Antithrombotics today.

Over the last 10 years some new drugs affecting blood clotting - antithrombotics - were invented. For more than half a century only warfarin and heparin were available. A better understanding of the pathways involved in activation of blood clotting, the links between these systems, and the impact of thrombosis on inflammation, have led to identification of new targets and development of new drugs, especially new antiplatelet drugs and anticoagulants. With the advent of new drugs into clinical practice, treatment options of thrombotic complications are expanding. However, it is always necessary to get familiar with the drug and its properties and to know its limitations. This is the only way to offer patients the best practices. Key words: anticoagulant - antithrombotic - Direct Oral AntiCoagulant (DOAC) - laboratory monitoring - Low-Molecu-lar-Weight Heparins (LMWH) - New Oral Anticoagulants/Non-vitamin K Oral AntiCoagulants (NOAC) - unfractionated heparin (UFH) - warfarin.

The impact of PROS1 mutation position on thrombotic risk in protein S-deficient patients.

Background: Inherited protein S deficiency is a thrombophilic risk factor associated with venous thromboembolism. However, there is not much data on the impact of mutation position on thrombotic risk. Objectives: The aim of this study was to evaluate the risk of thrombosis due to mutations located in the sex hormone-binding globulin (SHBG)-like region as opposed to the rest of the protein. Methods: Genetic analysis of PROS1 was performed in 76 patients with suspected inherited protein S deficiency, and the effect of missense mutations present in the SHBG region on thrombosis risk was analyzed by statistical methods. Results: We found 30 unique mutations (13 of them novel), of which 17 were missense mutations, in 70 patients. Patients with missense mutations were then divided into 2 groups: the "SHBG-region" mutation group (27 patients) and the "non-SHBG" group (24 patients). The multivariable binary logistic regression analysis showed that mutation position in the SHBG region of protein S is an independent risk factor for thrombosis in deficient patients (OR, 5.17; 95% CI, 1.29-20.65; P = .02). The patients with a mutation in the SHBG-like region also developed a thrombotic event at a younger age compared to the "non-SHBG" group in the Kaplan-Meier analysis (median thrombosis-free survival of 33 vs 47 years, respectively; P = .018). Conclusion: Our findings show that a missense mutation located in the SHBG-like region may contribute to higher thrombotic risk rather than a missense mutation located elsewhere in the protein. However, as our cohort was relatively small, these findings should be taken with this limitation.

[Haemopoiesis defects in HIV/AIDS-anaemia.].

Under physiological conditions haemopoiesis is continuous and maintains a stable number of blood elements. A defect at any stage presents as anaemia, neutropenia, thrombocytopenia or their combinations. The cause of haematological abnormalities with an HIV infection is multifactorial. HIV/AIDS patients may present identical haematological disorders as patients free of an HIV infection. Additionally, HIV-positive subjects tend to present disorders specific of an HIV infection. Anaemia may also be the first manifestation of an as yet undetected HIV infection. Moreover, many drugs used in the treatment of HIV/AIDS significantly affect haemopoiesis. Whatever the cause of anaemia, it is essential to initiate simultaneously with its treatment an appropriate highly active antiretroviral therapy. An antiretroviral therapy along the lines of state-of-the-art pharmacotherapy of HIV/AIDS significantly improves the efficacy of the actual haematological treatment. Key words: HIV infection-haemopoiesis-anaemia-antiretroviral therapy.