Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Megakaryocyte morphology was studied quantitatively in primary thrombocythaemia (PT) and in chronic myelogenous leukaemia (CML). The relation of thrombokinetics to megakaryocyte quantifications was evaluated in PT and compared to previously obtained results in polycythaemia vera (PV) and idiopathic thrombocytopenic purpura (ITP). Megakaryocyte area, number and volume per mul bone marrow were significantly higher in PT as compared to controls. The nuclear lobe number was significantly increased and the megakaryocytes were shifted towards more mature forms, suggesting a prolonged megakaryocyte generation time. In CML the megakaryocyte number and volume per mul bone marrow were also significantly above normal, but the megakaryocyte area, number of lobes and degree of megakaryocytic maturation were significantly below normal. Platelet production was in PT 6.2 times normal and proportional to the increase in megakaryocyte volume which was 6.8 times normal. In PV with major splenomegaly the mean platelet production rate was higher (9.5 times normal) although their peripheral platelet count was lower than in PT. This discrepancy is explained by the greatly enlarged splenic platelet pool in the PV patients. In ITP the mean platelet production rate was 2.2 to 3 times normal and was significantly lower than in PT and PV.
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PMID:Megakaryocyte quantifications in relation to thrombokinetics in primary thrombocythaemia and allied diseases. 106 Jan 75

The French-American-British classification scheme of myelodysplastic syndromes includes a category of refractory cytopenia that includes refractory thrombocytopenia (RTC). Because dysmegakaryopoiesis manifesting as an isolated cytopenia can be difficult to identify morphologically and because it may be accompanied by megakaryocytic hyperplasia, RTC may be confused with idiopathic thrombocytopenic purpura. A review of 1,220 cases of myelodysplastic syndromes at Mayo Clinic Jacksonville and Mayo Clinic Rochester from 1979 to 1990 yielded 9 cases (0.7%) of isolated thrombocytopenia (RTC) associated with clonal chromosome abnormalities. Review of 319 marrow chromosome analyses performed at the cytogenetics laboratory at Mayo Clinic Rochester from 1979 to 1990 for patients with low platelet count yielded two additional cases of RTC (0.6%). Of the 11 RTC cases, 3 previously had been misdiagnosed as idiopathic thrombocytopenic purpura. All patients had oval macrocytes in peripheral blood smears and abnormal megakaryocyte morphology in bone marrow aspirates, lacked antiplatelet antibodies, and did not have splenomegaly on clinical examination. The most common clonal chromosome abnormalities involved chromosomes 3, 5, 8, or 20. Steroid therapy was ineffective. Clinical and laboratory findings can establish the diagnosis of RTC and allow the physician to avoid recommending inappropriate therapy (steroids or splenectomy) for these patients.
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PMID:Refractory thrombocytopenia. A myelodysplastic syndrome that may mimic immune thrombocytopenic purpura. 148

A 61-year-old man was admitted to our hospital in April 18, 1988, with dyspnea and gingival bleeding. Physical examination revealed marked splenomegaly, and peripheral blood showed severe pancytopenia with 38% abnormal mononuclear cells. The abnormal cells were characterized by a hairy appearance under a phase contrast microscopy, and strong tartrate-resistant acid phosphatase activity. These cells reacted with CD19, CD25 and CD11c monoclonal antibodies by the immunostaining method. Bone marrow aspiration failed and bone marrow biopsy revealed diffuse proliferation of hairy cells (HC) with moderate fibrosis. In addition, the staining pattern of HC peroxidase is similar to that found in megakaryocyte series. He was diagnosed as HCL of the European-American type based on these findings. Interferon (IFN)-alpha was administered at a daily dosage of 3 x 10(6) IU by intramuscular injection. Although splenomegaly and hematological conditions improved gradually, he received splenectomy because of his incomplete hematological improvement. Normalization of peripheral blood cell counts and a marked decrease of HC in bone marrow were obtained. Tubuloreticular structure and tubular confronting cisternae were seen in peripheral mononuclear cells during IFN therapy.
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PMID:[Improvement with interferon-alpha therapy and splenectomy in hairy cell leukemia of European-American type]. 157 41

Both large, acute doses of erythropoietin (EPO) and short-term hypoxia increase platelet counts in mice, but long-term hypoxia causes thrombocytopenia. Therefore, we tested the hypothesis that EPO injected in large, chronic doses (a total of 80 U of EPO over a 7-day period) might cause thrombocytopenia. EPO caused increased red blood cell (RBC) production, ie, increased hematocrits, RBC counts, mean cell volume (MCV), and reticulocyte counts (from P less than .05 to P less than .0005), and decreased thrombocytopoiesis, ie, decreased platelet counts, percent 35S incorporation into platelets, and total circulating platelet counts (TCPC) (P less than .0005). Femoral marrow megakaryocyte size was unchanged, but megakaryocyte number was significantly (P less than .005) reduced in mice treated with EPO. EPO-injected mice had increased spleen volumes (P less than .0005), but blood volumes (BV) were unchanged. In EPO-treated, splenectomized mice, RBC production was also increased (P less than .05 to P less than .0005) and platelet counts, TCPC, and percent 35S incorporation into platelets were decreased (P less than .05), but BV was not altered. Therefore, the decrease in platelet counts observed in EPO-treated mice was not due to increased BV or to an enlarged spleen. In other experiments, mice were rendered acutely thrombocytopenic to increase thrombocytopoiesis, and platelet and RBC production rates were determined. In mice with elevated thrombocytopoiesis, RBC counts, hematocrits, percent 59Fe RBC incorporation values, and MCV were decreased (P less than .05 to P less than .0005). Because 59Fe RBC incorporation and MCV were not elevated, the decrease in RBC counts and hematocrits does not appear to be due to bleeding. Therefore, we show that large, chronic doses of EPO increase erythropoiesis and decrease thrombocytopoiesis. Conversely, acute thrombocytopenia causes increased thrombocytopoiesis and decreased erythropoiesis. These findings support the hypothesis of competition between precursor cells of the erythrocytic and megakaryocytic cell lines (stem-cell competition) as the cause of thrombocytopenia in EPO-treated mice and the cause of anemia in mice whose platelet production rates were increased.
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PMID:Large, chronic doses of erythropoietin cause thrombocytopenia in mice. 129 64

To determine the number of megakaryocyte precursors (pro- and megakaryoblasts), an immunomorphometric study was performed on paraffin-embedded trephine biopsies of the bone marrow using a monoclonal antibody against platelet glycoprotein IIIa. Eighteen control specimens from patients with no evidence of any hematological disorder and a normal platelet count were selected and assessed together with the same number of specimens from patients with reactive thrombocytosis, polycythemia vera rubra (P. vera) or primary (essential) thrombocythemia (PTH). A strikingly proportionate increase in early megakaryocytes occurred in all patients enrolled in this study, compared with the controls. Moreover, there were no significant correlations between counts for precursors or total megakaryocytes per square millimeter of bone marrow with the corresponding values for platelets. This indicates that despite an orderly increase in immature forms in the bone marrow, the number of platelets circulating in the blood is influenced by other additional factors, such as the expanded platelet pool in the enlarged spleen. The non-disproportionate expansion of megakaryocyte precursors extends previous findings on progenitor cells of this lineage in vitro, particularly in PTH. Histological evaluation of the bone marrow of patients with P. vera and PTH indicated that megakaryopoiesis proceeded to the production of appropriate mature forms with no obvious excess of very small or blastic elements.
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PMID:Megakaryocyte precursors (pro- and megakaryoblasts) in bone marrow tissue from patients with reactive thrombocytosis, polycythemia vera and primary (essential) thrombocythemia. An immunomorphometric study. 197 Jun 93

To evaluate the efficacy of recombinant murine granulocyte-macrophage colony-stimulating factor (rGM-CSF) in attenuating the myelosuppression associated with chemotherapy, the effects of 100 and 300 ng rGM-CSF, administered twice daily by intraperitoneal injection for 6 consecutive days to mice 24 hours after a dose of 200 mg/kg cyclophosphamide, were measured. Six days after the initial injection of rGM-CSF, a significant increase occurred in the absolute myeloid count compared to that of vehicle-treated animals. The difference was most pronounced on day 7, attaining levels of 327% and 428% of the control; these increases slowly declined to that of the control level by day 19. No significant effect was produced by rGM-CSF on the packed red cell volume or on the platelet count. Furthermore, the administration of rGM-CSF did not alter bone marrow cellularity or increase the number of marrow-derived hematopoietic stem cells. In contrast, a significant splenomegaly occurred, starting on day 6 and continuing until day 17. This was characterized by a pronounced increase in splenic-derived granulocyte (CFU-G), granulocyte-macrophage (CFU-GM), macrophage (CFU-M), megakaryocyte (CFU-MK), and erythroid (BFU-E, CFU-E) stem cells. The increases occurred between days 6 and 9 following the initial administration of rGM-CSF. These findings indicated that the administration of rGM-CSF to cyclophosphamide-treated animals causes an absolute increase in circulating myeloid cells and that these increases are derived from the spleen. The use of recombinant hematopoietic growth factors may permit the administration of more intensive chemotherapy through amelioration of chemically induced leukopenia.
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PMID:Effects of recombinant murine granulocyte-macrophage colony-stimulating factor in cyclophosphamide-treated mice. 201 56

A case of chronic myelogenous leukemia (CML) with marked thrombocytosis and its megakaryokinetics were reported. Patient was 57-year old woman who had a marked thrombocytosis (1,413 x 10(3)/microliters) and a bone marrow megakaryocytosis. Bone marrow karyotype demonstrated Ph1 chromosome in all cells examined. However, on physical examination, there was no splenomegaly. CBC showed no immature myeloid cells, and neutrophil alkaline phosphatase was elevated. These manifestations were consistent with so called essential thrombocythemia (ET) with Ph1 chromosome reported by Nissenblatt. To know the megakaryokinetics of this case, we examined the number of colony forming unit-megakaryocyte (CFU-M), platelet glycoprotein (PGP) IIb/IIIa positive cells, cytoplasmic area, and DNA content, comparing with those of normal subjects, CML, and ET. We found a marked increase of CFU-M and PGP IIb/IIIa positive cells, but in contrast, decreased DNA content and cytoplasmic area. This pattern of megakaryokinetics was consistent with that of CML. We conclude that ET with Ph1 chromosome may be a variant of CML rather than ET itself.
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PMID:[Chronic myelogenous leukemia with marked thrombocytosis--comparison with essential thrombocythemia with Ph1 in its megakaryokinetics]. 231 4

We report a case of acute myelofibrosis. This is a rare myeloproliferative disorder characterized by pancytopenia, minimal or absent anisopoikilocytosis, bone marrow fibrosis with hyperplasia and immaturity of the three main cellular lines with megakaryocyte predominance, absence of splenomegaly and rapidly fatal course. We discuss its relationship with acute megakaryocytic leukemia, as its blast elements correspond to megakaryocytes when ultrastructural and antifactor VIII immunoperoxidase techniques are used; these techniques disclose alpha granules and cell demarcating membranes.
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PMID:[Acute myelofibrosis: apropos of a case with immunocytochemical and ultrastructural studies]. 249 79

In 24 cases of thrombopenic purpura associated with human immunodeficiency virus infection the clinical, immunological and therapeutic features were evaluated. Thrombopenia resulted in clinical manifestations in 20 patients. Splenomegaly was found in only one fourth of patients. Antiplatelet antibodies were found in 9 patients, and thrombopenia was associated with anemia in 37% of cases and with leukopenia in 21%. Bone marrow examination showed megakaryocyte hyperplasia in two thirds of the patients. The major immunological abnormalities were an inverted helper/suppressor T lymphocytes ratio, a reduction in the number of helper T lymphocytes, polyclonal hypergammaglobulinemia, and increased serum concentrations of circulating immunocomplexes. The different therapeutic modalities, steroids, vincristine, danatrol and plasma exchange, resulted in short responses; only two patients had normal platelet counts. The median follow-up was 14 months; during this time three patients fulfilled the criteria of acquired immunodeficiency syndrome.
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PMID:[Thrombopenic purpura associated with human immunodeficiency virus infection. Analysis of 24 cases]. 274 29

IL-1 has been shown to stimulate the release of granulocyte-macrophage CSF, granulocyte-CSF, and macrophage-CSF from "accessory cell populations" in vitro, and it stimulates the appearance of colony-stimulating activity in the sera of mice in vivo. This cytokine has also been proposed to act on primitive hematopoietic progenitor cells to stimulate expression of receptors for the CSF. We sought to determine whether IL-1 beta could influence platelet and/or megakaryocytes and their progenitor cells following in vivo administration to normal mice. Our results demonstrated that, although administration of IL-1 beta clearly expands the pool of megakaryocyte-CFU and acetylcholinesterase-positive megakaryocytic cells (primarily in the spleen), it causes a transient and dose-dependent reduction of circulating platelets. The associated thrombocytopenia can be abolished by splenectomy before IL-1 beta administration, and is not temporally associated with the development of splenomegaly.
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PMID:Alterations in megakaryocyte and platelet compartments following in vivo IL-1 beta administration to normal mice. 278 31


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