American Society of Hematology

Figure 2

$Figure 2. Clinical case 2. A 68-year-old man sought medical help at the emergency unit of his local hospital because of weakness, bone pain, and night sweats over several weeks. He was admitted because of HL of ∼170 000/µL, anemia, and thrombocytopenia. After the diagnosis of AML M4 was made, HU and cytarabine were started, and the patient was transferred to our hospital, presenting with a WBC count 70 000/µL and central neurologic deficits with speech impairment. A magnetic resonance imaging (MRI) scan showed several meningeal lesions, but the cerebrospinal fluid cell count was normal, and infection parameters were negative. In order to avoid cerebrospinal fluid contamination with leukemic blasts, lumbar puncture was postponed until peripheral blast clearance. We continued cytarabine induction and added daunorubicin for 3 days. WBC counts declined rapidly after initiation of cytarabine; the patient’s ability to speak improved gradually, and a control MRI 7 days after admission showed multiple hemorrhagic lesions, most pronounced in the hemispheres, with no signs of extramedullary leukemic lesions or meningeosis (A). In the consecutive aplasia, our patient developed Escherichia coli septicemia and Systemic Inflammatory Response Syndrome (SIRS) requiring epinephrin support. Early response assessment revealed persisting AML in the bone marrow. After having recovered from the sepsis, he developed a rapid relapse with WBCs rising up to 150 000/µL within 1 week (B,C). Intermediate-dose cytarabine plus mitoxantrone was administered as salvage treatment. In the consecutive aplasia, our patient received allogeneic stem cell transplantation from a matched unrelated donor after reduced-intensity conditioning with busulfan and fludarabin, leading to a rapid engraftment and the establishment of a stable donor chimerism. This case is highly suggestive for cerebral manifestations of leukostasis, possibly associated with extravasation and extramedullary infiltration of myeloid blasts. Primary refractory disease could be overcome by higher-dose cytarabine salvage treatment, and sustained response of this high-risk disease could be achieved by allogeneic stem cell transplantation. (A) T2-weighted axial plane of cranial MRI scan showing multiple brain hemorrhages (in correlation with other sequences) at the stage of extracellular methemoglobin with marked perifocal edema. (B) Peripheral-blood sample from patient 2 at hyperleukocytotic relapse (containing EDTA for anticoagulation). Cell settlement revealed a pronounced buffy coat containing excessive numbers of leukemic cells (left tube) as opposed to blood from an age-matched healthy man (right tube). (C) Peripheral-blood smear of patient 2 at hyperleukocytotic relapse (May-Grünwald and Giemsa stain, ×400) showing numerous myeloid blasts with wide cytoplasm and large euchromatin-containing nuclei with 1 or more nucleoli.$

Clinical case 2. A 68-year-old man sought medical help at the emergency unit of his local hospital because of weakness, bone pain, and night sweats over several weeks. He was admitted because of HL of ∼170 000/µL, anemia, and thrombocytopenia. After the diagnosis of AML M4 was made, HU and cytarabine were started, and the patient was transferred to our hospital, presenting with a WBC count 70 000/µL and central neurologic deficits with speech impairment. A magnetic resonance imaging (MRI) scan showed several meningeal lesions, but the cerebrospinal fluid cell count was normal, and infection parameters were negative. In order to avoid cerebrospinal fluid contamination with leukemic blasts, lumbar puncture was postponed until peripheral blast clearance. We continued cytarabine induction and added daunorubicin for 3 days. WBC counts declined rapidly after initiation of cytarabine; the patient’s ability to speak improved gradually, and a control MRI 7 days after admission showed multiple hemorrhagic lesions, most pronounced in the hemispheres, with no signs of extramedullary leukemic lesions or meningeosis (A). In the consecutive aplasia, our patient developed Escherichia coli septicemia and Systemic Inflammatory Response Syndrome (SIRS) requiring epinephrin support. Early response assessment revealed persisting AML in the bone marrow. After having recovered from the sepsis, he developed a rapid relapse with WBCs rising up to 150 000/µL within 1 week (B,C). Intermediate-dose cytarabine plus mitoxantrone was administered as salvage treatment. In the consecutive aplasia, our patient received allogeneic stem cell transplantation from a matched unrelated donor after reduced-intensity conditioning with busulfan and fludarabin, leading to a rapid engraftment and the establishment of a stable donor chimerism. This case is highly suggestive for cerebral manifestations of leukostasis, possibly associated with extravasation and extramedullary infiltration of myeloid blasts. Primary refractory disease could be overcome by higher-dose cytarabine salvage treatment, and sustained response of this high-risk disease could be achieved by allogeneic stem cell transplantation. (A) T2-weighted axial plane of cranial MRI scan showing multiple brain hemorrhages (in correlation with other sequences) at the stage of extracellular methemoglobin with marked perifocal edema. (B) Peripheral-blood sample from patient 2 at hyperleukocytotic relapse (containing EDTA for anticoagulation). Cell settlement revealed a pronounced buffy coat containing excessive numbers of leukemic cells (left tube) as opposed to blood from an age-matched healthy man (right tube). (C) Peripheral-blood smear of patient 2 at hyperleukocytotic relapse (May-Grünwald and Giemsa stain, ×400) showing numerous myeloid blasts with wide cytoplasm and large euchromatin-containing nuclei with 1 or more nucleoli.

This Feature Is Available To Subscribers Only