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Relevant bibliographies by topics / Thrombocytemie

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Academic literature on the topic 'Thrombocytemie'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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Journal articles on the topic "Thrombocytemie"

1

Maneh, N., M. Banla, K. B. Nonon Saa, et al. "Complications retiniennes d’une thrombocytemie essentielle." Journal Français d'Ophtalmologie 39, no. 6 (2016): e149-e150. http://dx.doi.org/10.1016/j.jfo.2015.01.032.

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Fernandez-Robles, E., C. Vermylen, P. Martiat, J. Ninane, and G. Cornu. "Familial Essential Thrombocyteemia." Pediatric Hematology and Oncology 7, no. 4 (1990): 373–76. http://dx.doi.org/10.3109/08880019009033414.

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Fattori, B., M. De Ciccio, A. Casani, P. Casalino, A. Sagripanti, and P. L. Ghilardi. "Vestibular disorders in primary Thrombocytemia." Biomedicine & Pharmacotherapy 47, no. 6-7 (1993): 287. http://dx.doi.org/10.1016/0753-3322(93)90227-c.

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Rodríguez-Cuartero, A., F. Pérez-Blanco, M. Riera, J. Canora, and J. Roldán. "Spurious serum hyperkalemia in essential thrombocytemia." Clinical Nephrology 61, no. 03 (2004): 229–30. http://dx.doi.org/10.5414/cnp61229.

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5

Rinaldi, Ciro R., Donglan Li, Rosanna Ciancia, et al. "GATA1 Is Over-Expressed in Essential Thrombocytemia." Blood 110, no. 11 (2007): 1534. http://dx.doi.org/10.1182/blood.v110.11.1534.1534.

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Abstract GATA1, founding member of the GATA transcription factor family, is essential for cell maturation and differentiation within the erythroid and megakaryocyte (MK) lineages. Disruption of DNA- or protein-binding capacity of GATA1 causes severe hematopoietic dysfunction and plays a role in blood disorders such as thrombocytopenia, anemia or leukemia. GATA1 expression seems to be related to the MK commitment both in mice and in humans; indeed, similarly to the murine myeloid M1 cell line, in which the enforced expression of GATA1 induces the c-Mpl appearance and MK differentiation, transduction of human hematopoietic stem cells with a GATA1 highly expressing vector results in self-renewal block and in the exclusive generation of Meg-E lineages. More recently, a role for GATA1 also in myeloproliferative disorders (MPDs) was indicated by the “GATA1-low” mouse model which develop a disease closely resembling the human idiopathic myelofibrosis. Interestingly, patients affected by myelofibrosis was also shown to express decreased GATA1 levels by immunostaining of BM sections. In this study, we investigated by Real Time PCR the levels of GATA1 in a myeloproliferative disorders such as essential thrombocytemia (ET) tipically characterized by a neoplastic megakaryocitic proliferation. We have studied BM samples of 40 newly diagnosed patients (M:F ratio 1:1 - median age 53 years, range 18–84) affected by ET, as for the PVSG group criteria. These patients were selected from a cohort of 65 ET patients considering a similar erythroid/myeloid ratio at the FACS analysis to reduce a possible bias for the RT-PCR results due to the erythroid compartment interference. The median platelets count of the selected patients was 670,000/mL (range 493,000–1,400,000/mL), myelofibrotic index 0/1, and 18 out of 40 patients (45%) showed mild splenomegaly both at the physical examination and US scan (median spleen vol 550 ml - range 430–1400 mL). No chromosomal abnormalities were detected by cytogenetic analysis. JAK2 sequencing in 21/40 patients indicated that 9/21 patients (43%) were positive for the JAK2 V617F genomic mutation. At the end of observation time (median 18 mo.) no patients had evidence or signs of thrombotic or hemorrhagic complications. BM cells from six healthy donors were used as normal controls in the study. The relative GATA1 quantification was calculated in according to the DCt method with GAPDH as internal control. The results showed a significant increase of GATA1 expression in BM cells from ET patients (median DCt + 6,11 ; range −0,41/+18,11) compared to the controls (median DCt + 0,172 ; range −4,03/+1,7) (p < 0,003). Interestingly, the GATA1 overexpression is not a mere consequence of the proliferation and activation of MKs, indeed samples from three patients affected by idiopathic thrombocytopenic purpura, whose BM smears had the typical secondary megakaryocytic hyperplasia, showed GATA1 levels much lower than the ET patients (median DCt − 0,6 ; range − 3,21/−0,9). No significant difference in GATA1 level was found between patients harbouring a JAK mutation (median DCt +5,86 ; range 0,85/16,12) and those with wild type alleles (median DCt +4,75 ; range −0,41/10,21). In conclusion, our results suggest that GATA1 overexpression could be a trigger for MK neoplastic commitment and proliferation and, consequently, seems to have a central role for ET pathogenesis both in JAK2 mutated and in JAK2 WT patients.

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6

Caocci, Giovanni, Sandra Atzeni, Monica Usai, and Giorgio La Nasa. "Essential thrombocytemia following immune thrombocytopenia with JAK2V617F mutation." Leukemia Research Reports 9 (2018): 14–15. http://dx.doi.org/10.1016/j.lrr.2017.12.002.

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Garc??a-Ferreira, Joaqu??n, Joaqu??n Hern??ndez-Palaz??n, Antonio Garc??a-Candel, and Teresa Verd??-Mart??nez. "Subarachnoid Block in a Patient with Essential Thrombocytemia." Anesthesia & Analgesia 101, no. 1 (2005): 300. http://dx.doi.org/10.1213/01.ane.0000156705.90157.9a.

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8

Legrand, F., A. Fernex de Mongex, M. Delrue, et al. "Foot ischemia related to essential thrombocytemia and atherosclerosis." JMV-Journal de Médecine Vasculaire 46, no. 3 (2021): 123–28. http://dx.doi.org/10.1016/j.jdmv.2021.03.009.

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TOKURA, Masaaki, Yoshihiko SEIMA, Kunio UESAKA, and Takemi SUGIMOTO. "A CASE OF ESSENTIAL THROMBOCYTEMIA COMPLICATED BY GASTRIC CANCER." Nihon Rinsho Geka Gakkai Zasshi (Journal of Japan Surgical Association) 69, no. 11 (2008): 2872–76. http://dx.doi.org/10.3919/jjsa.69.2872.

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Erbag, Gokhan, Ibrahim Hakki Dursun, Yildiray Topcu, Ilhan Dolasik, and Selcuk Yusuf Sener. "Systemic Lupus Erythematosus in a patient with Essential Thrombocytemia." Abant Medical Journal 2, no. 2 (2013): 176–77. http://dx.doi.org/10.5505/abantmedj.2013.13008.

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Dissertations / Theses on the topic "Thrombocytemie"

1

Lemarie, Dechristee Dominique. "La thrombocytemie essentielle de l'enfant : sept observations." Nancy 1, 1989. http://www.theses.fr/1989NAN11310.

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BARAN, DOMINIQUE. "Etude de la thrombocytemie essentielle a partir de 68 cas." Clermont-Ferrand 1, 1991. http://www.theses.fr/1991CLF13074.

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Petit, Michel. "Thrombocytemie essentielle et thromboses arterielles multiples : a propos d'une observation." Reims, 1990. http://www.theses.fr/1990REIMM024.

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MARAVAL, FREDERIC. "Association d'une anemie sideroblastique acquise a une thrombocytemie essentielle : a propos de sept cas." Nantes, 1989. http://www.theses.fr/1989NANT130M.

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EL, KASSAR NAHED. "Thrombocytemie essentielle : physiopathologie et etude de la clonalite de l'hematopoiese." Paris 7, 1997. http://www.theses.fr/1997PA077204.

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La thrombocytemie essentielle (te) est un syndrome myeloproliferatif (smp) caracterise par une hyperplaquettose persistante et une hyperplasie megacaryocytaire. Le diagnostic de cette maladie repose sur l'elimination de toute cause d'hyperplaquettose. La preuve d'une hematopoiese monoclonale peut constituer un argument positif de diagnostic. Le phenomene d'inactivation du chromosome x chez la femme est un phenomene actif qui aboutit, dans la cellule femelle, a l'extinction transcriptionnelle de la quasi-totalite des genes portes sur le chromosome x inactive. Cependant, l'analyse de la clonalite selon ce principe se heurte a l'existence de femmes normales ayant la meme image d'inactivation inegale dans leur tissu hematopoietique. Nous avons etudie la clonalite chez 53 patientes avec une te et 123 femmes normales appartenant a differentes tranches d'age, par deux techniques : la premiere est basee sur la difference de methylation du gene humara ; la deuxieme sur l'analyse des transcrits polymorphes des genes ids (iduronate-2-sulfatase), p55 et g-6-pd, par pcr-rflp et technique d'extension d'amorce. Utilisant les lymphocytes t comme tissu temoin de lyonisation, nous avons retrouve une monoclonalite dans les granulocytes et les plaquettes chez la majorite des patientes (31/36). Une polyclonalite a ete retrouvee chez une minorite de patientes par les marqueurs arn (5/36). La moyenne d'age et les signes ischemiques etaient nettement plus eleves dans les patientes avec une hematopoiese monoclonale. La technique d'extension d'amorce s'est revelee la technique la plus fiable. Ces resultats confirment la frequence elevee d'une hematopoiese monoclonale dans la te et la possibilite d'utiliser les lymphocytes t comme tissu temoin de lyonisation. La te etant caracterisee par une proliferation de la lignee megacaryocytaire, nous avons elimine, dans un second temps, des anomalies d'expression du gene c-mpl, ainsi qu'une secretion inappropriee de son ligand, la thrombopoietine. En conclusion, la te est une maladie heterogene. Par analogie avec le modele des polyglobulies primitives, nous suggerons l'existence de deux maladies differentes chez ces patientes, en fonction de la clonalite de l'hematopoiese : l'existence d'un vrai smp en cas d'hematopoiese monoclonale ; et celle d'une thrombocytose primitive en cas d'hematopoiese polyclonale, en reponse probablement a un facteur extrinseque.

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Cohen, Raphaël-Dany. "Les hyperplaquettoses de l'enfant : a propos d'une observation de thrombocytemie essentielle." Université Louis Pasteur (Strasbourg) (1971-2008), 1986. http://www.theses.fr/1986STR1M271.

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7

DEGAEY, PHILIPPE. "Thrombocytemie essentielle : interet des parametres hematologiques dans le diagnostic et la surveillance : etude retrospective (63 cas) et analyse de la litterature." Reims, 1992. http://www.theses.fr/1992REIMM032.

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8

BARBAZA, LIBES MARIE-ODILE. "Deficit en proteine c, deficit en antithrombine iii, thrombocytemie essentielle pendant la grossesse." Lyon 1, 1989. http://www.theses.fr/1989LYO1M434.

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9

CLERY, PATRICE. "Thrombocytemies avec chromosome philadephie ou debuts thrombocytemiques de leucemie myeloide chronique." Lille 2, 1989. http://www.theses.fr/1989LIL2M410.

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10

Messaadi, Nassir. "Association d'un syndrome poems, d'un syndrome de gougerot-sjogren et d'une thrombocytemie essentielle : a propos d'une observation." Lille 2, 1992. http://www.theses.fr/1992LIL2M121.

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Conference papers on the topic "Thrombocytemie"

1

Mazzucato, M., M. G. Del Ben, A. Casonato, V. De Angelis, and L. De Marco. "PLATELET MEMBRANE GLYCOPROTEINS ABNORMALITIES IN MYELOPROLIFERATIVE DISORDERS. STRUCTURE/FUNCTION RELATIONSHIP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643508.

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The platelet membrane glycoproteins (GP) lb and GPIIb/IIIa were investigated in 10 patients with myeloproliferative disorders. 2 patients had essential thrombocytemia (ET), 2 had chronic myeloid leukemia (CML) and 6 policytemia vera (PV). The number of GP molecules were detected by radiolabelled monoclonal antibodies anti GPIb and anti GPIIb/IIIa complex (gift of dr. Z.M. Ruggeri) and their function was evaluated by using, in a binding assay, purified radiolabelled asialo von Willebrand factor (1251 ASvWF) and purified radiolabelled fibrinogen (1251 F). Binding isotherms were evaluated by Scatchard type analysis using the computer assisted programLigand. The binding of 1251 anti GPIb to the platelets of the ten patients showed 14,955 ∓ 4,636 molecules/platelet (M/Plt) compared to 19,790 ∓ 3,791 M/Plt of 11 normals with a p value < 0.01. The binding of 125IAsvWF to the GPIb of nonstimulated platelets in platelet rich plasma (PRP) was then measured and ound to be decreased. The dissociation constants (Kds) were within normal values except in one patient. There was a good correlation (r = 0.91, p < 0.01) between the amount of 1251 ASvWF bound and GPIb molecules. The binding of radiolabelled anti GPIIb/IIIa to the platelets of six patients (4 with PV and 2 with CML) was measured and found to be constantly decreased in all patients with a mean value of 25,349 ∓ 2,077 M/Plt compared to 43,192 ∓ 6,354 M/Plt found in normals (p < 0.01). 1251 fibrinogen binding to the GPIIb/IIIa complex of ADP + adrenalin stimulated washed platelet was studied in 2 patients and we found 16,267 M/Plt and 14,752 M/Plt respectively, significantly diminished when compared to the mean value of 36,591 M/Plt found in 2 normal controls. The Kds were within normal values. Our studies demonstrate a significant decrease of GPIb and GPIIb/IIIa on the platelet membrane of patients with myeloproliferative disorders. Furthermore this decrease is accompanied by a diminished binding of both vWF and F to their platelets receptors. These findings may partly explain the hemorragic tendency often encountered in these patients.

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