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At least 1,063 records · Page 59Linked to original sources
PubMed1989

Flow cytometric analysis of megakaryocytes from patients with abnormal platelet counts.

Megakaryocytes (MKs) from 40 patients with quantitative platelet disorders and 19 normal volunteers were analyzed by flow cytometry for size, fine cell internal structure and granularity, membrane expression of the glycoprotein (GP) IIb/IIIa complex, and for ploidy distribution. Analysis was performed on unfractionated minimally manipulated marrows obtained from routine bone marrow aspirates. MKs were labeled with a fluorescent lineage-specific monoclonal antibody to the GPIIb/IIIa complex followed by DNA staining with propidium iodide. Eight hundred to 3,000 MKs were analyzed in each sample. The modal ploidy distribution in normals was 16N, comprising about half of the megakaryocytic population, with 22.6% of the cells less than or equal to 8N and 22.0% greater than or equal to 32N. Twelve thrombocytopenic patients with decreased marrow MKs on biopsy (mean platelet count [MPC] 44,600/microliters) showed an increase in low ploidy cells with 53.2% less than or equal to 8N (P less than .01); cell size was reduced in three patients when compared to normal cells of identical ploidy (P less than .05). Eight thrombocytopenic patients with enhanced platelet destruction (with normal or increased MKs on biopsy and shortened platelet survival; MPC 41,400/microliters) showed an increased proportion of high ploidy cells greater than or equal to 32N to 39.2% (P less than .01). Increased cell size and granularity were found in four of these patients (P less than .05). Six patients with thrombocytopenia secondary to multiple mechanisms affecting both platelet production and destruction (MPC 66,700/microliters) showed no shift in ploidy. Four patients with primary thrombocytosis (two with thrombocythemia and two with polycythemia vera; MPC 822,500/microliters) showed a marked shift toward high ploidy cells with 42.3% greater than or equal to 32N and 7.6% greater than or equal to 64N cells (P less than .01). The shift was accompanied by a marked increase in cell size and granularity in the patients with thrombocythemia. Ten patients with thrombocytosis secondary to chronic blood loss, malignant or inflammatory disorders (MPC 714,000/microliters), showed variable distributions with four patients exhibiting a shift in ploidy to the right similar to that found in the patients with increased platelet destruction. Based upon the present data, flow cytometric ploidy distribution may be diagnostically useful in thrombocytopenic patients by discriminating between disorders of platelet production and destruction. (ABSTRACT TRUNCATED AT 400 WORDS)

Bone Marrow↗
PubMed1986

[Clinical trial of bestrabucil (KM 2210) in hematopoietic malignancies].

Thirteen patients with hematological neoplasms were treated with Bestrabucil (100 mg/day po, total dose 700-9,900 mg), which is the benzoate of an estradiol-chlorambucil conjugate. The diseases from which they suffered consisted of T-cell leukemia (3), lymphoma (3), myeloma (5) and essential thrombocytosis (2). Although this drug was less effective against myeloma, the other diseases were more or less relieved with this medication. That is, Bestrabucil was effective in all three patients with T-cell leukemia, both with essential thrombocytosis and two of the three with lymphoma. It is most interesting that adult T-cell leukemia (ATL) cells decreased remarkably with Bestrabucil, along with the disappearance of several symptoms (bone pain, hypercalcemia etc.). The main side effects during this medication were mammary pain (eight of 13 patients, 62%), anorexia (five of 13 patients, 39%) and loss of libido (three of 13 patients, 23%), but neither severe myelosuppression nor hepatorenal dysfunction was induced.

Aged↗
PubMed1987

High doses of recombinant erythropoietin stimulate platelet production in mice.

Previously, recombinant erythropoietin (rEpo) was shown to increase the number and size of megakaryocytic colonies in vitro, and in vivo it elevates the number of megakaryocytes in mouse spleens. To test the hypothesis that rEpo would stimulate platelet production in mice, both normal mice and mice in rebound-thrombocytosis were injected with rEpo and the %35S incorporation into platelets was measured. A thrombocytopoiesis-stimulating factor (TSF or thrombopoietin) was used as a positive control. rEpo increased isotopic incorporation into platelets of both normal mice and mice in rebound-thrombocytosis, as did TSF, but required large doses (15 U rEpo/mouse). In other mice, hematocrits, platelet counts, platelet sizes, and 24-hr %35S incorporation into platelets were measured 2 days after injection of two equally divided doses of either rEpo or TSF. Significant increases in both platelet sizes and %35S incorporation into platelets were found after injections of 15 U rEpo/mouse or 2.3 U TSF/mouse. These data indicate that rEpo, at high doses, will stimulate platelet production in mice, and may suggest molecular similarities between rEpo and TSF and their ability to compete for common receptor sites on megakaryocytes and their progenitor cells.

Animals↗
PubMed1977

Effect of a low dose of vincristine on platelet production in mice.

The effect of a single low dose (0.1 mg/kg) of vincristine (VCR) on platelet production was investigated in C57B1 mice. A parallel increase of circulating platelets and (75Se)-selenomethionine (Se-Met) uptake was observed. The total megakaryocyte count decreased insignificantly 6 hours after VCR injection, followed by an increase after 18 hours. Plasma taken from mice 24 hours after VCR injection was tested for thrombopoietic activity. The post-VCR plasma caused a significant thrombocytosis, increased Se-Met uptake and increased protein synthesis of the platelets, indicating an active overproduction of platelets. These results suggest that the thrombocytosis induced by a low dose of VCR is mediated by a thrombopoietin-like substance.

Animals↗
PubMed1984

Bleeding and thrombosis in the myeloproliferative disorders.

Bleeding and thrombosis are major causes of morbidity and mortality in patients with myeloproliferative disorders. The significance of uncontrolled polycythemia as a risk factor for thrombosis in these patients has been established. However, the role of thrombocytosis in the pathogenesis of hemostatic complications remains controversial. Abnormalities of platelet function and prolongation of the bleeding time occur in a highly variable number of cases. Specific platelet defects that have been identified in the myeloproliferative defects include abnormal platelet morphology, acquired storage pool disease, platelet membrane abnormalities, and abnormal arachidonic acid metabolism. Causal relationships between any of these specific abnormalities and either bleeding or thrombosis have not been clearly established. The therapeutic efficacy of myelosuppression to reduce the platelet count in patients with thrombocytosis and the role of antiplatelet drugs in the myeloproliferative disorders are controversial issues.

Alkylating Agents↗
PubMed1984

The effects of low-dose vincristine on megakaryocyte colony-forming cells and megakaryocyte ploidy.

The administration of low-dose vincristine (VCR) (0.1 mg/kg) to mice resulted in thrombocytosis without prior thrombocytopenia. No significant changes in marrow megakaryocyte numbers were found. However, after a minor early decrease, mean megakaryocyte ploidy increased, with a peak at 3 d. The number of megakaryocyte colony-forming cells (MEG-CFC) in bone marrow did not change significantly. In contrast with the effects on marrow, the concentration of megakaryocytes and the content of MEG-CFC in the spleen were significantly reduced for 1-2 d after VCR. This reduction was followed by a compensatory rise in the splenic content of MEG-CFC (peak 3-fold increase at 3 d), and 1-2 d later, an increase in splenic megakaryocytes which was concurrent with the increased platelet count. Culture of marrow and spleen cells in the presence of VCR resulted in inhibition of megakaryocyte colony formation at concentrations greater than 5 ng/ml and parallel reduction of the number of megakaryocytes per colony and the mean ploidy of colony megakaryocytes. The results suggest that the thrombocytosis induced by low-dose VCR does not result simply from an effect on platelets, but reflects compensatory changes in megakaryopoiesis secondary to toxic suppression of megakaryocytes and their progenitors.

Animals↗
PubMed1981

Early splenectomy in chronic myelogenous leukemia: surgical aspects.

A retrospective study was conducted to analyze the surgical aspects of the splenectomy in chronic myelogenous leukemia. Twenty patients, Philadelphia chromosome-positive, were initially treated with busulfan until remission was reached. Elective splenectomy was then performed and chromosomal studies repeated at four- and six-month intervals yielding the indication for cyclic intensive chemotherapy. There ws no mortality, one episode of gram-negative sepsis with shock, and five instances of minimal complications. The spleen weights averaged 265 g, ranging from 60 to 800 g. All patients had normal coagulation profiles at the time of surgery, but four of them developed a postoperative thrombocytosis without related complications. A specific correlation was noted between postoperative thrombocytosis and splenomegaly (average weight 570 g). Eleven patients showed a high postoperative leukemoid reaction (average 40,500 cells/cu mm). The interval between diagnosis and splenectomy was shorter (average 7.5 months) in this group than for the patients who had a lower granulocytosis (average 19.5 months).

Adult↗
PubMed1981

Platelet number and function in Diamond-Blackfan anemia.

Congenital red cell aplasia (Diamond-Blackfan anemia) is occasionally associated with hematologic defects other than a deficiency of red blood cell progenitors, but such alterations have not been well studied. The frequency and magnitude of abnormalities in platelet count and platelet function were therefore examined in 38 patients. Thrombocytosis was seen in 21 patients, and 12 had mild thrombocytopenia on at least one occasion. Elevated platelet counts were demonstrated repeatedly in nine children. The three patients with the lowest platelet counts also had leukopenia. Platelet aggregation was normal in all 16 patients in whom it was studied, and bleeding times were within the normal range in 14 of them. Bleeding signs and symptoms were not observed. It is concluded that thrombocytosis or thrombocytopenia often occurs but that platelet function is normal in patients with Diamond-Blackfan anemia.

Adolescent↗
PubMed1981

Evidence that essential thrombocythemia is a clonal disorder with origin in a multipotent stem cell.

Essential thrombocythemia is characterized by proliferation of hematopoietic tissue predominantly involving megakaryocytes and resulting in marked thrombocytosis. The disorder has some clinical and laboratory features that resemble those seen in the clonal multipotent stem cell disorders chronic myelogenous leukemia, polycythemia vera, and agnogenic myeloid metaplasia. It has been argued that essential thrombocythemia should be classified together with those disorders as a myeloproliferative syndrome. However, without knowledge of the numbers and types of cells that are involved in essential thrombocythemia, this suggestion remains speculative. Three patients with thrombocytosis were studied. The diagnosis of essential thrombocythemia was considered to be firm in two patients and probable in the third one. The X-linked glucose-6-phosphate dehydrogenase locus was used as a cell marker. Whereas both A and B types of glucose-6-phosphate dehydrogenase were found in nonhematopoietic tissues, only a single-enzyme type was found in the granulocytes, red cells, and platelets from each patient. These data indicate that the disorders in these three patients are clonal and involve multipotent stem cells.

Adult↗
PubMed1993

Acute myeloid leukemia possibly producing thrombopoietic factor(s).

A 75-year-old man developed a cluster of differentiation (CD)4-positive but human T-cell lymphotropic virus type I (HTLV-I)-negative T lymphoid neoplasm with overwhelming cutaneous involvement and mild thrombocytosis. Twelve courses tetrahydropyranyl adriamycin, cyclophosphamide, vincristine and prednisone (THP-COP) combination chemotherapy led him to complete remission. After four months of complete remission, however, atypical immature cells (blasts) appeared in peripheral blood and bone marrow. Surface marker analysis revealed the blasts to be CD2-, CD3-, CD4-, CD5-, CD7+, CD8-, CD10, CD13 +/-, CD19-, CD20-, CD25-, CD33+ and human leukocyte antigen-DR (HLA-DR+). Staining for myeloperoxidase, esterases, PAS and platelet peroxidase were all negative. The patient was diagnosed as having both CD7 and CD33 positive acute myeloid leukemia (AML). The relation between the T cell lymphoid neoplasm and AML was not clear. Thrombocytosis became more marked after acute leukemia occurred and the platelet count varied in parallel with the blast cell count in peripheral blood. When the leukemic cell count was high, thrombopoietic activity could be detected in the serum. In addition, conditioned medium obtained from primarily-cultured blasts had detectable thrombopoietic activity, which implied the blasts directly to produce a thrombopoietic factor(s). Analysis of the serum concentration for cytokines with associated thrombopoietic activity indicated that the blasts possibly produced a thrombopoietic factor(s) distinct from interleukin (IL)6, IL3, leukemia inhibitory factor (LIF), erythropoietin and granulocyte macrophage-colony stimulating factor. To our knowledge, this is the first reported case of an acute myeloid leukemia with marked thrombopoiesis (more than 2000 x 10(3)/microliter of maximum platelet count in peripheral blood.

Acetylcholinesterase↗
PubMed1993

Platelet counts in thalassemic children before and after splenectomy.

Even though thrombotic risks in thalassemia patients from standpoints of platelet dysfunction and coagulation factors are controversial, they are in favor of thrombosis due to thrombocytosis. From the study of 74 cases of thalassemia in children, marked thrombocytosis occurred during day 8 to 4 months during which one should be aware of the thrombosis. However, none of thalassemia children had acute thrombosis even at platelet counts of 1.6 million/microliters.

Blood Platelets↗
PubMed1994

Erythromelalgic, thrombotic and haemorrhagic manifestations of thrombocythaemia.

OBJECTIVES: In order to document a relationship between platelet counts and clinical complication of thrombosis or bleeding in patients with myeloproliferative thrombocythaemia, 200 consecutive published cases of thrombocythaemia were reviewed for thrombotic or haemorrhagic manifestations and haematological findings at the time of the thrombohaemorrhagic complication. METHODS: Cases selected from the literature included all those complying with the diagnosis of thrombocythaemia as mandated by the Polycythemia Vera Study Group. One hundred consecutive cases of thrombocythaemia complicated by bleedings and one hundred consecutive cases of thrombocythaemia complicated by thrombosis were reviewed for clinical manifestations and haematological findings. RESULTS: In the reviewed cases of thrombocythaemia haemorrhagic complications (platelet count 2016 +/- 1070 x 10(9)/1) occurred at significantly (p < 0.001) higher degrees of thrombocytosis than thrombotic complications (platelet count 1110 +/- 477 x 10(9)/1). CONCLUSIONS: In the reviewed cases of thrombocythaemia arterial complications, especially erythromelalgia, can already be documented at platelet counts in excess of 400 x 10(9)/1, whereas bleeding complications usually occur at significantly higher degrees of thrombocytosis (> 1000 x 10(9)/1).

Adult↗
PubMed1995

Effect of intraperitoneal zinc on the haematological profiles of C57/6J mice.

Zinc is included in a number of medications and haematotoxic effects due to zinc excess have been reported. In this study, the haematological profiles (haematocrit, haemoglobin, total white blood cell count, differential white blood cell count and platelets) of mice treated with zinc were evaluated. Intraperitoneal zinc chloride was administered to C57/6J mice in varying dosages from 1.4-14 micrograms/g body weight, four times a week for a period of three weeks. Zinc chloride had no effect on the haematological profiles of these mice since the blood cell counts of treated mice were not significantly different from the controls (p < 0.05), with the exception that at half LD50 of zinc chloride (14 micrograms/g body weight) a reactive thrombocytosis resulted. (The platelet counts between the control and experimental group of mice were significantly different, exceeding 95% confidence limits; p = 0.016). We postulate that the specific effect on platelets was due to zinc being a potent inhibitor of phenol sulfotransferase (PST), an enzyme which is involved in many metabolic pathways. Platelets are a rich source of PST and the thrombocytosis observed was probably a compensatory mechanism to raise the levels of PST in the body.

Animals↗
PubMed1995

Platelet count and platelet factor 3 (PF-3) availability in sickle cell disease.

In view of the effect of red blood cell membrane on platelet factor 3 release in sickle cell disease, platelet count and platelet factor 3 (PF-3) availability were measured in 30 sickle cell patients in a stable state and 15 with thrombocytosis, and these were compared with 60 non-sickle cell individuals as controls. There were no significant differences in platelet counts, but there was a slightly higher PF-3 availability in sickle cell patients not in crisis than in the controls (P < 0.025). Sickle cell patients with thrombocytosis made PF-3 available more readily than did the control individuals and sickle cell patients not in crisis (P < 0.001). We conclude that sickle cell patients are capable of making platelet factor 3 readily available for coagulation activation, and this may play a decisive role in vaso-occlusive crisis.

Anemia, Sickle Cell↗
PubMed1997

[Effect of patients' gender on the course of chronic myeloid leukemia].

Chronic myeloid leukemia course was evaluated versus sex in 271 patients. Chronic stage involved more pronounced leukocytosis, thrombocytosis and splenomegaly in females, the latter showing higher susceptibility to anemia. As a result, treatment has to deal with a greater mass of tumor. A relatively longer survival time in males (44 and 42 months, respectively) suggest a higher effectiveness of therapy in such patients. When diagnosed, leukocytosis, thrombocytosis, enhanced splenomegaly and anemia should be regarded as factors of unfavorable prognosis.

Adolescent↗
PubMed1993

Inflammatory myofibroblastic tumor in children.

The authors presented the cases of two children with inflammatory myofibroblastic (IMF) tumor and reviewed the literature to facilitate the preoperative recognition, delineate the clinical features, and describe the natural history of this entity. The first child had IMF tumor arising from the mesentery of the small intestine. He presented with an abdominal mass associated with severe inflammatory response manifested by fever, impaired growth, thrombocytosis, and microcytic, hypochromic anemia. After surgical resection, his fever resolved and his growth rate and the laboratory abnormalities normalized. Five months after initial diagnosis, the fever, anemia, and thrombocytosis recurred along with two tumors arising from the omentum and the abdominal soft tissue. After the second surgery, he remains free of recurrent disease for 30 months. The second child presented with a lung mass that was radiologically indistinguishable from pulmonary sequestration. After surgical resection, she remains free of recurrent disease for 18 months. IMF tumor should be considered in any solid tumor that occurs in association with a chronic inflammatory response. IMF tumor should also be considered in the differential diagnosis of pulmonary sequestration.

Child↗
PubMed2000

Avascular necrosis of the femoral head in chronic myeloid leukemia patients treated with interferon-alpha: a synergistic correlation?

BACKGROUND: The objectives of this study were to describe cases of avascular necrosis of the femoral head (ANFH) observed in chronic myeloid leukemia (CML) patients who were treated with interferon-alpha and to review the literature. METHODS: The authors undertook a case review of the M. D. Anderson experience with ANFH occurring in CML patients who were managed with interferon-alpha-based therapy. MEDLINE (from 1966 to November 1999) and CancerLit (from 1983 to November 1999) searches were conducted to identify cases of avascular necrosis (AVN) associated with either CML or interferon-alpha. RESULTS: Three patients with ANFH were identified from the authors' experience. No common features related to the disease or therapy were seen among them, except for the presence of thrombocytosis and loss of response. A literature review revealed seven cases of ANFH associated with CML with or without interferon-alpha-based therapy. ANFH was not reported in association with interferon-alpha use for indications other than the treatment of patients with CML. CONCLUSIONS: ANFH may be the result of an interaction between CML and interferon-alpha therapy. ANFH that occurs in patients with CML who are treated with interferon-alpha should be recognized for treatment implications. Thrombocytosis with consequent microvascular thrombi and avascular necrosis manifesting in susceptible vascular or weight-bearing areas (e.g., the femoral head) may be an associated finding along with loss of response to interferon-alpha therapy.

Adult↗
PubMed1989

Evaluation of the clinical utility of platelet aggregation studies.

To determine the diagnostic importance of platelet aggregation studies, we evaluated the clinical utility of these assays by a retrospective review of 188 adult patients initially studied for bleeding abnormalities with platelet aggregation tests at a tertiary care hospital from 1984 to 1987. The primary indications for requesting the tests in our patient population were for the evaluation of a positive bleeding history or abnormal bleeding time (68%), hypercoagulability (17%), thrombocytosis (9%), or a family history of a bleeding disorder (6%). There was a statistically higher incidence of platelet aggregation test abnormalities in patients with highly abnormal bleeding times (40%), in patients with thrombocytosis from myeloproliferative disorders (65%), and in patients with a family history of a bleeding disorder (58%), compared to the other groups studied (16-29%). Of the 64 platelet aggregation tests performed that were abnormal, the following abnormalities were identified: 19 aspirin-like defects (poor response to arachidonate and decreased second wave responses to weak agonists), which were presumably drug-induced, ten myeloproliferative-type disorder defects (abnormal response to epinephrine predominantly) in patients known to have myeloproliferative disease, 34 abnormal patterns not characterized as aspirin or myeloproliferative disorder related, four of which ultimately led to a diagnosis of storage pool disease, and one spontaneous aggregation defect. Our results suggest that platelet aggregation tests rarely lead to the diagnosis of a specific, previously undiagnosed platelet function disorder. Specific recommendations are given for efficient utilization of platelet aggregation tests.

Bleeding Time↗