Circulating micromegakaryocytes in myelodysplasia.

Erber, Wendy N.; Jacobs, A.; Oscier, David; O'hea, A. M.; Mason, D Y

doi:10.1136/jcp.40.11.1349

Cited by 29 publications

(8 citation statements)

References 8 publications

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“…All functional platelet responses must be tightly regulated to ensure that the formation of blood clots is of sufficient size to seal off the damaged area, while not disrupting blood flow to vital organs by causing vessel occlusion [ 145 – 147 ]. With the observation that dengue viral antigens are associated with proplatelets [ 148 , 149 ] or micromegakaryocytes [ 137 , 150 ] in blood during acute dengue virus infection ( Figure 3 ), it is likely that a platelet lineage parental cell, megakaryocytes, may be involved in the production of dengue virus during acute infection. In addition, platelets contain several key elements related to dengue virus infection, such as DC-SIGN [ 151 ] as well as complement and Fc receptor, which have been implicated in virus uptake [ 152 , 153 ].…”

Section: In Vivo Dengue Patientsmentioning

confidence: 99%

“…Furthermore, a unique and previously neglected cell population, which has ultrastructural and morphological appearance similar to that of micromegakaryocytes [ 137 , 150 ] and a possible source of dengue viremia [ 22 , 123 ], were seen in circulation during the acute phase of infection [ 129 , 160 ], though the likely phenotypes of these neglected cells are not well defined.…”

Section: In Vivo Dengue Patientsmentioning

confidence: 99%

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Cells in Dengue Virus Infection In Vivo

Noisakran

Onlamoon

Songprakhon

et al. 2010

Advances in Virology

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Dengue has been recognized as one of the most important vector-borne emerging infectious diseases globally. Though dengue normally causes a self-limiting infection, some patients may develop a life-threatening illness, dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). The reason why DHF/DSS occurs in certain individuals is unclear. Studies in the endemic regions suggest that the preexisting antibodies are a risk factor for DHF/DSS. Viremia and thrombocytopenia are the key clinical features of dengue virus infection in patients. The amounts of virus circulating in patients are highly correlated with severe dengue disease, DHF/DSS. Also, the disturbance, mainly a transient depression, of hematological cells is a critical clinical finding in acute dengue patients. However, the cells responsible for the dengue viremia are unresolved in spite of the intensive efforts been made. Dengue virus appears to replicate and proliferate in many adapted cell lines, but these in vitro properties are extremely difficult to be reproduced in primary cells or in vivo. This paper summarizes reports on the permissive cells in vitro and in vivo and suggests a hematological cell lineage for dengue virus infection in vivo, with the hope that a new focus will shed light on further understanding of the complexities of dengue disease.

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Section: In Vivo Dengue Patientsmentioning

confidence: 99%

Section: In Vivo Dengue Patientsmentioning

confidence: 99%

Cells in Dengue Virus Infection In Vivo

Noisakran

Onlamoon

Songprakhon

et al. 2010

Advances in Virology

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“…That the presence of nearly no normal megakaryocytes in our patients and that nearly all megakaryocytes displayed characteristics of naked megakaryocyte nuclei, emperipolesis, or abnormal morphology like peripheral vacuolization (showing non-classical apoptosis: para-apoptosis) and directly destructed megakaryocytes (showing necrosis) and presence of many stage 1 megakaryocytes (megakaryoblasts), some of which were aberrantly releasing thrombocytes, imply defective megakaryocyte maturation, heavy intramedullary premature cell death of megakaryocytes, and increased megakaryopoiesis [ 14 , 69 , 70 , 71 , 72 , 73 ] (Supplemental Discussion, Text 3).…”

Section: Discussionmentioning

confidence: 99%

Both granulocytic and non-granulocytic blood cells are affected in patients with severe congenital neutropenia and their non-neutropenic family members: An evaluation of morphology, function and cell death

Olcay¹,

Ünal²,

Önay³

et al. 2018

Tjh

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Objective:To examine granulocytic and non-granulocytic cells in children with severe congenital neutropenia (SCN) and their non-neutropenic parents.Materials and Methods:Fifteen patients with SCN and 21 non-neutropenic parents were evaluated for a) CD95, CD95 ligand, annexin V, propidium iodide, cell cycle, and lymphocyte subsets by flow cytometry; b) rapid cell senescence (of leukocytes) by senescence-associated β-galactosidase stain; c) aggregation tests by aggregometer; d) in vitro bleeding time by PFA-100 instrument; e) mepacrine-labeled dense granule number of thrombocytes by fluorescence microscope; and f) hematomorphology by light and electron microscope. HAX1, ELANE, G6PC3, CSF3R, and JAGN1 mutations associated with SCN were studied in patients and several parents.Results:Significant increase in apoptosis and secondary necrosis in monocytes, lymphocytes, and granulocytes of the patients and parents was detected, irrespective of the mutation type. CD95 and CD95 ligand results implied that apoptosis was non-CD95-mediated. Leukocytes of 25%, 12.5%, and 0% of patients, parents, and controls showed rapid cell senescence. The cell cycle analysis testable in four cases showed G1 arrest and apoptosis in lymphocytes of three. The patients had HAX1 (n=6), ELANE (n=2), G6PC3 (n=2), and unidentified (n=5) mutations. The CD3, CD4, and NK lymphocytes were below normal levels in 16.6%, 8.3%, and 36.4% of the patients and in 0%, 0%, and 15.4% of the parents (controls: 0%, 0%, 5.6%). The thrombocytes aggregated at low rates, dense granule number/thrombocyte ratio was low, and in vitro bleeding time was prolonged in 37.5%-66.6% of patients and 33.3%-63.2% of parents (vs. 0% in controls). Under electron and/or light microscope, the neutrophils, monocytes, lymphocytes, and thrombocytes in the peripheral blood of both patients and parents were dysplastic and the bone marrow of patients revealed increased phagocytic activity, dysmegakaryopoiesis, and necrotic and apoptotic cells. Ultrastructurally, thrombocyte adhesion, aggregation, and release were inadequate.Conclusion:In cases of SCN, patients’ pluripotent hematopoietic stem cells and their non-neutropenic parents are both affected irrespective of the genetic defect.

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“…However, some megakaryocytes are able to pass through the pulmonary capillaries and are thus detectable in PB smears, especially in buffy coat preparations or in leukocyte concentrates [1]. Their number is found between 5 and 7 cells per millilitre in healthy adult subjects, and is increased in neonates, young infants, after delivery, following surgery, in patients with inflammatory, infectious and solid malignant disorders, disseminated intravascular coagulation, as well as in MPN and MDS [1,[35][36][37][38][39].…”

Section: Circulating Megakaryocytes Micromegakaryocytes and Megakarymentioning

confidence: 99%

“…Occasionally, a "budding" of platelets from the surface can be observed [11]. Micromegakaryocytes can be apparent in various haematopoietic disorders such as MDS, acute megakaryoblastic leukaemia, transient abnormal myelopoiesis of Down syndrome, PMF, post polycythaemia or post thrombocythaemia myelofibrosis and chronic myeloid leukaemia (CML) [1,[38][39][40]. In CML, the occurrence of circulating micromegakaryocytes may indicate the transformation to blast crisis [39].…”

Section: Circulating Megakaryocytes Micromegakaryocytes and Megakarymentioning

confidence: 99%

Platelet morphology

Robier

2020

Journal of Laboratory Medicine

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BackgroundThe examination of a peripheral blood smear is mandatory in case of unexplained thrombocytopenia or thrombocytosis. First, the number of platelets should be estimated in order to confirm the platelet count determined by the haematology analyser, and to rule out causes of spuriously low or elevated platelet counts. Second, the size and morphological features of the platelets, which may provide information on the underlying cause of the low or enhanced platelet count, have to be assessed.ContentThis review summarizes the physiological and pathological features of platelet size and morphology, circulating megakaryocytes, micromegakaryocytes and megakaryoblasts, and provides an overview of current guidelines on the reporting of platelet morphology.SummaryIn the diagnostic work-up of a patient with thrombocytopenia, the size of the platelets is of diagnostic relevance. Thrombocytopenia with small platelets is suggestive of a defect in platelet production, whereas the presence of large platelets is more likely to be associated with enhanced platelet turnover or hereditary thrombocytopenias. Morphological platelet abnormalities may affect the granulation and the shape and are frequently associated with abnormalities of platelet size. Platelet anomalies can be found in various haematologic disorders, such as myelodysplastic syndromes, myeloproliferative neoplasms, acute megakaryoblastic leukaemia or hereditary thrombocytopenias.

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Circulating micromegakaryocytes in myelodysplasia.

Abstract: SUMMARY The alkaline phosphatase-antialkaline phosphatase (APAAP)

Cited by 29 publications

References 8 publications

Cells in Dengue Virus Infection In Vivo

Cells in Dengue Virus Infection In Vivo

Both granulocytic and non-granulocytic blood cells are affected in patients with severe congenital neutropenia and their non-neutropenic family members: An evaluation of morphology, function and cell death

Platelet morphology

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