RESUMO
Venous thromboembolism is a common complication of patients with hematologic malignancies, due both to release of procoagulant factors by tumor cells and to external factors, such us drugs. In multiple myeloma patients, the risk is increased by use of immunomodulants, especially when associated to multidrug therapy, during the induction phase. Prevention of venous thromboembolism in myeloma patients is highly recommended but specific guidelines are still lacking. The most common approach is to stratify the thrombotic risk according to individual, myeloma-related and therapy-related risk factors and to use aspirin for all patients, except those with two or more thrombotic risk factors who should be treated with traditional oral or parenteral anticoagulant. A more controversial approach indicates for prophylaxis either anticoagulant or aspirin, regardless of risk stratification. Recent trials investigate prophylaxis in myeloma patients with direct oral anticoagulants, based on studies showing efficacy and safety of this new class of drugs in the treatment and prophylaxis of thrombosis in patients with any malignancy. The results of these trials are encouraging but they need to be confirmed by larger studies. An international consensus about best prophylaxis to prevent venous thromboembolism in patients with multiple myeloma on treatment is still missing. Therefore, thrombosis in multiple myeloma remains an ongoing issue.
Assuntos
Mieloma Múltiplo , Preparações Farmacêuticas , Trombose , Tromboembolia Venosa , Anticoagulantes/uso terapêutico , Aspirina/uso terapêutico , Quimioterapia Combinada , Humanos , Hansenostáticos/uso terapêutico , Mieloma Múltiplo/complicações , Mieloma Múltiplo/tratamento farmacológico , Trombose/tratamento farmacológico , Tromboembolia Venosa/tratamento farmacológico , Tromboembolia Venosa/etiologia , Tromboembolia Venosa/prevenção & controleRESUMO
INTRODUCTION: Corticosteroids and/or thalidomides have been associated with thromboembolism events (TBE) in multibacillary (MB) leprosy. This report aimed to determine genetic and laboratory profiles associated with leprosy and TBE. METHODS: Antiphospholipid antibodies (aPL), coagulation-related exams, prothrombin and Leiden's factor V mutations, and ß2-glycoprotein-I (ß2GPI) Val247Leu polymorphism were assessed. RESULTS: Six out of seven patients with leprosy were treated with prednisone and/or thalidomide during TBE and presented at least one positive aPL. All patients presented ß2GPI polymorphism, and one showed prothrombin mutation. CONCLUSIONS: Corticosteroid or thalidomide adverse effects and aPL and ß2GPI polymorphisms may cause TBE in patients with MB leprosy.
Assuntos
Corticosteroides/administração & dosagem , Síndrome Antifosfolipídica , Hanseníase Multibacilar/imunologia , Talidomida/administração & dosagem , Corticosteroides/efeitos adversos , Adulto , Idoso , Anticorpos Antifosfolipídeos/sangue , Anticorpos Antifosfolipídeos/efeitos dos fármacos , Anticorpos Antifosfolipídeos/genética , Síndrome Antifosfolipídica/sangue , Síndrome Antifosfolipídica/tratamento farmacológico , Síndrome Antifosfolipídica/genética , Ensaio de Imunoadsorção Enzimática , Fator V/análise , Feminino , Humanos , Imunoglobulina G/sangue , Imunoglobulina M/sangue , Hanseníase Multibacilar/tratamento farmacológico , Hanseníase Multibacilar/genética , Masculino , Pessoa de Meia-Idade , Mutação , Polimorfismo Genético , Protrombina/análise , Talidomida/efeitos adversos , Tromboembolia Venosa/tratamento farmacológico , beta 2-Glicoproteína I/sangueRESUMO
Abstract INTRODUCTION Corticosteroids and/or thalidomides have been associated with thromboembolism events (TBE) in multibacillary (MB) leprosy. This report aimed to determine genetic and laboratory profiles associated with leprosy and TBE. METHODS Antiphospholipid antibodies (aPL), coagulation-related exams, prothrombin and Leiden's factor V mutations, and ß2-glycoprotein-I (ß2GPI) Val247Leu polymorphism were assessed. RESULTS Six out of seven patients with leprosy were treated with prednisone and/or thalidomide during TBE and presented at least one positive aPL. All patients presented ß2GPI polymorphism, and one showed prothrombin mutation. CONCLUSIONS Corticosteroid or thalidomide adverse effects and aPL and ß2GPI polymorphisms may cause TBE in patients with MB leprosy.