration. The patient was treated with radiotherapy and chemotherapy with protocol COP. He survived 7 months and expired due to renal insufficiency.