Srpski arhiv za celokupno lekarstvo 2015 Volume 143, Issue 11-12, Pages: 734-738
https://doi.org/10.2298/SARH1512734C
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Acute myocardial infarction during induction chemotherapy for acute MLL t(4;11) leukemia with lineage switch and extreme leukocytosis
Čolović Nataša (School of Medicine, Belgrade + Clinical Center of Serbia, Clinic of Hematology, Belgrade)
Bogdanović Andrija (School of Medicine, Belgrade + Clinical Center of Serbia, Clinic of Hematology, Belgrade)
Virijević Marijana (Clinical Center of Serbia, Clinic of Hematology, Belgrade)
Vidović Ana (School of Medicine, Belgrade + Clinical Center of Serbia, Clinic of Hematology, Belgrade)
Tomin Dragica (School of Medicine, Belgrade + Clinical Center of Serbia, Clinic of Hematology, Belgrade)
Introduction. In patients with acute leukemias hemorrhage is the most
frequent problem. Vein thrombotic events may appear rarely but arterial
thromboses are exceptionally rare. We present a patient with acute leukemia
and bilateral deep leg vein thrombosis who developed an acute myocardial
infarction (AMI) during induction chemotherapy. The etiology and treatment of
AMI in patients with acute leukemia, which is a rare occurrence, is
discussed. Case Outline. In April of 2012 a 37-year-old male presented with
bilateral deep leg vein thrombosis and malaise. Laboratory data were as
follows: Hb 118 g/L, WBC 354x109/L (with 91% blasts in differential leukocyte
count), platelets 60Ч109/L. Bone marrow aspirate and immunophenotype revealed
the presence of acute lymphoblastic leukemia. Cytogenetic analysis was as
follows: 46,XY,t(4;11)(q21:q23) [2]/62-82,XY,t(4;11)[18]. Molecular analysis
showed MLL-AF4 rearrangement. The patient was on low molecular weight heparin
and combined chemotherapy according to protocol HyperCVAD. On day 10 after
chemotherapy he got chest pain. Three days later AMI was diagnosed (creatine
kinase 66 U/L, CK-MB 13U/L, troponin 1.19 μg/L). Electrocardiogram showed the
ST elevation in leads D1, D2, aVL, V5 and V6 and “micro q” in D1. On
echocardiography, hypokinesia of the left ventricle and ejection fraction of
39% was found. After recovering from AMI and restoring left ventricle
ejection fraction to 59%, second course of HyperCVAD was given. The control
bone marrow aspirate showed 88% of blasts but with monoblastic appearance.
Flow cytometry confirmed a lineage switch from lymphoblasts to monoblasts. In
further course of the disease he was treated with a variety of
chemotherapeutic combinations without achieving remission. Eventually,
palliative chemotherapy was administered to reduce the bulk of blasts. He
died five months after the initial diagnosis. Conclusion. AMI in young adults
with acute leukemia is a very rare complication which may occur in patients
with very high white blood cell count in addition with presence of a CD56
adhesion molecule and other concomitant thrombophilic factors. The treatment
of AMI in patients with acute leukemias should include antiplatelet and
anticoagulant therapy, even with more aggressive methods depending on
patient’s age and clinical risk assessment.
Keywords: acute myeloid leukemia, chest pain, myocardial infarction, chemotherapy, leukocytosis
Projekat Ministarstva nauke
Republike Srbije, br. 41004