Imatinib-induced platelet dysfunction and hypofibrinogenemia in chronic myeloid leukemia
| Autor: | Richa Chauhan, Manoranjan Mahapatra, R Ragesh R Nair, Renu Saxena, Shivangi Harankhedkar |
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| Rok vydání: | 2019 |
| Předmět: |
Male
medicine.medical_specialty Platelet dysfunction Hemorrhage 030204 cardiovascular system & hematology Gastroenterology Red cell transfusion 03 medical and health sciences Myelogenous 0302 clinical medicine Melena hemic and lymphatic diseases Internal medicine Leukemia Myelogenous Chronic BCR-ABL Positive medicine Humans Protein Kinase Inhibitors business.industry Myeloid leukemia Imatinib Hematology General Medicine Hypofibrinogenemia medicine.disease Afibrinogenemia Leukemia Pyrimidines Imatinib Mesylate Blood Platelet Disorders medicine.symptom business 030215 immunology medicine.drug |
| Zdroj: | Blood coagulationfibrinolysis : an international journal in haemostasis and thrombosis. 30(5) |
| ISSN: | 1473-5733 |
| Popis: | We aim to present a case of chronic myeloid leukemia (CML) in chronic phase, in major molecular response for 5 years of treatment with imatinib 400 mg OD. He presented with recurrent melena for one and a half years, requiring 11 U of packed red cell transfusion since then. Various causes of bleeding in CML, such as thrombocytopenia, disease progression related to accelerated phase/blast crisis or imatinib-induced cytopenia were ruled out. His investigations revealed reduced plasma fibrinogen (150 mg/ml; range 200-450 mg/ml). The platelet count, prothrombin time, activated partial thromboplastin time and thrombin time were 314 × 10/l, 13 s (control 13 s), 31 s (control 30 s) and 16 s (control 16 s), respectively. Platelet aggregometry revealed normal platelet aggregation with adenine-di-phosphate, epinephrine and ristocetin, and reduced response with arachidonic acid (30%). Bleeding subsided with transfusion of fresh frozen plasma. Moreover, his medication was changed to nilotinib 300 mg BD. Thereafter, his subsequent repeat investigations were normal. Platelet function defects in CML both pretherapy and on tyrosine kinase inhibitors has been described in the literature. However, concomitant hypofibrinogenemia has rarely been reported. |
| Databáze: | OpenAIRE |
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