12th Congress of the European Hematology ... - Haematologica

12 th Congress of the European Hematology Association
1529
EXTRAMEDULLARY RELAPSE AFTER ALLOGENIC BONE MARROW TRANSPLANTATION
IN THREE PATIENTS DIAGNOSED OF ACUTE MYELOBLASTIC LEUKEMIA
J. López, P. Martin, S. Jiménez, C. Campo, A. Suárez, R. Mataix,
T. Molero, S. Iglesia, M.T. Gomez Casares
Hospital Dr. Negrin G.C., ARUCAS, Spain
Background. Extramedullary relapses of tumors composed of malignant
myeloid cells after allogenic bone marrow transplantation are uncommon.
In fact, there is little known about biology, treatment or prognosis
of this kind of tumors. Aims. Due to the fact of being exceptional, we
expose three cases of Acute Myeloblastic Leukemia diagnosed patients,
who suffered this type of relapse after allogenic bone marrow transplantation.
Methods. We studied three patients diagnosed of acute
myeloblastic leukemia (M6, M1 and M4 FAB classification). Two of
them showed complex cariotype (45,XX,-7 and 47,XY,inv(16)(p13q22))
and all of them were in molecular complete chimerism. They suffered
extramedullary relapse (granulocytic sarcoma) after allogenic bone marrow
transplantation. Results. In our experience and reviewing the bibliography,
extramedullary relapses after allogenic bone marrow transplantation
in acute myeloblastic leukemia are scarce. This kind of relapse
is usually related to M2 subtype, but it has also been described in M3,
M4 and M5 FAB subtypes. In this case, one of our patients was diagnosed
of M4 acute myeloblastic leukemia. As a matter of fact, two of
the patients showed cytogenetics alterations known to be linked to this
type of tumors: monosomy of chromosome 7 and inversion of chromosome
16. Conclusions. Generally speaking, extramedullary granulocytic
sarcoma is very rare as a way of relapse after allogenic bone marrow
transplantation in acute myeloblastic leukemia. In most cases, it appears
at diagnosis of acute myeloblastic leukemia or during its follow-up. We
describe three cases with this unusual presentation, not only because of
the timing but also because of the location( central nervous system and
breasts). It is also important to note the different evolutions that patients
have followed; two of them in complete remission and one exitus.
1530
CONTINUOUS INFUSION OF FLAG AND IDARUBICIN FOR PATIENTS YOUNGER THAN 60
YEARS WITH RESISTANT ACUTE MYELOID LEUKEMIA
H. Kim, 1 J.-H. Park, 1 J.-H. Lee, 2 J.-H. Lee, 2 Y.-D. Joo, 3 W.-S. Lee, 3
S.-H. Bae, 4 K.H. Lee2 1 Ulsan University Hospital, ULSAN, South-Korea; 2 Asan Medical Center,
SEOUL, South-Korea; 3 Busan Paik Hospital, BUSAN, South-Korea; 4 Daegu
Catholic University Hospital, DAEGU, South-Korea
Continuous infusion (CI) of cytarabien and fludarabine can accentuate
drug activities. We studied the feasibility and the efficacy of fludarabine
and cytarabin as a continuous infusion plus idarubicin for resistant
AML under 60 years old. Inclusion criteria were AML except for acute
promyelocytic leukemia, patients with resistant acute myeloid leukemia
(failure to achieve CR after initial induction chemotherapy including
standard dose cytarabine; early relapse, occurring after a first CR lasting
less than 12 months; relapse after allogeneic hematopoietic stem cell
transplantation [SCT]; relapses more than 2 times). Induction
chemotherapy consists of idarubicin 12 mg/m 2 iv infusion (day 1- 3), fludarabine
30 mg/m 2 /d and Cytarabine 1000 mg/m 2 /d (day 1-5) as a 24hour
CI. G-CSF was added on day 1-5. More 3 cycles of FLAG as CI
were followed for consolidation. All 24 patients were enrolled. Median
age was 38.5 (18-57). Disease status were primary refractory in 5
(20.8%), early relapse in 17 (70.8%), multiple relapse in 1 (4.2%), and
relapse after SCT in 1 (4.2%). Translocation (8;21) and variants (8,
33.3%) and 2 or 3 abnormalities (5, 20.8%) were most common chromosomal
abnormalities. Twenty two patients (91.7%) could complete
induction. Hematological recoveries were follows: ANC > 500/mm 3 in
11 (45.8%, median 29 days); ANC >1000/mm 3 in 11 (45.8%, median 32
days); platelet >20K/mm 3 in 9 (37.5%, median 29 days); platelet
>100K/mm 3 in 4 (16.7%, median 43 days). Response for induction were
CR in 7 (29.2%), CRp in 1 (4.2%), and treatment failure in 16 (66.7%,
aplasia in 13, indeterminate course in 3). Median days required for CR
was 42 (37-63) days. Consolidation stopped in 7/8: 5 patients underwent
SCT; 1 patient died during consolidation; 1 patient stopped due to toxicity.
Six patients are alive. Seventeen patients died of induction aplasia
(13), toxicity during consolidation (1), relapse after SCT (3). Autolous
SCT performed in 2 and allogeneic SCT in 4. Median overall survival in
all and CR patients were 2.47 (0.67-4.26) and 11.38 (3.12-19.64) months,
respectively. Relapse after autologous SCT in 2/2 and after allogeneic
542 | haematologica/the hematology journal | 2007; 92(s1)
SCT in 2/4. Median event-free and disease-free survival were 2.47 (0.66-
4.28) and 8.32 months, respectively. Continuous infusion of FLAG plus
idarubicin showed high toxic deaths during induction chemotherapy.
Conventional infusion schedule will be more suitable for resistant AML.
1531
HEMATOPOIETIC COLONY STIMULATING FACTORS CAN CAUSE CATARACT
S. Al Jaouni, H. Al Jedani
King Abdulaziz University, JEDDAH, Saudi Arabia
Background. Granulocyte-colony stimulating factor (G-CSF) is a lineage-restricted
hematopoietic growth factor as it induces proliferation
and maturation of neutrophilic precursors and progenitors, mobilizes
myeloid progenitors into peripheral blood and activates neutrophil
functions. Other cells like stromal cells and endothelial cells are activated
too. It has been used to ameliorate or prevent profound neutropenia
and its consequences. Congenital neutropenia such as Kotsmann’s
or Schwachmann-Diamond syndromes are associated with severe neutropenia,
which causes serious infectious complications that may be life
threatening. CSF therapy in these disorders showed increased number
of circulating neutrophils and improvement of infectious complications.
Aim. Awareness of the uncommon side effect of high dose G-CSF.
Method. Two-years-old boy who had repeated admission to the Hospital
due to febrile illnesses and infection, associated with severe neutropenia
in the range of 0.1-0.3×109 /L since early infancy. Bone marrow
aspiration was consistent with the diagnosis of Kotsmann’s syndrome
disease. Other reasons of neutropenia and immune deficiency were
excluded. The patient received granulocyte-colony stimulating factor
(G-CSF) and three times granulocytes monocytes-colony stimulating
factor (GM-CSF) in a dose of subcutaneous 5 microgram/kilogram body
weight (mcg/kg per day) during admission then once weekly for 7
months and neutrophil count was maintained in the range of 0.3 ' 0.6
×109 /L. This dose was increased to 15 mcg/kg per day weekly but no
increase in neutrophil count was observed. After 3 months of the high
dose of the G-CSF, the patient developed bilateral eye cataract more at
the left eye that required left lensectomy and its histological evaluation
revealed chronic inflammation, many macrophages and some fibrosis
and there were no positive cultures for the lens tissues. Discussion and
Results. G-CSF can raise the granulocytes count and its usage is usually
with febrile neutropenia and infections. The dose required for congenital
neutropenia is usually 5-12 microgram/kg/day, the dose can be escalated
until adequate response. Small number of patients experience
bone pain during therapy. High dose of G-CSF can cause fever, rashes,
pericarditis and pleural effusion. In chronic sitting, thrombocytopenia,
splenomegaly, and vasculitis may be also seen at increased doses. GM-
CSF is a potent hemopoietic cytokine that stimulates stem cell proliferation
in the bone marrow and inhibits apoptotic cell death in leukocytes.
Transgenic mice expressing a hemopoietic growth factor gene
(GM-CSF) develop accumulations of macrophages, blindness, and a
fatal syndrome of tissue damage. Summary. High dose of G-CSF can
cause cataract. Regular opthalmological examination is needed. Higher
dose need close follow-up.
1532
DIAGNOSTIC UTILITY OF 18-FDG PET IN THE ASSESSMENT OF PATIENTS WITH MULTIPLE
MYELOMA
A. Jurczyszyn, 1 B. Malkowski, 2 A.B. Skotnicki3 1 University Hospital, CRACOW; 2 Centrum Onkologii Zaklad Medycyny Nuklea,
BYDGOSZCZ; 3 Department of Hematology University Hosp, CRACOW,
Poland
Objective. The role of whole-body PET with 18-FDG in detection of
bone marrow involvement in patients with multiple myeloma was evaluated.
The presence of extramedullary plasmocytomas and distribution
of diffuse or focal lesions in the bones was also detected. Materials and
methods. Between November 2006 and February 2007 the whole-body
FDG PET scans (60 min after intravenous administration of 370-555
MBq FDG) were performed in 15 patients (age 51-71, median 59 years,
5 males) with multiple myeloma. Five patients were referred before
therapy and ten patients were referred for evaluation of therapy
response (chemotherapy, radiation therapy, bone marrow transplant).
Standardized uptake values were obtained to quantify FDG uptake.
Results of other imaging examinations (MRI, CT, radiography), laboratory
data, bone marrow biopsies and the clinical course were used for
verification of detected lesions. Results. FDG PET was able to detect