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At least 919 records · Page 51Linked to original sources
PubMed1993

Circulating megakaryocyte progenitors in myeloproliferative disorders are hypersensitive to interleukin-3.

Previous studies have reported that megakaryocyte progenitors in myeloproliferative disorders (MPD) formed spontaneous megakaryocyte colonies without the addition of megakaryocyte colony-stimulating factor (Meg-CSF). To determine whether this spontaneous colony formation is due to autocrine proliferation of MPD megakaryocyte progenitors or to hypersensitivity to Meg-CSF that might exist in the culture system, we investigated colony-forming unit-megakaryocytes (CFU-Meg) in the peripheral blood of 11 MPD patients, using serum-free cultures. Spontaneous megakaryocyte colonies were observed in serum-free cultures of nonadherent mononuclear cells (NAdMNC) obtained from MPD patients with thrombocytosis, whereas the NAdMNC of MPD patients without thrombocytosis, that of patients with reactive thrombocytosis and normal subjects never formed spontaneous colonies. However, the spontaneous colonies from MPD patients with thrombocytosis disappeared in cultures using highly purified CD34-positive cells as target cells. To study the hypersensitivity of megakaryocyte progenitors to Meg-CSF, dose-response experiments were performed with interleukin-3 (IL-3). CFU-Meg from MPD patients with thrombocytosis showed maximal growth at the concentrations of IL-3 lower than those for normal subjects. CFU-Meg of MPD patients without thrombocytosis and that of patients with reactive thrombocytosis showed the same colony growth response to IL-3 as that of normal subjects. This result indicates that the CFU-Meg of MPD patients with thrombocytosis are hypersensitive to IL-3. It also suggests that spontaneous colony formation by NAdMNC is not due to the autocrine growth of megakaryocyte progenitors but is due to the hypersensitivity of megakaryocyte progenitors to Meg-CSF, such as IL-3, released by accessory cells. Furthermore, it is possible that such hypersensitivity of CFU-Meg to IL-3 might be a pathogenic factor in MPD with accompanying thrombocytosis.

Adult↗
PubMed2006

Thrombopoietin and interleukin-6 levels in Henoch-Schönlein purpura.

BACKGROUND AND PURPOSE: Depending on the severity of the illness, thrombocytosis is found in about 60% to 70% of patients with Henoch-Schönlein purpura (HSP). Whether thrombocytosis is the result of an inflammatory reaction mediated by thrombopoietin (TPO) or other inflammatory cytokines such as interleukin (IL)-6 remains unknown. METHODS: Thirty two patients who met the diagnostic criteria for HSP were included. They were divided into two groups - HSP patients with thrombocytosis (n = 14) and those without thrombocytosis (n = 18) with a platelet count of 400,000/microL. Eight normal healthy controls were also included. TPO and IL-6 serum levels during the acute phase were measured by enzyme-linked immunosorbent assay. RESULTS: Patients with platelet counts greater than 400,000/microL in the acute stage had significantly lower TPO levels than patients with platelet counts lower than 400,000/microL (310 +/- 65.6 pg/mL vs 608 +/- 97.8 pg/mL, p=0.013). However, HSP patients with or without thrombocytosis had similar TPO levels as the healthy controls (441 +/- 176 pg/mL, p=0.89 and 0.29, respectively). IL-6 serum levels were significantly elevated in HSP patients during the acute stage of HSP (28.6 +/- 61.7 pg/mL vs 3.16 +/- 1.35 pg/mL, p=0.049). In patients with complications of glomerulonephritis or gastrointestinal hemorrhage (n = 12), IL-6 levels were significantly lower than in those without such complications (8.07 +/- 3.79 pg/mL vs 40.9 +/- 16.9 pg/mL, p=0.007). CONCLUSIONS: This study showed that thrombocytosis in HSP patients is a type of inflammatory reactive thrombocytosis, and that IL-6 may also play a role in the pathogenesis of HSP.

Child↗
PubMed2000

Artefactual serum hyperkalaemia and hypercalcaemia in essential thrombocythaemia.

AIM: To investigate possible abnormalities of serum potassium and calcium levels in patients with essential thrombocythaemia and significant thrombocytosis. METHODS: 24 cases of essential thrombocythaemia with significant thrombocytosis (platelet count > 700 x 10(9)/litre) had serum potassium and calcium estimations performed at the time of maximum thrombocytosis before treatment, and at the time of low platelet count after treatment with cytoreductive drugs. Selected patients were further investigated with plasma sampling and estimation of ionised calcium and parathyroid hormone. RESULTS: At the time of maximum thrombocytosis six patients had serum hyperkalaemia (> 5.5 mmol/litre) and five had serum hypercalcaemia (> 2.6 mmol/litre). Following treatment and reduction of the platelet count, hyperkalaemia resolved in all cases and hypercalcaemia in four of the five cases. Mean serum potassium and calcium concentrations were raised (p < 0.0001) at maximum thrombocytosis compared with the values when the platelet count was low. Serum potassium and calcium values were significantly correlated at all stages. Measurements on plasma consistently corrected the hyperkalaemia but not the hypercalcaemia. Serum hypercalcaemia was associated with raised ionised calcium and normal parathyroid hormone concentrations. CONCLUSIONS: Essential thrombocythaemia with significant thrombocytosis is associated with serum hyperkalaemia and hypercalcaemia. The probable mechanism of hypercalcaemia is the secretion of calcium in vitro from an excessive number of abnormally activated platelets. It is thus likely that the hypercalcaemia is an artefact, as is the hyperkalaemia.

Adolescent↗
PubMed2004

Iron deficiency and thrombosis: literature review.

Compared to primary thrombocytosis such as that caused by essential thrombocytosis, reactive thrombocytosis is generally regarded as benign. However, reactive thrombocytosis has infrequently been reported to cause severe and even fatal complications. Two fatal cases of reactive thrombocytosis and iron deficiency anemia associated with peripheral/pulmonary vascular and cerebrovascular thrombosis are described. The literature on thrombosis and reactive thrombocytosis associated with iron deficiency anemia is reviewed.

Adult↗
PubMed1983

In vitro studies of megakaryocytopoiesis in thrombocytotic disorders of man.

Increased numbers of bone marrow megakaryocytes and thrombocytosis are frequently observed in patients with myeloproliferative disorders (MPD). Increased marrow megakaryocytes and thrombocytosis are also noted in a variety of inflammatory and neoplastic disease leading to the phenomenon of reactive thrombocytosis (RT). The pathogenesis of this finding remains incompletely understood. Using methodology developed in our laboratory, we investigated the causative role of megakaryocyte colony-stimulating activity (Meg-CSA) in generating this phenomenon. We also examined the cloning efficiency of colony-forming units-megakaryocyte (CFU-M) and their responsiveness to an exogenous source of Meg-CSA in patients with these diseases. The results of our investigations suggest that: (1) increased production of Meg-CSA is not responsible for the megakaryocyte hyperplasia and thrombocytosis noted in these patients; (2) the intrinsic stem cell defect described in MPD appears to affect the CFU-M of these patients as well, resulting in an effective expansion of the CFU-M pool with consequent megakaryocyte hyperplasia and thrombocytosis; (3) the CFU-M of patients with MPD remain responsive to an exogenous source of Meg-CSA, suggesting that this megakaryocyte hyperplasia may not be entirely autonomous of its effects; and (4) the CFU-M pool in RT is normal both in size and responsiveness to Meg-CSA, suggesting that in these disorders, the stimulus leading to megakaryocyte hyperplasia and thrombocytosis is active at the post-CFU-M level of megakaryocyte differentiation.

Cells, Cultured↗
PubMed1978

Regulation of megakaryocytes in W/Wv mice.

W/Wv mice were injected with antiplatelet serum to produce thrombocytopenia or with platelet transfusions to induce thrombocytosis. The responses of their platelets and megakaryocytes were followed to determine if proliferative abnormalities of the megakaryocytic system would be detected. W/Wv mice responded normally to the stimulation from thrombocytopenia with rebound thrombocytosis, macromegakaryocytosis, and macrothrombocytosis. The megakaryocytes of these mice became smaller than normal in response to post-thrombocytopenic rebound thrombocytosis but not to transfusion-induced thrombocytosis. Thus, endogenous thrombocytosis appeared to be a more potent suppressor of megakaryocyte growth than exogenous. These results failed to reveal an effective abnormality of the thrombocytopoietic regulatory system of W/Wv mice in spite of their intrinsically reduced numbers of megakaryocytes and the well known defect of stem cell proliferation. Thrombocytopoietic regulation appeared, therefore, to occur mainly at the committed, rather then pluripotential, stem cell level, and normal responses of the platelet system were observed in spite of severe abnormalities at the pluripotential stem cell level.

Anemia, Hemolytic↗
PubMed2001

Cytokines, endothelium, and adhesive molecules in pathologic thrombopoiesis.

Clonal thrombocytosis (CT) associated with myeloproliferative disorders (MPD) is believed to be secondary to autonomous unregulated platelet production. Secondary or reactive thrombocytosis (RT) can be observed in a number of clinical circumstances and may be related to persistent production of some thrombopoietic factors acting on megakaryocytes (MK). The goal of this study is to assess the serum concentrations of these cytokines in control subjects and patients with MPD associated with thrombocythemia, RT, and autoimmune thrombocytopenic purpura (ATP). Eleven patients with MPD, five with chronic myeloid leukemia (CML), three with polycythemia vera (PCV), two with essential thrombocythemia (ET), one with myelofibrosis, 15 with RT, eight with ATP, and 12 healthy volunteers were enrolled in the study. Serum interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha (TNF), fibronectin, intracellular adhesion molecule-1 (ICAM-1), and thrombomodulin (TM) were measured in these groups. Interleukin- 1beta, IL-6, and TNF levels were high in patients with RT and ATP, suggesting that these cytokines act on early uncommitted progenitors, promoting commitment along the MK lineage and leading to thrombocytosis or compensation for thrombocytopenia. TM was significantly increased in patients with MPD compared to all other groups, probably indicating the presence of subclinical endothelial damage. Fibronectin levels were high in MPD and RT patients. This finding can be secondary to high platelet turnover in these patients. We found that ICAM-1 levels were high in patients with clonal thrombocytosis. ICAM-1 can be one of the factors initiating the events ultimately leading to clonal thrombocytosis. Thrombocythemia associated with MPD is an autonomous phenomenon not regulated by cytokines.

Case-Control Studies↗
PubMed2004

Anagrelide: an update on its mechanisms of action and therapeutic potential.

Thrombocytosis is an increasingly recognized clinical problem due to the widespread availability of automated cell counters. While reactive thrombocytosis does not require any therapeutic intervention, clonal thrombocytosis may require therapy to prevent thrombohemorrhagic complications. The clinician has a number of therapeutic options available when confronted with a patient having clonal thrombocytosis. One of these agents is anagrelide (Agrylin, Bristol-Myers Squibb). In this drug profile, a synopsis of the available data on this agent and its role in the control of thrombocytosis will be provided. The main side effects of the medication are discussed, as well as the potential future developments in the field.

Clinical Trials as Topic↗
PubMed2006

The role of megakaryocytes in skeletal homeostasis and rheumatoid arthritis.

PURPOSE OF REVIEW: This review provides an update on the role of megakaryocytes in skeletal homeostasis, and discusses these findings in the context of rheumatoid arthritis. RECENT FINDINGS: Thrombocytosis is a common complication of rheumatoid arthritis, and is presumably caused by an up-regulation in megakaryocytopoiesis. In general, patients with rheumatoid arthritis exhibit localized joint bone erosion with systemic bone loss, and rheumatoid arthritis patients with thrombocytosis tend to have more severe disease. Interestingly, in addition to their role in rheumatoid arthritis with thrombocytosis, it has been demonstrated recently that megakaryocytes play a dual role in regulating skeletal mass by inhibiting bone resorption while simultaneously stimulating bone formation. This seeming contradiction in the putative role of megakaryocytes in skeletal regulation and rheumatoid arthritis is the focus of this review. SUMMARY: In rheumatoid arthritis there are substantial increases in the levels of several pro-inflammatory pleiotropic cytokines. As would be expected, in addition to their role in inflammation, these cytokines play a critical role in the megakaryocytopoiesis seen in patients who develop reactive thrombocytosis, and these cytokines also are known to regulate osteoclastogenesis. Thus, it appears that in rheumatoid arthritis with reactive thrombocytosis, the ability of the cytokines to enhance osteoclastogenesis outweighs the ability of megakaryocytes to inhibit osteoclastogenesis.

Arthritis, Rheumatoid↗
PubMed1999

[Massive thrombosis of the superior mesenteric artery following splenectomy. A coincidence?].

Postsplenectomy thrombocytosis is a well recognised complication about which there is little published information. Therefore, postoperative complications of this effect have not been emphasised. An experience with a case of superior mesenteric artery thrombosis and small intestinal ischemia following splenectomy is reported. We reviewed the literature, but we wasn't able to find any case, whereas the association between splenectomy and mesenteric or portal vein thrombosis is well known. Pathogenesis of postsplenectomy thrombocytosis is poorly understood. Theories to explain it include removal of the splenic sequestration effect or removal of a regulatory humoral factor produced by the spleen. Both mechanisms could be operative at the same time, explaining the observation that some patients develop thrombocytosis related complications soon after surgery, while others after a longer time. The literature on the thromboembolic risk of postsplenectomy thrombocytosis is inconclusive and no studies have established whether patients with thrombocytosis following splenectomy should be treated with anticoagulants or antiplatelet medications in order to prevent thrombotic complications. Certainly, a recommendation for the routine use of these drugs cannot be made on the basis of one observation, but the need for controlled studies must be stressed.

Aged↗