OBJECTIVE:Myelodysplastic syndrome (MDS) is a clonal hematopoietic stem cell disease. Patients are at risk of developing cytopenias or progression to acute myeloid leukemia. Different classifications and prognostic scoring systems have been developed. The aim of this study was to compare the different prognostic scoring systems.MATERIALS AND METHODS:One hundred and one patients who were diagnosed with primary MDS in 2003-2011 in a tertiary care university hospital's hematology department were included in the study.RESULTS:As the International Prognostic Scoring System (IPSS), World Health Organization Classification-Based Prognostic Scoring System (WPSS), MD Anderson Prognostic Scoring System (MPSS), and revised IPSS (IPSS-R) risk categories increased, leukemia-free survival and overall survival decreased (p<0.001). When the IPSS, WPSS, MPSS, and IPSS-R prognostic systems were compared by Cox regression analysis, the WPSS was the best in predicting leukemia-free survival (p<0.001), and the WPSS (p<0.001) and IPSS-R (p=0.037) were better in predicting overall survival.CONCLUSION:All 4 prognostic systems were successful in predicting overall survival and leukemia-free survival (p<0.001). The WPSS was found to be the best predictor for leukemia-free survival, while the WPSS and IPSS-R were found to be the best predictors for overall survival.

Objective: Many studies reported an improved prognosis in patients with Burkitt's lymphoma obviating the need of stem cell transplantation. However, prognosis of the advanced disease [i.e. Burkitt's cell leukemia (BCL)] has not been reported with current treatment modalities except for a few prospective trials. The aim of this study is to compare the prognoses of BCL patients with similarly treated and nontransplanted patients with other types of acute lymphoblastic leukemia (ALL) and with ALL patients that underwent allogeneic stem cell transplantation (ASCT) in their first remissions.Materials and Methods: In this retrospective analysis, BCL patients aged between 16 and 63 who were admitted between 2000 and 2014 to the hospitals of Hacettepe or Gazi University and were treated with intensive therapies aimed at cure were included. All ALL patients who were treated with a similar protocol not including transplantation during the same period (NT-ALL group) and all ALL patients who underwent ASCT in the first complete remission during the same period (T-ALL group) served as control groups.Results: The central nervous system or extramedullary involvement rates, lactate dehydrogenase levels, and white blood cell counts at diagnosis were higher in the BCL group than the NT-ALL group and these differences were significant. BCL patients had disease-free survival (DFS) durations comparable with the T-ALL cohort but NT-ALL patients had significantly shorter DFS durations. Both cumulative relapse incidence and cumulative nonrelapse mortality were higher in NT-ALL patients compared to the T-ALL group and BCL patients.Conclusion: DFS in BCL patients treated with a widely accepted modern regimen, R-HyperCVAD, is comparable to results in other ALL patients receiving allogeneic transplantation. Our results are in agreement with a few prospective noncomparative studies suggesting no further need for stem cell transplantation in BCL.

We admire the efficiency of the authors asking, “Is dasatinib really a safe choice for imatinib-induced rhabdomyolysis?” and their kind efforts spent on the evaluation of our article. On the other hand, we do have some objections to their comments. First, the authors describe our patient’s clinical condition as hyperCKemia instead of rhabdomyolysis. However, according to the recently updated data, the diagnosis of rhabdomyolysis was made with either an acute neuromuscular illness or dark urine without other symptoms plus an acute increase in serum creatine kinase (CK). There is no certain cutoff level for CK that can be identified, and the CK should be taken into account, with the clinical context of the history and examination findings. Also, there are several issues that should be taken into account during the diagnosis. For instance, muscle biopsy, electromyography, and magnetic resonance imaging are generally not required for the diagnosis of rhabdomyolysis. Furthermore, altered serum calcium and phosphorus levels are not required for the diagnosis of rhabdomyolysis, and abnormal urine analysis is not a “must” for the diagnosis either. The reddishbrown urine of myoglobinuria is observed in only half of the cases, and thus, its absence does not exclude the diagnosis. The triad of rhabdomyolysis is myalgia, weakness, and myoglobinuria; however, this triad is only detected in <10% of cases. Moreover, we have performed the Naranjo algorithm that confirms that these clinical findings are related to the adverse drug reaction. From our point of view, the comments of Uz and Dolasik are more likely related to the Crush syndrome. Urine myoglobin, serum creatine phosphokinase, and serum electrolyte data are necessary in the laboratory evaluation of Crush syndrome. Myoglobinuria and/or hematuria and laboratory values of CK of 10 000 U/L, oliguria (urine output 400 mL/24 h), and elevated blood urea nitrogen (40 mg/dL), serum creatinine (2 mg/ dL), uric acid (8 mg/dL), potassium (6 mg/dL), or phosphorus (8 mg/dL) and a decreased serum calcium (8 mg/dL) are generally observed in Crush syndrome. To conclude, for all these reasons, we preferred to name our patients’ clinical condition “rhabdomyolysis” instead of “hyperCKemia.” Second, the authors have commented that nilotinib is a safer choice in comparison to dasatinib for those chronic myeloid leukemia (CML) patients who have experienced rhabdomyolysis with imatinib. However, in the literature in English, there are reports indicating that dasatinib can be safely used in patients who have experienced rhabdomyolysis. Augustyn et al and our group had administered dasatinib to CML patients with rhabdomyolysis, and there were no complications, including CK increase, in the clinical and laboratory follow-up of the patients. Nevertheless, we agree with Uz and Dolasik that if there is rhabdomyolysis in a given CML patient who has been using imatinib, one of the second-generation TKIs (tyrosine kinase inhibitors), including nilotinib, could be administered to the patient. The choice between nilotinib and dasatinib should be made with the clinical background in mind because the management of CML patients depends on personalized treatment as well as evidence-based medicine.

The aim of this report is to describe a newly diagnosed chronic myeloid leukemia (CML) patient who had imatinib mesylate (IM)-induced rhabdomyolysis and tolerated the second-generation tyrosine kinase inhibitor (TKI) dasatinib that controlled CML disease progression without precipitating the already present muscle damage. A 42-year-old man was admitted to the local hospital with left lumbar region pain. He had polycystic kidney disease, and leukocytosis in the routine tests had been observed. The patient admitted to our hematology outpatient unit for the evaluation of leukocytosis. After the investigations, he had been diagnosed as de novo chronic phase CML. In June 2014, he had been given IM 400 mg once a day. He was not taking any other drug. Pain began in both lower extremities 15 days after the start of medication. The patient’s baseline creatinine level was 1.5 mg/dL before the admission. The laboratory tests were as follows: creatinine 1.4 mg/dL, serum calcium and phosphorus levels in normal range, and creatine kinase (CK) levels 1533 U/L. Therefore, the patient was diagnosed as having rhabdomyolysis. The urine was clear in appearance, yellow colored, with a pH of 5, density 1010, protein glucose bilirubin ketone nitrite negative, and urobilinogen normal, with a few erythrocytes and leukocytes. Other causes of rhabdomyolysis (trauma or direct injury, excessive muscle activity, hereditary muscle enzyme defects, drugs and toxins, muscle hypoxia, metabolic and endocrine disorders, infections, temperature alterations, myocardial infarction, and stroke) were ruled out, and rhabdomyolysis was considered to have been caused by IM. We performed the Naranjo algorithm, and the score was 9 points. Therefore, IM treatment was stopped and secondgeneration TKI (dasatinib) was given instead. We preferred dasatinib because there are trials that confirmed the efficiency of dasatinib in patients with imatinib intolerance. Nilotinib could have also been used; however, its molecular mimicry cast doubts that it might cause the same intolerance and/or adverse events in terms of rhabdomyolysis. Two weeks after IM withdrawal, the pain in the patient’s extremities decreased, and CK levels were 195 U/L. His real-time polymerase chain reaction (PCR) analysis revealed that the disease was controlled with dasatinib treatment, and CK levels remained in normal ranges (Figure 1). He is still on follow-up with dasatinib in our clinic, without any sign of rhabdomyolysis. CML is a slowly progressive clonal malignant disease characterized by myeloid neoplastic expansion with heterogeneous clinical manifestations. CML could be functionally cured by the TKI drugs. IM is the first TKI to be used widely for CML treatment. Diarrhea, edema, myalgia, and skin reactions are common side effects of IM. In one previous study, myalgia occurred in 39% versus 22% of newly diagnosed chronic-phase CML patients who were treated with imatinib and dasatinib, respectively. Rarely, IM-induced rhabdomyolysis cases have been reported. Myalgia is a common side effect of IM. However, rhabdomyolysis with CK elevations is quite rare. In such a patient with CML, IM should be discontinued, and second-generation TKIs (such as dasatinib) should be administered. Because rhabdomyolysis recurs with the reintroduction of IM, the patient should be followed up while under secondgeneration TKIs. Dasatinib treatment could be used as an alternative TKI, so that CML remains under control during the rhabdomyolysis phase, and dasatinib does not precipitate the muscle damage with imatinib already present. It would have been better if we had investigated the plasma levels of imatinib in our patient; however, we failed to perform the plasma analyses. The interrelationships between IM and CK elevations are not well known. Some researchers suggest that IM-induced electrolyte imbalance is the reason for CK elevations. However, although our patient had polycystic kidney disease and creatinine levels of 1.4 mg/dL, he had no electrolyte imbalance. Monitoring the CML disease and TKI drug off-target risks are vital in clinical practice. Expected hematological, cytogenetic, and molecular responses to those drugs during the monitoring of CML vary based on some parameters. These parameters are the disease phase, mutational status, resistance profile, molecular BCR-ABL dynamics, compliance, patient drug adherence, and drug adverse effects. If there is myalgia with muscle weakness after the initiation of IM, rhabdomyolysis should be considered. No reports of rhabdomyolysis occurred during the clinical trial conducted for imatinib approval; however, postmarketing surveillance has captured some case reports of rhabdomyolysis. We have compared such cases in Table 1. In these cases, CK; complete blood count, including differential and platelet count; blood urea nitrogen; creatinine; routine electrolytes, including potassium, calcium, 579425 AOPXXX10.1177/1060028015579425Annals of PharmacotherapyMalkan et al research-article2015

Thank you very much for your valuable comments and sharing your experience. We agree for your contribution. In thalassemia patients, several transplantation centers categorised risk factors prior to allogenic hematopoietic stem cell transplantation. Pesaro classification assigned patients to three arms according to the absence or presence of one, two or three risk factors: hepatomegaly > 2 cm, portal fibrosis, and irregular chelation history [1]. It should be kept in mind that in a study by Ghavamzadeh et al., liver iron overload did not change after transplant (p=0.61) but hepatic fibrosis progressed (p=0.01) [2]. Allogeneic stem cell transplantation did not reduce liver iron overload and in fact liver fibrosis increased. Also steps for reducing iron overload should be taken in the post transplant setting [3]. Iron overload is still an essential issue in both pre and post transplant settings. Survival in transfusion-dependent thalassemia patients can be improved with proper understanding of the pathophysiology of thalassemia and iron toxicity.

Abstract Introduction: Interferon (IFN-α) is frequently used in various hematologic neoplastic disorders either at failure of first-line treatment or as first-line therapy in selected patients. IFN-α has shown significant activity in treatment, but the therapy is handicapped by high dropout rates due to side effects and cumbersome dosing schedules. Pegylated (peg) IFN- α is formulated by the covalent binding of one 40 kDa branched PEG-polymer to a lysine side chain of IFN- α. This modification prolongs serum half-life and patient exposure to medicine, decreases renal excretion, thus allowing for weekly administration, acceptable toxicity, tolerability and activity profiles. The results of peg-IFN in polycythemia vera (PV) and essential thrombocythemia (ET) in phase 2 studies are encouraging, with molecular responses in some patients. There is at least one phase 3 study of hydroxyurea versus peg-IFN as first-line cytoreductive therapy for PV. In spite of ongoing international efforts to evaluate peg-IFN in PV, there is limited experience on peg-IFN use in other hematologic neoplasms. Method: <>All patients who were put on peg-IFN in our center were found in our institutional electronic database. The patients had been recorded prospectively. All patients who had been treated with peg-IFN had been approved by national health authority and all patients had given informed written consent. Responses were evaluated by ELN (chronic myeloid leukemia), IWG-MRT (PV and ET), EUMNET (myelofibrosis), Nordic proposal criteria (hypereosinophilic syndrome), modified consensus criteria (systemic mastocytosis) (Am. J. Hematol 2009;84:790), Cheson criteria (lymphomatoid granulomatosis) and PET response criteria (Erdheim Chester disease) standardized criteria. Adverse effects were classified according to Common Terminology Criteria for Adverse Events (CTCAE4.0). Categorical and continuous data were expressed as ratio (%) and median (range). Statistical analyses were done by SPSS v17 (Chicago, IL). Results: There were 30 patients with 8 different hematologic neoplasms: 12 PV, 6 ET, 2 chronic myeloid leukemia (CML), 3 systemic mastocytosis (SM), 4 Erdheim-Chester disease (ECD), 1 primary myelofibrosis (PM), 1 hypereosinophilic syndrome (HES), and 1 lymphomatoid granulomatosis (LG). Detailed descriptive data, toxicity and treatment results are presented in table 1. Responses were observed in all disease categories. Toxicities were frequent in PV/Et, including significant autoimmune disorders (nephritic syndrome, autoimmune hepatitis) Conclusion: Peg-IFN is effective in many hematologic neoplastic disorders. Unfortunately, toxicity is a major concern in this treatment. Disclosures No relevant conflicts of interest to declare.

Phosphatidylinositol 3-kinases (PI3Ks) are considered as lipid kinases that are very active in the pathobiology of lymphoproliferative disorders (LPDs). Idelalisib, a selective inhibitor of the delta isoform of PI3K, provides significant clinical efficacy and has an acceptable side-effect profile in the treatment of B-LPDs. The aim of this review is to outline the pharmacobiological basis of idelalisib that is located at the crossroads of B-LPDs. The PI3K signaling pathway with downstream targets including Akt is involved in hematologic malignancies and lymphomas. Idelalisib has been most widely studied in chronic lymphoid leukemia (CLL) and B-lymphoma. The activity of idelalisib in high-risk FL with early relapse following front line immunochemotherapy was recently shown. The unique immunological toxicity pattern of idelalisib was also decribed in this review. Further clinical investigations will help for the better selection of the subsets of the patients with B-LPD that would be best candidates for the clinical utilization of idelalisib. Other indications such as marginal zone lymphoma, mantle cell lymphoma, Waldenstrom's Macroglobulinemia and other B-cell disorders could likely to be expanded. Future clinical and experimental data combined with the next-generation genomics strategies and personalized medicine for the treatment of malignant disorders will enlightened us for better placement of idelalisib in the treatment algorithm of the patients.

Ruxolitinib as a JAK1 and JAK2 inhibitor drug has recently been approved for the treatment of patients with highor intermediate-risk myelofibrosis with symptomatic splenomegaly. Clinical development of ruxolitinib has currently focused on the Ph* negative myeloproliferative neoplastic disorders (MPN). The aim of this study is to assess the impact of ruxolitinib treatment on the clinical course of Ph* negative myeloproliferative disorders. Forty-three patients who were under ruxolitinib treatment and followed-up between years 1987-2015 in Hacettepe University Medical School Hematology Clinic and Ondokuz Mayis University Hematology Clinic with myeloproliferative disease without Philadephia chromosome translocation were retrospectively analyzed. The constitutional symptoms were decreased in 97% of patients after ruxolitinib treatment. The mean spleen sizes before and after ruxolitinib treatment were 229±35 versus 202±31 mm, respectively (p< 0.001). In this study, we observed a reduction in spleen size after ruxolitinib treatment in Turkish patients with MPN and this reduction was statistically significant. Moreover, nearly all of the MPN patients’ constitutional symptoms were improved. Those observations are concordant with other geographical MPN data obtained from different countries. Further experimental and clinical studies into the efficacy and safety of ruxolitinib in patients with MPN are necessary to elucidate its role in special subgroups of MPN patients, such as patients undergoing hematopoietic stem cell transplantation and the patients with vascular disorders such as hepatoportal thrombosis.

Objective: Multiple myeloma (MM) is currently incurable due to refractory disease relapse even under novel anti-myeloma treatment. In silico studies are effective for key decision making during clinicopathological battles against the chronic course of MM. The aim of this present in silico study was to identify individual genes whose expression profiles match that of the one generated by cytotoxicity experiments for bortezomib.Materials and Methods: We used an in silico literature mining approach to identify potential biomarkers by creating a summarized set of metadata derived from relevant information. The E-MTAB-783 dataset containing expression data from 789 cancer cell lines including 8 myeloma cell lines with drug screening data from the Wellcome Trust Sanger Institute database obtained from ArrayExpress was "Robust Multi-array analysis" normalized using GeneSpring v.12.5. Drug toxicity data were obtained from the Genomics of Drug Sensitivity in Cancer project. In order to identify individual genes whose expression profiles matched that of the one generated by cytotoxicity experiments for bortezomib, we used a linear regression-based approach, where we searched for statistically significant correlations between gene expression values and IC50 data. The intersections of the genes were identified in 8 cell lines and used for further analysis.Results: Our linear regression model identified 73 genes and some genes expression levels were found to very closely correlated with bortezomib IC50 values. When all 73 genes were used in a hierarchical cluster analysis, two major clusters of cells representing relatively sensitive and resistant cells could be identified. Pathway and molecular function analysis of all the significant genes was also investigated, as well as the genes involved in pathways.Conclusion: The findings of our present in silico study could be important not only for the understanding of the genomics of MM but also for the better arrangement of the targeted anti-myeloma therapies, such as bortezomib.

The impacts of serum iron parameters and/or radiological evidence of systemic iron overload on the prognosis of hematopoietic stem cell transplantation (HSCT) in acute leukemia are controversial.Unfortunately, some of the studies evaluating iron overload in transplant setting did not precisely show the patients with iron overload, mainly due to ignoring consideration of transferrin saturation along with hyperferritinemia for elimination of non-iron overload etiologies of hyperferritinemia.The aim of this study is to assess the effect of iron overload on transplantation related complications and prognosis in acute leukemia.Patients who undergone allogeneic HSCT for acute leukemia in Hacettepe University Medical School Department of Hematology were screened retrospectively in order to find cases with serum iron tests within 9 months before transplant.The endpoints investigated were overall and disease-free survivals, acute and chronic graft-versus-host disease and veno-oclussive disease (VOD).There were 84 patients suitable for inclusion.When various ferritin plus transferrin saturation (TS) cut-off values were investigated for a possible relationship with major transplant-related complications/results only ferritin> 2000 plus TS> 45% was found to have an association with VOD at borderline significance (p= 0.067).In conclusion, we observed a non-significant borderline relationship between iron overload and post-transplant VOD.We did not confirm other post-transplant complications reported in the literature.It must be noticed that although many studies intended to investigate the relationship between iron status and transplant outcomes, only a few of them have really looked for the effect of iron overload.

Background/aim: To compare plasma vitamin D concentrations among patients with normal cognitive function (control group), mild cognitive impairment (MCI), and Alzheimer disease (AD).Materials and methods: In total, 158 patients with AD, 228 patients with MCI, and 603 control subjects were included. Plasma levels of 25-hydroxyvitamin D were measured after comprehensive geriatric assessment and compared among groups. SPSS 15.0 was used for statistical analysis.Results: Mean levels of 25-hydroxyvitamin D were significantly different among the 3 groups of AD patients, MCI patients, and controls (P < 0.001). Post hoc analysis revealed that the levels were significantly lower in the MCI group than the control group (P = 0.002) and significantly lower in the AD group than the control group (P = 0.003). Multivariate analysis showed that age (OR: 1.070, 95% CI: 1.025-1.116, P = 0.002), instrumental activities of daily living score (OR: 0.920, 95% CI: 0.850-0.995, P = 0.037), 25-hydroxyvitamin D level (OR: 0.959, 95% CI: 0.932-0.987, P = 0.004), and diabetes mellitus (OR: 2.476, 95% CI: 1.153-5.319, P = 0.020) were factors independently associated with AD.Conclusion: This study demonstrated that there is a correlation between plasma 25-hydroxyvitamin D levels and cognitive functions.

INTRODUCTION:Acquired erythroblastopenia (AE) is a rare clinical situation. It is characterized by the reduction of erythroid precursors in the bone marrow together with the low reticulocyte counts in the peripheral blood.BACKGROUND:Main secondary causes of AE are drugs, Parvovirus B19 and other infectious reasons, lymphoid and myeloid neoplasia, autoimmune diseases, thymoma and pregnancy. The aim of this study is to assess the frequencies and clinical associations of AE via analyzing 12340 bone marrow samples in a retrospective manner.MATERIAL AND METHOD:Bone marrow aspirations which were obtained from patients who applied to Hacettepe University Hematology Clinic between 2002 and 2013, were analyzed retrospectively.RESULTS:Thirty four erythroblastopenia cases were found. Patients ranged in age from 16 to 80 years with a median of 38 years. Fifteen patients were men (44%) and nineteen were women (56%). In these patients, detected causes of erythroblastopenia were MDS, idiopathic pure red cell aplasia (PRCA), parvovirus infection, post chemotherapy aplasia, plasma proliferative diseases, copper deficiency due to secondary amyloidosis, fever of unknown origin, hemophagocytic syndrome, enteric fever and legionella pneumonia. We found that between those reasons the most common causes of erythroblastopenia are MDS (17.7%) and idiopathic PRCA (17.7%).DISCUSSION:As a result, erythroblastopenia in the bone marrow may be an early sign of MDS. In those AE cases possibility of being MDS must be kept in mind as it can be mistaken for PRCA.CONCLUSION:To conclude, in adults MDS without excess blast is one of the most common causes of erythroblastopenia in clinical practice and in case of erythroblastopenia the presence of MDS should be investigated.

e18005 Background: In acute leukemia (AL) relapse after allogeneic stem cell transplantation (ASCT) is a devastating complication. Although this problem has been well studied in the literature there are limited systematic data on extramedullary (EM) relapse. In this study we aimed to evaluate EM relapse in an AL and CML ASCT cohort including its patterns, cumulative incidence and risk factors. Methods: 131 ASCT patients (57 F, 74 M; median age, range: 35, 17-66; 51 ALL, 61 AML, 12 CML, 7 others) transplanted between June 2001 and September 2014 were analyzed retrospectively. Results: Types of transplantations were reduced intensity conditioning in 105 and myeloablative in 26 patients. The conditioning regimens were Bu/Flu/ATG, Mel/Flu, total body irradiation (TBI) based regimens, Bu/Cy, Bu/Flu and its variants. Relapse was observed in 53 patients. Types of the relapses were bone marrow (BM) in 31, BM and EM in 18 [14 central nervous system (CNS), 2 breast, 2 bone, kidney, and mediastinum 1 each] and isolated EM in 5 patients (2 bone, CNS, skin, testicle 1 each). Significantly more frequent EM relapses were observed in ALL compared to AML or CML, (chi-squared test, p = .02). Only-BM relapse and non-relapse mortality were accepted as competing risks for cumulative extramedullary relapse (CEMR) incidence. EM relapse and non-relapse mortality were considered as competing risks for cumulative only-BM relapse (CBMR) incidence. Estimated CBMR and CEMR incidences [ratio (standard error)] at 60 months were 13.6 (5.3) % and 29.3 (7.5) % in ALL, 26.9 (6) % and 10.8 (4.2) % in AML, and 47.9 (17.1) % and 10.4 (10.6) % in CML (competing risk analyzes by Gray’s test, p = .01 for CBMR incidence and p = .16 for CEMR incidence). Only type of conditioning regimen (p = .06) and GVHD status were found to be related with EM relapse risk. GVHD significantly decreased the EM relapse risk (Cox regression analysis, Exp(B) = 3.46, p = .01). EM relapse risk was lower with TBI-based regimens and significantly higher with Mel/Flu and its variants. Conclusions: EM relapse is quite frequent after ASCT, especially in ALL. GVHD and TBI-based regimens may prevent this devastating complication.

There are very few data about the relationship between acute myeloid leukemia (AML) prognosis and bone marrow recovery kinetics following chemotherapy. In this study, we aimed to assess the prognostic importance and clinical associations of neutrophil and platelet recovery rates and rebound thrombocytosis (RT) or neutrophilia (RN) in the postchemotherapy period for newly diagnosed AML patients. De novo AML patients diagnosed between October 2002 and December 2013 were evaluated retrospectively. One hundred patients were suitable for inclusion. Cox regression analysis using need for reinduction chemotherapy as a stratification parameter revealed RT as the only parameter predictive of OS, with borderline statistical significance (p = 0.06, OR = 7; 95% CI 0.92-53), and it was the only parameter predictive of DFS (p = 0.024, OR = 10; 95% CI 1.3-75). In order to understand whether RT or RN was related to a better marrow capacity or late consolidation, we considered neutrophil recovery time and platelet recovery time and nadir-first consolidation durations in all patients in the cohort. Both the marrow recovery duration and the time between marrow aplasia and first consolidation were shorter in RT and RN patients. To our knowledge, this is the first study to report a correlation between RT/RN and prognosis in AML.

There are some improvements in management of acute myeloid leukemia (AML). However, induction-induced deaths still remain as a major problem. The aim of this study is to assess clinical parameters affecting early death in patients with AML. 199 AML patients, who were treated with intensive, non-intensive or supportive treatment between 2002 and 2014 in Hacettepe Hematology Department, were analyzed retrospectively. In our study early death rate for elderly was found to be lower than previous reports whereas it was similar for those who were under age of 60. Better ECOG performance (ECOG performance score 0 and 1) and non-intensive treatment associated with lower early death rates, however APL-type disease associated with higher early death rates. ECOG performance score at diagnosis was found to be the most related independent factor with higher rate of early death in 15 days after treatment (P<0.001). Therefore we decided to understand the factors which were related with ECOG. WBC count at diagnosis was found to be the only related parameter with ECOG performance score. Leucocyte count at diagnosis appears like to have an indirect effect on early death in AML patients. It maybe suggested that in recent years there is an improvement in early death rates of elderly AML patients. The currently reported findings require prospective validation and would encourage the incorporation of other next generation genomics for the prediction of early death and overall risk status of AML.