Deep venous thrombosis or pulmonary embolism and factor V Leiden: enigma or paradox.

Kebriaei P, et al. Low-dose azacitidine after allogeneic stem cell trans-plantation for acute leukemia. relapse after allo-geneic bone marrow transplantation for haematological malignancy. Early prediction of extramedullary relapse of leukemia following allogeneic stem cell transplantation using the WT1 transcript assay. Repeated relapses of acute myelogenous leukemia in the isolated extramedullary sites following allogeneic bone marrow transplanta-tions. Myeloid leukemia and myelodysplastic syndrome relapsing as gran-ulocytic sarcoma (chloroma) after allogeneic bone marrow transplan-tation. al. Establishment of a novel granulocytic sarcoma cell line which can adhere to dermal fibroblasts from a patient with granulocytic sarco-ma in dermal tissues and myelofibrosis. Specific skin manifestations in CD56 positive acute myeloid leukemia. Management of relapse after allo-SCT for AML and the role of second transplantation. Tanizawa Y. Gemtuzumab ozogamicin therapy for isolated extramedullary AML relapse after allogeneic hematopoietic stem-cell transplantation. Gemtuzumab therapy for isolated extramedullary AML relapse following allogeneic stem-cell transplant. T he study of factor V Leiden (FVL) has created many expectations but also engendered much controversy. Factor V Leiden is widely considered the first and most common prothrombotic polymorphism, but in 1965, the non-O blood group, present in 50% of the population , was associated with a 2-fold increased risk of venous thrombosis. Factor V Leiden may have developed through genetic drift or natural selection in Caucasians, possibly by conferring a reduced risk of bleeding and an evolutionary advantage, but no similar prothrombotic polymorphism has been described in other populations. The risk of venous thrombosis (OR: 4 for heterozygous) and the relatively high prevalence in Caucasians (4-10%), together with its simple genotyping explain why testing for factor V Leiden has been widely studied and is still commonly requested. However, the utility of such testing is under debate, as it might complicate more than facilitate the clinical management of carriers, particularly the pro-phylaxis of venous thrombosis in asymptomatic carriers. Moreover, factor V Leiden has a very mild effect on arterial thrombosis. These controversies may be explained by the moderate functional consequences of the activated protein C (APC) resistance caused by this polymorphism and the requirements of additional genetic and environmental risk factors and triggering factors that are ultimately responsible for the development of a thrombotic event. Additionally, there are two apparent paradoxes concerning the clinical consequences of factor V Leiden. Pulmonary embolism (PE) is usually considered to be a complication of deep vein thrombosis (DVT) and therefore the genetic risk factors for both DVT and …