A síndrome de Legg-Calvé-Perthes ou doença de Perthes é uma doença degenerativa da articulação da anca (quadril em português brasileiro) em que ocorre. El absceso del psoas es una enfermedad infrecuente en niños. Puede tener una en pediatría es primario; sin embargo, en ocasiones, puede ser de origen secundario y médula espinal, enfermedad de. Legg-Calvé-Perthes, entre otros Download Citation on ResearchGate | Enfermedad de Legg Calvé Perthes (LCP) en varios aspectos de la enfermedad de Legg Calvé Perthes y la evolución de caderas de August · Anales espanoles de pediatria.
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To improve our services and products, we use “cookies” own or third parties lediatria to show advertising related to client preferences through the analyses of navigation customer behavior. Are you a health professional able to prescribe or dispense drugs? J Lab Clin Med,pp.
Thromb Haemost, 62pp. Association of idiopathic venous thromboembolism with single point-mutation at Arg of factor. Thromb Haemost, 71pp. Conclusions Epidemiological and laboratory data from this group ofpediatric patients and from enfrmedad control prrthes do not supportthe hypothesis that a thrombogenesis defect couldbe the underlying cause of avascular necrosis of the hipjoint.
Variability of thrombosis among homozigous siblings with resistance to activated protein C due to an Arg-Gln mutaion in gen for factor V.
Clin Chem, 32pp. Thromb Res, 11pp. Blood collection in strongly acid citrate anticoagulant used in a study of dietary influence of basal Tpa activity. Determination of plasminogen activator and its fast inhibitor in plasma.
Am J Hematol, 44pp. Mutation in blood coagulation factor V associated with resistance to activated protein C. The remaining patients were considered withinthe normal range when age was taken into account. Maturation of the hemostatic system during childhood.
Pathophysiology of osteonecrosis of the jaw: Necesidades del alumnado con diabetes tipo 1 en Lancet,pp.
Enfermedad de Legg-Calve-Perthes | HCA Healthcare
Genetics aspects of Perthes disease: Familial idiopathic oeteonecrosis mediated by familial hypofibrinolysis witn high levels of plasminogen activator inhibitor. Patients and method Complete study of hemostasis with coagulation and antithrombinfactors as well as study pertnes thrombophilia andfibrinolysis in these patients could determine the prevalenceof hemostasis and fibrinolysis in this group of patients.
Association of antithrombotic factor deficiencies and hy-pofibrinolysis with Legg-Perthes disease. Perthes’ disease and the relevance of thrombophilia.
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Antithrombin heparin cofactor assay with new chromogenic substrates. Blood, 87pp. Relation of altered hemostasis to etiology. Special laboratory evaluation of coagulation.
Resistance to activated protein C and Legg-Perthes disease.
Síndrome de Legg-Calvé-Perthes – Wikipédia, a enciclopédia livre
Severe thrombotic disease in a young man with bone marrow and skeletal changes and with a high content of an inhibitor in the fibrinolytic system. Identification of the same factor V gene mutation in 47 of 50 thrombosis-prone families with inherited resistance to activated protein C. Idiopathic osteonecrosis, hypofibrinolysis, high plasminogen activator inhibitor, high Lp aand therapy with stanozolol.
Br J Hematol, 71pp. Results Alterations in hemostasis and thrombosis were detectedin one patient who had moderate-to-light protein Sdeficiency. Thromb Haemost, 78pp.
Síndrome de Legg-Calvé-Perthes
The Kinston antiphospholipid group. Non traumatic osteonecrosis of the femoral head: J Med,pp. It has been suggested that peciatria cause of Perthes diseasemay be intravascular thrombosis induced by a potentialcongenital hemostatic disorder leading to conditions ofthrombophilia or hyperfibrinolysis.
Complete study of hemostasis with coagulation and antithrombinfactors as well as study of thrombophilia andfibrinolysis in these patients could determine the prevalenceof hemostasis and fibrinolysis in this group of patients.
Blood, 84pp. Thromb Haemost, 69pp. Aguirre Canyadell aI. Nature,pp. Background It has been suggested that the cause of Perthes diseasemay be intravascular thrombosis induced by a potentialcongenital hemostatic enffrmedad leading to conditions ofthrombophilia or hyperfibrinolysis.
Anal Biochem,pp. Epidemiological and laboratory data from this group ofpediatric patients and from the control group pertues not supportthe hypothesis that a thrombogenesis defect couldbe the underlying cause of avascular necrosis of the hipjoint. The second international anticardiolipin standardization workshop.
Alterations in hemostasis and thrombosis were detectedin one patient who had moderate-to-light protein Sdeficiency.