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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet antibodies either bound to the surface of platelets or free in the serum were sought in patients who had low platelet counts for a variety of reasons. They were detected by finding excess IgG on the surface of washed platelets either directly or after incubation of the serum with normal platelets. The technique used was a modification of that described recently (Dixon et al, 1975) in which the greater the amount of anti-IgG consumed by the reaction with platelets the less the subsequent lysis of sheep red cells coated with IgG. This test could be calibrated by adding known quantities of IgG to the antisera and thus the amount of bound IgG could be measured. Platelets from normal donors and those with thrombocytopenia due to non-immunological causes such as aplastic anaemia or acute leukaemia were found to have 15-70 ng IgG/10(7) platelets (mean 53 ng). 37 out of 38 thrombocytopenic patients in whom immune destruction of platelets was suspected were found to have excess IgG on their platelets ranging from 70 to 720 ng/10(7) (mean 297 ng, P less than 0.001) and there was a significant inverse correlation between this amount and the platelet count (r = 0.85, P less than 0.001). Antibody in the serum was found in 14 of 22 patients with 'idiopathic' thrombocytopenic purpura (ITP), three of four patients with underlying lymphoma and in all five cases of systemic lupus erythematosus (SLE). Four non-thrombocytopenic patients with autoimmune haemolytic anaemia (AIHA) due to IgG on the red cells were also studied and were shown to have no increase in platelet-bound IgG. Our results confirm the work of Dixon et al (1975) that platelet antibody as excess IgG can be readily detected on the surface of platelets in patients with immune thrombocytopenia. The clinical implications of these findings are discussed.
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PMID:Platelet antibodies in thrombocytopenic patients. 86 90

Advances in the methodologic study of megakaryocytopoiesis are discussed, and their effect on the understanding of the production of platelets is included. This knowledge has led to a better understanding of disorders of megakaryocytopoiesis and platelet production. Specific diseases discussed are congenital megakaryocyte hypoplasia, acquired amegakaryocytic thrombocytopenic purpura, myeloproliferative disorders, reactive thrombocytosis, megakaryoblastic leukemia, and megakaryocyte and marrow fibrosis.
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PMID:Human megakaryocyte production: cell biology and clinical considerations. 217 14

The availability of safe and effective preparations of human immune globulin that can be administered intravenously has revolutionized replacement therapy for patients suffering from hypogammaglobulinaemia. Of equal importance and greater interest, however, has been the recognition that super physiological doses of IgG can manipulate an abnormal immune system. Future prospects for the use of immunoglobulin preparations to supply specific antibodies includes the standardization of procedures, whereby patients with acute sepsis may receive antibiotics and immunoglobulin simultaneously. Already there is in vitro evidence that suggests that opsonized bacteria are more readily affected by aminoglycosides. It seems certain that gamma globulin will be used routinely in the management of patients with a number of immunomalignancies, such as chronic lymphatic leukaemia and multiple myeloma that feature hypogammaglobulinaemia, especially when chemotherapy is being administered. Control trials are underway to determine whether gamma globulin given intravenously to premature babies will satisfactorily correct their immuno-deficient state and improve their chances of survival. The immunomanipulative capacity of immunoglobulin is yet to be fully realized. Success in ideopathic thrombocytopenic purpura had led to a trial of gamma globulin in a number of autoimmune conditions. Success has been reported in myasthenia gravis, rheumatoid arthritis, diabetes, patients with circulating antibodies to factor VIII and Kawasaki's disease. The mechanism of action is unknown but almost certainly multifactorial. Two proven mechanisms that will be added to in the future, include blockade of the Fc receptors on cells of the reticulo-endothelial system and manipulation of immunoregulatory T cells by the presence of anti-idiotypic antibodies in the preparation.
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PMID:The clinical use of intravenous gammaglobulin. 244 Jul 43

We present 25 new cases of blood dyscrasia, including leukemias, production defects, and thrombocytopenic purpura, generally following home termite treatment with the chlorinated hydrocarbon pesticides chlordane and heptachlor (C/H). These newly reported cases are consistent with 34 previously published case reports associating blood dyscrasias with C/H exposure. Additionally, the newly reported leukemias are consistent with epidemiologic evidence of excess risk of leukemia and other cancers in C/H-exposed populations and with the carcinogenic action of C/H in animals. The importance of case reports in warning of the association of blood dyscrasias to C/H exposure is emphasized. Until the voluntary halt in production in July 1987, millions of homes in the United States were treated with chlordane and heptachlor for termites even though their agricultural uses were phased out in 1978, largely on the grounds of "imminent hazard" because of carcinogenicity. In view of the recognized myelotoxicity, carcinogenicity, and other chronic toxic effects of these pesticides, a national program for monitoring all homes treated is urgently needed to detect persistent contamination.
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PMID:Leukemias and blood dyscrasias following exposure to chlordane and heptachlor. 289 66

Thrombocytopenic purpura developed in a 64-year-old woman seropositive for human T-cell leukemia virus type I (HTLV-I). She had no underlying disorders and HTLV-I is suggested as a possible cause of her thrombocytopenia.
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PMID:Thrombocytopenic purpura in a carrier of human T-cell leukemia virus type I. 289 42

We describe a prospective study comparing four different assays for PAIgG. Platelets from patients with a variety of thrombocytopenic disorders were collected into ACD, washed, and the PAIgG then measured using three assays for surface PAIgG. These included: (a) a direct binding assay using 125I-monoclonal anti-IgG (MoAb); (b) a direct binding assay using 125I-staphylococcal protein A (SPA); and (c) a two-stage assay. PAIgG also was measured using an assay for 'total' PAIgG following platelet lysis. The mean +/- SD number of molecules of IgG per platelet on washed platelets from 29 healthy, non-thrombocytopenic controls was: 86 +/- 80 (125I-MoAb); 94 +/- 96 (125I-SPA); 3520 +/- 1890 (two-stage surface assay); and 10,850 +/- 3720 (total PAIgG). A total of 62 different patients with idiopathic thrombocytopenic purpura or thrombocytopenia complicating systematic lupus erythematosus, and 73 different patients with 'non-immune' thrombocytopenia, were tested using each of the four assays. These 'non-immune' thrombocytopenic patients included patients with carcinoma, septicaemia, pre-eclampsia, chronic leukaemia, thrombotic thrombocytopenic purpura, haemolytic uraemic syndrome, acute leukaemia and myelodysplasia. All four assays gave similar results for both the immune and non-immune thrombocytopenic patients. The sensitivity of the assays for the most severely thrombocytopenic patients with immune thrombocytopenia was: MoAb 60%; SPA 88%; two-stage 82%; and 'total' PAIgG 88%. The specificity of the four assays in the non-immune thrombocytopenic patients was 57% 'total' PAIgG; 63% two-stage surface; 25% SPA; 38% MoAb.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A prospective comparison of four techniques for measuring platelet-associated IgG. 291 34

Marked elliptocytosis and schistocytosis are described as unusual manifestations of haematopoietic dysplasia in two patients. The first patient, whose history was negative for inherited haemolytic anaemias, presented these prominent features on his first admission; 22 months later he developed an acute myeloblastic leukaemia. In the second patient, followed since 4 years for an autoimmune thrombocytopenic purpura, elliptocytosis and schistocytosis appeared 17 months before a pancytopenia established. The patient is now on follow-up and is treated for a refractory anaemia. In both cases bone marrow examinations revealed the typical criteria for myelodysplasia and this diagnosis was confirmed by cytogenetic analysis.
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PMID:Elliptocytosis and schistocytosis in myelodysplasia: report of two cases. 309 35

Three groups of patients were studied to assess the effect of oral corticosteroid therapy on erythropoiesis in vivo as measured by changes in haemoglobin concentration (Hb) and red blood cell count (RBC). Fifteen patients with acute lymphoblastic leukaemia, who were in remission and receiving pulses of vincristine and prednisone during maintenance chemotherapy, showed no rise in Hb or RBC with steroid therapy. Likewise, 15 patients completing chemotherapy for ALL did not show a rise in Hb or RBC after stopping treatment. However, 14 children with acute immune thrombocytopenic purpura demonstrated a significant increase in Hb and RBC during a course of treatment with prednisone. These findings complement the results of in vitro studies, indicating that erythropoiesis in normal human bone marrow is stimulated by corticosteroid therapy.
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PMID:The influence of corticosteroids on human erythropoiesis. An in vivo study. 323 7

The authors present a patient with the typical clinical picture of an acquired amegakaryocytic thrombocytopenic purpura. After 16 months of observation, the patient developed acute myelomonocytic leukemia. During the preleukemic phase and after progression to overt leukemia, serial in-vitro analyses of megakaryocytic, granulocytic, erythrocytic and T-lymphocytic colony growth were carried out in a microagar culture system. At presentation, a marked diminution of CFU-M was observed, whereas CFU-E, BFU-E, CFU-C and CFU-TL were in the normal range. The CFU-M number remained at its low level during the whole observation period. The CFU-C number declined steadily during the preleukemic period, while BFU-E, CFU-E and CFU-TL remained constant until January 1985 when the patient developed AML. After progression to overt leukemia, a distinct reduction became evident in all colony-forming cells. Cytogenetic studies performed during the preleukemic phase indicated the presence of a 5q- chromosome. The authors submit evidence here that the patient was not only characterized by defective megakaryocytic colony formation but also by a deficiency of functional megakaryocyte colony-stimulating activity. No humoral or cellular inhibitors of CFU-M colony formation were found. It is concluded that in preleukemia with a 5q- chromosome the megakaryocytic cell lineage may be involved in the process that precedes overt leukemia at an earlier time than cells of granulocytic and erythrocytic lineages. In addition, it is shown here that megakaryocytopoiesis during the preleukemic period can be characterized by two different defects: first, an intrinsic megakaryocytic stem cell defect and, second, a deficiency of functional megakaryocytic colony-stimulating activity.
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PMID:Progressive preleukemia presenting amegakaryocytic thrombocytopenic purpura: association of the 5q- syndrome with a decreased megakaryocytic colony formation and a defective production of Meg-CSF. 349 97

The kidney is involved in a variety of systemic diseases and conditions including collagen, endocrine, liver, infectious, neoplastic, and cardiac diseases, as well as pregnancy. Renal involvement in hematologic diseases has not been stressed. In this review we will summarize the role of coagulation in the pathophysiology of renal disease and present renal involvement in sickle cell anemia, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, leukemia, and other less common hematologic diseases.
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PMID:The kidney in hematologic disease. A review. 354 73


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