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Dalteparin-sodium/fondaparinux-sodium/heparin Heparin-induced thrombocytopenia and cross-reactivity: case report

A 67-year old man developed heparin-induced thrombocytopenia following treatment with dalteparin-sodium and heparin for non-ST segment elevation myocardial infarction. Subsequently, he developed cross-reactivity to fondaparinux-sodium during treatment with fondaparinux-sodium for heparin-induced thrombocytopenia [not all routes stated; duration of treatment to reaction onset and outcome not stated]. The man was hospitalised with left-sided hemiplegia and confusion. Six months prior to the presentation, he was diagnosed with type 2 myelodysplastic syndrome with excessive blasts and started receiving azacitidine. Subsequently, he was scheduled for bone marrow examination and allogeneic haematopoietic stem cell transplant. He had no history of heparin-induced thrombocytopenia or thrombosis. His concomitant medications included aciclovir [acyclovir] and cotrimoxazole. During the follow-up of myelodysplastic syndrome, he remained transfusion-independent and his haemoglobin levels remained more than 100x109/L and platelet count was more than 100x109/L. Fourteen days prior to the hospitalisation, he was admitted due to non-ST segment elevation myocardial infarction. Hence, IV heparin [unfractionated heparin] 5000 IU/L bolus was given and he was shifted for coronary angiography. His coronary angiography results were unremarkable; therefore, he received conservative therapy with dalteparin sodium (low-molecular weight heparin) twice a day for a total of 7 days in combination with aspirin [acetylsalicylic acid] and clopidogrel. His platelet counts were found in the range of 121-147x109/L and he was discharged good health condition. Fourteen days after the myocardial infarction, during last admission, he was normotensive and afebrile. His blood results showed WBC 3.2 x 109/L without myeloblasts in the peripheral blood smear, haemoglobin 108 g/L and erythrocyte count 3.45x1012/L; but, his platelet count was low at 32x109/L. His Brain MRI demonstrated acute right-sided parieto-occipital ischaemic stroke. His serological investigation results were negative for autoimmune disorders were negative. His indirect and direct antiglobulin test results were negative. Even though there were no signs of haemolysis and peripheral blood smear showed no presence of shistocyte, a possibility of acquired thrombotic thrombocytopenic purpura was considered. Based on his laboratory test results and considering his pervious exposure to heparins, possibility of delayed onset heparin-induced thrombocytopenia was considered. On the second day of hospitalisation, an enzyme-linked immunosorbent assay showed negative results and subsequently he underwent 4T risk score evaluation. Risk of heparin-induced thrombocytopenia was still considered as his 4T score was found to be 6 (a more than 50% fall in platelet count: 2 points, arterial thrombosis: 2 points, timing of thrombocytopenia more than 10 days: 1 point and other possible causes of