[ JAK2 mutation in myeloproliferative neoplasms: a predictive factor of thrombosis]

Background: BCR-ABL negative myeloproliferative neoplasms [MPN] include polycythemia Vera [PV], essential thrombocythemia [ET] and primitive myelofibrosis [PMF]. the JAK2 V617F mutation has been introduced since 2008 as a major diagnostic criterion on the one hand and on the other hand, it would be linked to increased risk of thrombotic complications

Aim: This study aimed to evaluate the association of JAK2 mutation and thrombotic events in MPN

Methods:A retrospective study concerning 45 BCR-ABL negative MPN patients [mean age=53 old years, sex ratio=0.8] was conducted

Results: They were classified as PV [22 patients], ET [17 patients], PMF [3 patients] and atypical MPN [3 patients]. The JAK2 mutation was found in 64.4% of patients: 72.7% of PV patients, 47% of ET patients and 66.7% of PMF patients. Thrombotic events were recorded in 11 patients [24.4%]. Cerebral arteries and portal vein were the most frequent localizations. The JAK2 mutation was an independent risk factor of thrombotic events

Conclusion: Consequently, it seems that screening for JAK2 mutation in BCR-ABL negative MPN could play a role in identifying patients at high risk of vascular complications

[Protein S, C and antithrombin deficiency: Association to myocardial infarction and thromboembolism in young]

The pathogenesis of myocardial infarction [MI] in young involves new factors including constitutional or acquired thrombophilia. To determine in patients

[Transfusion safety: state of the arts]

Blood transfusion is a high risk activity. To evaluate transfusion safety in planned cardiac surgery. This study was conducted in the blood bank of the Rabta Hospital in two phases: a phase to observe transfusion acts followed by corrective actions and a phase to evaluate the impacts of these corrections on the transfusion practices. Characteristics of the potentially transfused patients, the eventually prescribed, dispensed and transfused blood products and transfusion practices were studied. During the observation phase, 70 patients were enrolled, 51 potentially transfused. Weaknesses concerned the mention of phenotype and transfusion history when ordering blood components as well as the double ABO/D group typing, the phenotype and the cross match performing. Final bedside controls were done in a wrong way. The distribution and the blood administration were established respectively for 208 and 232 blood products. The traceability was established for 86 blood products. During the evaluation phase, 30 patients were enrolled, 15 potentially transfused. Improvement was achieved in the transfusion history notification, phenotype and antibodies screen performing and cross matching. Optimisation of blood transfusion can be conceived only with collaboration between the different transfusion structures