Thrombocytopenia: Clinicobiologic validation and classification
Service d'hématologie biologique, CHU Nancy.Annales de biologie clinique (Impact Factor: 0.28). 11/2005; 63(6):599-610.
Thrombocytopenia occurs frequently. We will illustrate, through the presentation of a clinical case, the difficulties encountered to identify and characterize thrombocytopenia. The clinicobiological validation of a low platelet count implies, at the same time, the biologist, who must assume the validation of numeration while mentioning the morphological characteristics of the platelets and other blood cells, as well as the clinician who must interpret these data according to the clinical context. Firstly, we will detail the basic rules to correctly ensure this validation. Secondly, we will see which are the arguments which that make it possible to direct the diagnosis towards an acquired or inherited thrombocytopenia. Lastly, we will approach the classification of inherited thrombocytopenias.
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ABSTRACT: Inherited diseases and metabolism inborn errors with hematologic abnormalities such as cytopenias are observed early in the infant or childhood. Most of them require an acute observation of the bone marrow to determine quantitative and qualitative morphological peculiarities of each cell line in order to charatherize cytological signs of these childhood hereditary diseases and differentiate them from acquired disorders, which are particularly frequent in pediatric. So, after a brief review of hematopoietic physiology in healthy neonates and infant, we'll consider the physiopathology and bone marrow aspect of the erythroid (Blackfan-Diamond anemia, congenital dyserythropoietic...), megacaryocytic (Wiskott-Aldrich syndrome, congenital amegakaryocytic thrombocytopenia...) and granulocytic cell line (Kostmann syndrome, WHIM syndrome...) in hereditary disorder. Considering the hematologic consequences of metabolism inborn errors and storage diseases, the last part of this review will be dedicated to the examination of the bone marrow encountered in those diseases such as mitochondrial cytopathy, orotic aciduria or lysinuric aciduria intolerance.Annales de biologie clinique 09/2007; 65(5):483-503. DOI:10.1684/abc.2007.0160 · 0.28 Impact Factor
Article: HématologieRevue Francophone des Laboratoires 06/2012; 2012(443):67–68. DOI:10.1016/S1773-035X(12)71505-8
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ABSTRACT: We report a case of a 47 years old woman. In her case of medical history, there were vein thrombosis and an allergic to tinzaparin. The patient entered in critical care unit under medical supervision for a multivisceral infarction due to an arterial mesenteric, renal and splenic thrombosis. An heparinotherapy was introduced. A laparotomy was realized because of an occlusion. Small intestine necrozed was removed. 8 days after the introduction of the heparin, there was a thrombocytopenia. Considering the background and the initiale situation, an heparin-induced thrombocytopenia of type II (HTI) was suspected. Whereas the heparinotherapy was stopped, the thrombocytopenia maked worse. Biological tests infirmed HIT's diagnosis. A recurrent anemia in spite transfusions associated to a renal failure suggest a thrombotic microangiopathy which was secondary confirmed. The intensivist is sensibilized to evoke an heparin induced thrombocytopenia when there is a thrombocytopenia under heparin. However, he must not forget diagnosis of thrombocytopenia which required specific investigations and emergency treatment such as thrombotic microangiopathy.02/2013; 71(1):113-119. DOI:10.1684/abc.2012.0786
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