Consistent Hypofibrinogenemia Associated with Induction Anti-Tumor Chemotherapy for Acute Myeloid Leukemia

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1400-1400
Author(s):  
Zeina G Elamil ◽  
Hande H. Tuncer ◽  
Roy Tara ◽  
Samer A. Al Homsi

Abstract Abstract 1400 Introduction: Hemostatic abnormalities are frequently encountered during initial presentation of acute myeloid leukemia (AML) as well as during induction treatment. Patients often present with decreased platelet counts and sometimes with abnormalities of the coagulation parameters with or without bleeding manifestations. In the absence of overt disseminated intravascular coagulopathy (DIC), transfusion practices during treatment are essentially based on the platelet count. Fibrinogen is an important element of the clotting mechanisms, constituting a template for both thrombin binding and the fibrinolytic system. We sought to determine the prevalence of altered serum fibrinogen levels during induction treatment in AML and its clinical significance. Methods: We prospectively measured serum fibrinogen on a daily basis in patients with newly diagnosed AML treated with induction anti-tumor chemotherapy at our institution from February 2007 to July 2010. Inclusion criteria included the diagnosis of AML and no overt DIC. Results: The study population included 17 patients (47% females) with mean age of 55.3 years (range 18 –80 years). At presentation, the mean platelet count was 62 × 109/L (range 3 – 252 × 109/L), the mean prothrombin time was 11.4 seconds (range 9.6–13.4 secs, normal range 10—13.7 secs), the mean international normalized ratio was 1.1 (range 0.9–1.3; normal range 0.9–1.1) and the mean activated partial thromboplastin time was 26.56 seconds (range 20.1–41 secs, normal range 22.3–34.0 secs). All patients had normal serum fibrinogen levels at presentation (mean 380.6 mg/dl; range 258–567 mg/dl; normal range 200–400 mg/dl). Thirteen patients were treated with idarubicin and cytarabine, 3 patients received a FLAG (fludarabine, cytarabine and G-CSF) regimen and one patient had amonafide and cytarabine. Serum fibrinogen levels were recorded on all patients on a daily basis (Figure 1). Nine (53%) developed hypofibrinogenemia on the fourth day of induction, 2 (12%) on day 5, 3 (17%) on day 6, 2 (12%) on day 7, and one (6%) on day 8 of the induction. Eight patients (47%) received prophylactic cryoprecipitate when the serum fibrinogen levels fell below 150 mg/dl. We did not observe a significant trend difference in serum fibrinogen levels between patients who received cryoprecipitate and those who did not. Serum fibrinogen levels were back to normal without transfusion support by day 6 for one patient (5.88 %), day 7 for 2 patients (11.76 %), day 8 for 3 patients (17.65 %), day 9 for one patient (5.88 %), day 10 for one patient (5.88 %), day 11 for 3 patients (17.65 %), day 12 for 6 patients (35.3 %). Conclusion: Patients with acute myeloid leukemia receiving induction chemotherapy may frequently develop isolated hypofibrinogenemia without evidence of disseminated intravascular coagulation. This finding is usually self-limited and disappears shortly after the completion of antitumor chemotherapy, usually by day 12. The mechanism of this under-recognized phenomenon is unclear. Its common occurrence raises questions about the appropriateness of transfusion practices in AML based solely on the platelet count and argues in favor of the need of more global tests such as thromboelastography. Disclosures: No relevant conflicts of interest to declare.

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4896-4896 ◽  
Author(s):  
Luisa C A Koury ◽  
Lorena Lobo Figueiredo-Pontes ◽  
Belinda Pinto Simoes ◽  
Luciana C O Oliveira ◽  
Leandro F F Dalmazzo ◽  
...  

Abstract The overexpression of P-glycoprotein (Pgp) in leukemic blasts of Acute Myeloid Leukemia (AML) is associated with lower complete remission (CR) rates and shorter disease-free (DFS) and overall survival (OS). Cyclosporine A (CSA) is a competitive inhibitor of Pgp capable of reduce the P-gp mediated drug efflux. List et al. reported that CSA addition to treatment with cytarabine and daunorubicine reduced the resistance to induction treatment (IT) and prolonged DFS and OS. The effect was greater in AML patients with higher Pgp expression (Blood 2001; vol 98, n 12: 3212-20). Based on this study, we tested the effect of the association of CSA to IT in cases with high Pgp expression, which was established using the Rhodamine effux test as previously described (Pétriz, J. and García-López, J. Leukemia 1997; vol 11: 1124-30). The cut off value of the mean fluorescence intensity adopted to define high P-gp expression was ≥ 1.10. A total of 21 high P-gp AML patients were randomized in two groups: 1. Daunorubicin (DNR) 60mg/m² in continuous infusion -CI- 3x+Cytarabine 100 mg/m² CI 7x + CSA 16mg/m² CI 3x; (CSA group) and 2. DNR 60mg/m² CI 3x + Cytarabine 100 mg/m² CI 7x (Conventional IT group). Patients who did not achieve Complete Hematological Remission (CHR) in the first cycle of chemotherapy received a second course. The 2 groups did not differ regarding age (mean ± S.D.: 44.5 ± 11.9 vs. 48.5 ± 15.2 years in CSA and conventional IT group, respectively), leukocyte counts at diagnosis (44,200 ± 56,100 vs. 21,540 ± 20,200/µl), frequency of de Novo AML (81.8 vs. 80%) and of Core Binding Factor Leukemia cases (18.2 vs. 10%). The median follow up among survivors was of 6.2 years. The mean serum levels of CSA at 24 hours after infusion was of 1,157 ng/mL (range: 4 - 1,600ng/mL), which was similar to that reported by List et al. The CHR rate after the first cycle of induction was higher in the group using CSA (63.6% vs. 30%; p = 0.09) but the DFS (2.05 years vs. not reached; p= 0.27) and OS (4.08 vs. 21.12 months; p = 0.19) were higher in conventional IT group. These results may reflect the effect of the second course of induction in patients who failed to achieve CHR (CHR after second IT: 0% vs. 33.3%, p=0.34, in CSA and conventional IT group, respectively) and higher relapse rate in CSA group (42.8% vs. 33.3%, p=0.78). Furthermore, there was a lower frequency of induction deaths (18.2% vs. 9%; p = 0.59) and of hyperbilirubinemia (bilirubin > 1,5x the upper limit of normality) in the Conventional IT group (6 vs. 0 patients; p = 0.02). There were no cases of acute cardiac toxicity. The study was interrupted due to the cost of CSA and the lack of significant improvement in the outcomes. In conclusion, despite the higher rate of CR after one cycle of chemotherapy, there was not improvement in long term survival of AML patients with high Pgp expression treated with CSA in combination with anthracyclines and cytarabine. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1011-1011
Author(s):  
Marek Seweryn ◽  
Jerzy Wojnar ◽  
Dariusz Kata ◽  
Slawomira Kyrcz-Krzemien

Abstract Abstract 1011 Poster Board I-33 Background: Addition of purine analogues to standard induction therapy of acute myeloid leukemia (AML) had previously been demonstrated to increase complete remission rate. The aim of this study was to analyze whether the use of cladribine or fludarabine during induction and consolidation increases the risk of infectious complications. Material and methods: 118 AML patients, included in two consecutive randomized trials between 1999-2006 in a single centre were analyzed. Induction therapy consisted of daunorubicin + cytarabine (DA-7, n=53) alone or in combination with cladribine or fludarabine (DAC-7 + DAF-7, n=65 ). Consolidation included one course of high-dose AraC + mitoxantrone and one course of high-dose AraC +/- purine analogues. A median age was 45(17-58) years and 48(20-60) years for patients treated with and without purine analogues, respectively. Results: The frequency of neutropenic fever as well as microbiologically documented bacterial, fungal and viral infections during induction and consolidation did not differ between two compared groups - receiving or not purine analogues. Time to infection occurrence and infection duration were similar in both study groups. During induction and both consolidation treatments significant lower values of lymphocytosis were observed in the group of patients treated with purine analogues. There was a slight tendency to increased rate of mucositis for patients treated with purine analogues (60% vs. 44.3%, p=0.07) during induction treatment, while infections affecting skin and soft tissues were significant frequent for patients treated without purine analogues (43.3% vs. 18%, p=0.03) during second consolidation treatment (high dose AraC). The usage of intravenous anti-infectious medications (antibiotics, antifungal, antiviral) and periods of hospitalization did not differ between two groups in this study. Conclusions: We conclude that the use of purine analogues, either cladribine or fludarabine along with conventional induction and consolidation therapy does not aggreviate infectious complications in adults with AML. Disclosures: No relevant conflicts of interest to declare.


Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5046-5046
Author(s):  
David Martínez-Cuadrón ◽  
Pau Montesinos ◽  
Federico Moscardo ◽  
Lineth Lopez ◽  
Guillermo Martin ◽  
...  

Abstract Background Patients with hyperleukocytic acute myeloid leukemia (AML) have a high mortality rate during induction treatment. This mortality is mainly due to bleeding complications, tumor lysis syndrome and symptoms of hyperleukocitosis. Although there is no clear evidence of benefit, leukapheresis is indicated to reduce the number of leukocytes (WBC) in peripheral blood and prevent or relieve leukostasis symptoms before starting cytotoxic therapy. Objetives Analyze the characteristics of a series of patients with hyperleukocytic AML who started induction treatment and assess the outcome depending on whether leukapheresis was performed or not. Methods All adult patients with hyperleukocytic AML (WBC> 95 x 109 / L) who received induction therapy in the Hospital La Fe between 1979 and 2012 were included. The leukapheresis was indicated according to physician discretion. The characteristics and mortality of both groups, patients who underwent leukapheresis and non-leukapheresis, were compared. Then a “matched-paired analysis” was performed according to ECOG, WBC and coagulopathy in a 2:1 ratio to compare results from two homogeneous cohorts. Results One hundred and forty patients diagnosed with hyperleukocytic AML received induction therapy, 18 of them underwent leukapheresis. Patients who underwent leukapheresis compared with non-leukapheresis showed a median age of 55 years (16-71) vs 58 (14-75) and WBC at diagnosis of 198 ´ 109 / L (101-620) vs 141 (97-375), respectively. The leukapheresis group had a worse ECOG (p = 0.03), more leukocytes (p = .003), more coagulopathy (p = .03), more leukostasis symptoms (p <.001) and more mortality at 7 days (p = .02). From the “matched-paired analysis”, 2 cohorts were obtained, whose characteristics are shown in Table 1. After comparing the group of leukapheresis and non-leukapheresis (n = 36), there were no significant differences between them, including leukocyte count, ECOG, coagulopathy and leukostasis. There were also no significant differences in mortality at 7, 14, 21 and 28 days (p = .60, p = .99, p = .92, p = .99, respectively). Conclusions Patients diagnosed with hyperleukocytic AML who underwent leukapheresis showed more leukocytes, leukostasis and coagulopathy. After analizying two comparable groups, leukapheresis failed to reduce mortality. Disclosures: No relevant conflicts of interest to declare.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 935-935
Author(s):  
Friedrich Stöolzel ◽  
Thomas Illmer ◽  
Claudia Dill ◽  
Michael Kramer ◽  
Brigitte Mohr ◽  
...  

Abstract Abstract 935 Background: Previous work of our group led to the identification of several differentially regulated microRNAs in patients with acute myeloid Leukemia (AML) harboring a mutation of the Nucleophosmin 1 gene (NPM1) – amongst these was miR-149 which is reported to regulate Lysyloxidase (LOX). LOX is described as necessary for premetastatic niche formation in various epithelium-derived malignancies and its expression level correlates with distant metastasis free- and overall survival (OS). Animal models have demonstrated that inhibition of LOX sufficiently eliminates metastasis. Therefore, we were interested to investigate whether the LOX-concentration in AML plasma samples is of prognostic relevance and whether it is associated with certain characteristics such as extramedullary disease. Patients and methods: Plasma samples of 156 patients with AML (n=63 with reported extramedullary manifestation and n=93 without reported extramedullary manifestation; age 17–60 years) who were treated within the prospective AML2003 trial (NCT00180102) of the SAL study group were analyzed for LOX concentration using the Amplite Fluorimetric LOX Assay Kit (AAT Bioquest, Sunnyvale, CA, USA). All fluorescence reads were performed in triplicate with recombinant human LOXL2 (R&D Systems, Minneapolis, MN, USA) for standard curve estimation. Signals were read by a fluorescence microplate reader at Ex/Em 540/590 nm. Supernatant of the NPM1 mutated AML cell line OCI/AML3 served as internal control. LOX values were compared for statistical significance using the two tailed t test for continuous variables and chi-square test for dichotomized variables. The method of Kaplan-Meier was used to estimate OS and event-free survival (EFS). Survival distributions were compared using the log-rank test. Results: The mean LOX concentration for all patients was 58 ng/mL (standard error of the mean (SEM) 12). Dichotomizing at the mean LOX level (n=29 patients > mean = LOX-high; n=126 ≤ mean = LOX-low), survival comparing LOX-high and LOX-low patients in a univariate analysis revealed a 3-year OS of 22% (95% CI: 6–39%) and 53% (95% CI: 43–62%, p=.004), and 2-year EFS of 14% (95% CI: 2–28%) and 43% (95% CI: 34–52%, p=.001), respectively. In the Lox-high group 79% of patients exposed extramedullary AML compared to 32% in the Lox-low group, p<0.001. The mean LOX concentration in AML patients with extramedullary disease (n=63) was 131 ng/mL (SEM 26) as compared to 9 ng/mL (SEM 4) in patients without reported extramedullary AML manifestation (n=93), p<0.001. Conclusions: This analysis is the first study so far investigating the role of LOX in AML. High LOX levels are associated with statistically significant worse OS and EFS in AML patients. The positive correlation between high LOX levels and extramedullary AML suggests a potentially pathophysiological relevant mechanism involved in extramedullary homing and growth of AML and may offer further insights into AML biology. Future studies will need to address the functional modalities of how LOX is regulated and how it contributes to migratory and adhesion properties in AML. Disclosures: No relevant conflicts of interest to declare.


Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1488-1488
Author(s):  
Paolo Strati ◽  
Hagop M. Kantarjian ◽  
Jorge E. Cortes ◽  
Farhad Ravandi ◽  
Naveen Pemmaraju ◽  
...  

Abstract Abstract 1488 Background: Individuals with congenital Trisomy 21 (+21) (Down syndrome) have an increased risk of developing acute myeloid leukemia (AML). As +21 in AML frequently occurs in association with other karyotypic abnormalities, its prognostic impact remains poorly defined. Thus +21 has been empirically categorized as an intermediate risk cytogenetic aberration. This study focuses on the biological and clinical features of +21 AML. Methods: We analyzed the records of all AML patients treated at MD Anderson Cancer Center (MDACC) between January 1995 and December 2011. Only patients presenting to MDACC at the time of diagnosis with no prior therapy were included. Four cytogenetic groups were defined: +21 alone, +21 plus favorable cytogenetics, +21 plus intermediate cytogenetics and +21 plus unfavorable cytogenetics (Grimwade D et al, Blood 2010). Progression free survival (PFS) was defined as time from diagnosis to relapse or last follow up. Survival curves were calculated using Kaplan-Meier estimates and were compared using the log-rank test. Results: A total of 90 patients harboring +21 aberrations at diagnosis were identified. Median age was 59 years (range, 18–88) and 58% were male. At diagnosis, median white cell count was 4.6 (0.6–190) × 109/L, hemoglobin 8.6 (3.3–13.4)g/dL, platelets 53 (4–395) × 109/L, peripheral blasts 17% (0–96), and bone marrow blasts 48% (0–97). FAB classification: M0–2 64%, M3 1%, M4–5 20%, M6 10%, M7 4%. Cytogenetic subgroups included: +21 alone: 12%, +21 with favorable: 8%, +21 with intermediate: 8%, and +21 with unfavorable: 72%. Molecular mutations: FLT3 4/49 (2 ITD, 2 D835) (8%), NRAS 4/53 (7%), NPM1 1/25 (4%), CEBPA 2/13 (15%) and CKIT 0/26 (0%). Induction regimens included: Idarubicin+AraC-based (IA) 36%, fludarabine-based (FLU) 24%, clofarabine-based (CLO) 11%, topotecan-based (CAT) 10%, hypomethylating-based (HMT) 11%, and miscellaneous (MISC) 8%. Overall Response Rate (ORR) was 54%. Clofarabine-based induction showed the highest frequency of complete remission (CR) (70%) and HMT the lowest frequency of CR (56%) (Table 1). Median time to CR (TTCR) from initiation of therapy for those patients achieving CR was 5 (3–19) weeks. Patients with +21 alone or treated with HMT had a significantly longer TTCR (p=0.038 and 0.006; respectively). Median PFS was 11 (2–130) months and median CR duration was 5 (1–100) months. PFS was significantly higher in patients with +21 alone (101 months) as compared to the intermediate and unfavorable group (11 and 2 months, respectively) (p=0.006). CR duration did not differ significantly among the 4 cytogenetic groups. Both PFS and CR duration did not differ significantly by induction regimen. Median Overall Survival (OS) for the entire group was 9 (0–130) months. Median OS for stem cell transplant (SCT) recipients (14 months) was significantly higher than those who did not undergo SCT (8 months) (p=0.003). Patients with +21 alone had better OS (32 months) than those in the intermediate and unfavorable groups (5 months and 2 months; respectively) (p <0.01). On multivariate COX regression, +21 alone group maintained an improved OS as compared to the intermediate and unfavorable groups (covariates were WBC, peripheral blasts, previous hematological malignancies, performance status, age and induction treatment)(p<0.001). Conclusions: Patients with AML harboring +21 aberrations have unique biological and clinical features. When present as a sole aberration it is associated with significantly improved PFS and OS. Thus +21 alone may be a favorable prognostic factor in AML. Disclosures: No relevant conflicts of interest to declare.


Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 4408-4408
Author(s):  
Lifen Kuang ◽  
Juan Li

Abstract Objective: This single-arm prospective research (ChiCTR2100044731) aimed to evaluate the efficacy and safety of azacitidine combined with IA regimen in the induction treatment of newly diagnosed acute myeloid leukemia (AML), with a view to further improving the efficacy of acute myeloid leukemia with poor prognosis. Methods: Newly diagnosed AML (non-M3) patients who received azacitidine combined with IA regimen induction chemotherapy in the Department of Hematology of the First Affiliated Hospital of Sun Yat-sen University from November 2019 to February 2021 were enrolled, and the efficacy and side effect were analyzed. Results: A total of 33 patients were enrolled. The median age of the enrolled patients was 43.36 years (17-63), including 16 males (48.5%) and 17 females (51.5%). According to NCCN risk stratification, there were 3 patients (9.1%) in the favor group (9.1%) ,13 cases (39.4%) in the intermediate group and 17 cases (51.5%) in the poor group.The CR rate of one cycle of azacitidine combined with IA regimen was 66.7%, with a PR rate of 12.1% and a NR rate of 21.2%. After propensity score matching with the newly diagnosed AML patients who received IA regimen as induction chemotherapy in our center, a paired study was carried out. The results showed that there was no significant difference between the 2 groups in the treatment CR rate (66.7% for azacitidine combined with IA vs 54.5% for IA, P=0.592, Fig1). Subgroup analysis (table 1) showed combination of azacitidine with IA significantly improved the CR rate of patients with a ratio of blasts in the bone marrow greater than 67% (83.3% vs 30.8%, P=0.014) and patients in the intermediate NCCN risk group (100.0% vs 37.5%, P=0.001).The duration of agranulocytosis in the azacitidine combined with IA chemotherapy group was longer than that in the IA group (21 days vs 19 days, P=0.045). There was no significant difference in the number of platelet transfusions and the number of red blood cell transfusions between the two groups, and there was no significant difference in the incidence of infection between the two groups (table 2). Conclusions: The remission rate of induction chemotherapy for azacitidine combined with IA regimen and IA regimen in newly diagnosed non-M3 AML patients is comparable. Patients with a ratio of immature cells in bone marrow greater than 67% and patients in the intermediate NCCN risk group may benefit from azacitidine combined with the IA regimen. The combination of azacitidine with IA regimen aggravated granular bone marrow suppression. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.


2021 ◽  
Vol 8 ◽  
pp. 204993612110365
Author(s):  
Kundan Mishra ◽  
Suman Kumar ◽  
Sandeep Ninawe ◽  
Rajat Bahl ◽  
Ashok Meshram ◽  
...  

Introduction: Acute myeloid leukemia (AML) is the commonest leukemia in adults. Mortality in thew first 30-days ranges from 6% to 43%, while infections account for 30–66% of early deaths. We aim to present our experience of infections in newly-diagnosed AML. Method: This prospective, observational study, was undertaken at a tertiary care hospital in Northern India. Patients with confirmed AML (bone marrow morphology and flow cytometry) and who had developed febrile neutropenia (FN), were included. Result: A total of fifty-five patients were included in the study. The median age of the patients was 47.1 years (12–71) and 28 (50.9%) were males. Fever (33, 60%) was the commonest presentation at the time of diagnosis. One or more comorbid conditions were present in 20 patients (36.36%). Infection at presentation was detected in 17 patients (30.9%). The mean duration to develop febrile neutropenia since the start of therapy was 11.24 days. With each ten-thousand increase in white blood cell (WBC) count, the mean number of days of FN development decreased by 0.35 days ( p = 0.029). Clinical and/or radiological localization was possible in 23 patients (41.81%). Thirty-four blood samples (34/242, 14.04%) from 26 patients (26/55, 47.3%) isolated one or more organisms. Gram negative bacilli (GNB) were isolated in 24 (70.58%) samples. Burkholderia cepacia (8/34, 23.52%) was the commonest organism. The number of days required to develop febrile neutropenia was inversely associated with overall survival (OS). However, when compared, there was no statistically significant difference in OS between patients developing fever on day-10 and day-25 ( p = 0.063). Thirteen patients (23.63%) died during the study period. Discussion: Low percentage of blood culture positivity and high incidence of MDR organisms are a matter of concern. Days to develop febrile neutropenia were inversely associated with overall survival (OS), emphasizing the importance of preventive measures against infections. Conclusion: Infections continues to be a major cause of morbidity and mortality among AML patients.


PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e4139 ◽  
Author(s):  
Qianying Zhang ◽  
Kanchun Dai ◽  
Laixi Bi ◽  
Songfu Jiang ◽  
Yixiang Han ◽  
...  

Background Pretreatment platelet count has been reported as a potential tool to predict survival outcome in several solid tumors. However, the predictive value of pretreatment platelet count remains obscure in de novo acute myeloid leukemia (AML) excluding acute promyelocytic leukemia (M3). Methods We conducted a retrospective review of 209 patients with de novo non-M3 AML in our institute over a period of 8 years (2007–2015). Receiver operating characteristic (ROC) curve analysis was used to determine the optimal platelet (PLT) cutoff in patients. We analyzed the overall survival (OS) and disease free survival (DFS) using the log-rank test and Cox regression analysis. Results By defining the platelet count 50 × 109/L and 120 × 109/L as two cut-off points, we categorized the patients into three groups: low (<50 × 109/L), medium (50–120 × 109/L) and high (>120 × 109/L). On univariate analysis, patients with medium platelet count had longer OS and DFS than those with low or high platelet count. However, the multivariate analysis showed that only longer DFS was observed in patients with medium platelet count than those with low or high platelet count. Conclusion Our findings indicate that pretreatment platelet count has a predictive value for the prognosis of patients with non-M3 AML.


1991 ◽  
Vol 9 (7) ◽  
pp. 1210-1214 ◽  
Author(s):  
S Amadori ◽  
W Arcese ◽  
G Isacchi ◽  
G Meloni ◽  
M C Petti ◽  
...  

Thirty-two patients with refractory acute myeloid leukemia (AML) received salvage therapy with a single course of mitoxantrone 6 mg/m2 intravenous (IV) bolus, etoposide 80 mg/m2 IV for a period of 1 hour, and cytarabine (Ara-C) 1 g/m2 IV for a period of 6 hours daily for 6 days (MEC). Eighteen patients were primarily resistant to conventional daunorubicin and Ara-C induction treatment; eight patients had relapsed within 6 months from initial remission; six patients had relapsed after a bone marrow transplantation (BMT) procedure. Overall, 21 patients (66%) achieved a complete remission (CR), two (6%) died of infection during induction, and nine (28%) had resistant disease. Age greater than 50 years was the only factor predictive for a significantly lower response rate (P = .03). The median remission duration was 16 weeks; the overall median survival was 36 weeks. Severe myelosuppression was observed in all patients resulting in fever or documented infections in 91% of patients. Nonhematologic toxicity was minimal. We conclude that the MEC regimen has significant antileukemic activity and acceptable toxicity in salvage AML. Its benefit in front-line AML therapy is being investigated.


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