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P Bettelheim

Publications and source records attributed to P Bettelheim.

At least 19 recordsLinked to original sources
PubMed2001

Impact of the factor II: G20210A variant on the risk of venous thromboembolism in relatives from families with the factor V: R506Q mutation.

OBJECTIVES: Factor V: R506Q mutation and the prothrombin G20210A variant (factor II: G20210A variant) are associated with an increased risk of venous thromboembolism (VTE). In cohorts of unrelated patients a cosegregation of both mutations has been shown to be associated with an increased risk of developing VTE. The aim of this study was to investigate the impact of the coinheritance of both mutations on the risk of VTE in relatives of symptomatic carriers of the factor V: R506Q mutation and the factor II: G20210A variant. PATIENTS AND METHODS: Four families with 48 family members were investigated for the presence of the factor V: R506Q mutation and the factor II: G20210A mutation, and their clinical history was evaluated. RESULTS: VTE was more frequent in family members with a combined defect (3/10; 30%) compared to those with a single mutation (1/16; 6%) or without a defect (1/12; 8%). The probability for VTE for 40-yr-old individuals with both mutations, a single mutation and no mutation was 56%, 12% and 20%, respectively. CONCLUSIONS: These data suggest that the G to A transition at position 20210 of the prothrombin gene leads to an increase in the risk of VTE in carriers of the factor V: R506Q mutation. The determination of the factor II: G20210A variant in index patients carrying a factor V: R506Q mutation and, if present, in family members may help to identify individuals who are at high risk for VTE.

Adolescent↗
PubMed1998

Chemotherapy in patients with acquired immunodeficiency virus syndrome associated with non-Hodgkin's lymphoma.

We retrospectively analyzed our chemotherapy results in patients with the Acquired Immunodeficiency Virus syndrome (AIDS) and lymphoma over a 10 year period. Thirty out of 492 (6%) Human Immunodeficiency Virus (HIV) positive patients developed a non-Hodgkin's lymphoma. Thirteen patients with high-grade histology were treated with chemotherapy, 6 patients received CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisolone) and 7 patients received CEOP/IMVP-Dexa (cyclophosphamide, epirubicin, vincristine, prednisolone, ifosfamide, methotrexate, VP-16, and dexamethasone). The overall response rate was 77%, with no difference between the CHOP and CEOP/IMVP-Dexa regimens. There was no difference between the two treatment groups with respect to median overall survival (9 months for CHOP and 11.4 months for CEOP/IMVP-Dexa) or median lymphoma free survival (10.7 months for CHOP and not reached for CEOP/IMVP-Dexa). All patients treated with CEOP/IMVP-Dexa had WHO grade 3 or 4 infections, while only 2 of 6 patients treated with CHOP had WHO grade infections, and no grade 4 infection occurred (P < 0.01). Intensive regimens such as CEOP/IMVP-Dexa seem to be too toxic for patients with HIV-associated non-Hodgkin's lymphoma.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Superiority of high-dose over intermediate-dose cytosine arabinoside in the treatment of patients with high-risk acute myeloid leukemia: results of an age-adjusted prospective randomized comparison.

Although cytosine arabinoside (AraC) represents the most effective single agent in the treatment of adults with acute myeloid leukemia (AML) when given at doses exceeding 200 to 500 mg per application, its optimal dosage is still a matter of controversial discussion. While pharmacokinetic investigations suggest that the AraC-activating enzyme deoxycytidine kinase is saturated at drug concentrations achieved by short-term infusion of 0.5 to 1.0 g/m2 AraC and that higher doses are therefore not more effective, recent evidence indicates that additional mechanisms of AraC cytotoxicity may exist which could be enhanced by further dose escalation. In order to test this thesis in the clinical setting, a prospective randomized comparison of high-dose (HD-AraC) vs intermediate-dose (ID-AraC) AraC was carried out in patients with refractory or relapsed AML on the basis of the sequential high-dose AraC and mitoxantrone regimen (S-HAM). AraC was given as a 3-h infusion q 12 h on days 1, 2, 8 and 9. Patients younger than 60 years were randomized to AraC doses of 3.0 g/m2 vs 1.0 g/m2 while older patients received either 1.0 g/m2 or 0.5 g/m2 per single dose. Mitoxantrone was given to all patients on days 3, 4, 10 and 11 at a daily dose of 10 mg/m2. Randomization was stratified for primary refractoriness against induction therapy and length of first remission in relapsed patients. From 186 evaluable patients, 88 (47%) and 10 cases (5%) achieved a complete (CR) or partial (PR) remission, 39 patients (21%) had persisting leukemia (non-response (NR)), and 49 cases (26%) died within 6 weeks after the start of therapy (early death (ED)). In patients younger than 60 years the higher dose level resulted in a significant reduction of NR (12% vs 31%; ordinal chi2 test: P = 0.01) but also a higher rate of ED (32% vs 17%) thus leading to a marginally higher CR rate only (52% vs 45%). Within the subgroup of patients with refractory AML the tendency towards a higher CR rate after HD-AraC was more pronounced (46% vs 26%; P = 0.045). In patients older than 60 years, corresponding though less evident differences were observed with a higher rate of NR in the lower dose group (26% vs 16%) and ED occurring more frequently after higher doses (36% vs 26%). These data indicate that HD-AraC reveals a significantly higher antileukemic efficacy than ID-AraC as expressed by a significant reduction of failure from NR. This advantage, however, does not fully translate into an increase in remission rate due to a higher incidence of ED after HD-AraC predominantly from uncontrolled infections. In order to take full advantage of the higher antileukemic activity of HD-AraC an improvement of supportive care and infection control is warranted.

Acute Disease↗
PubMed1997

First-line treatment of Waldenström's disease with cladribine. Arbeitsgemeinschaft Medikamentöse Tumortherapie.

PURPOSE: To assess the activity and side effects of cladribine (2-CdA) treatment in patients with advanced Waldenström's disease. PATIENTS AND METHODS: Ten symptomatic patients without prior therapy were included in a prospective multicenter trial. 2-CdA was administered daily at 0.12 mg/kg body weight in a 2-h i.v. infusion over 5 consecutive days: this was repeated every 28 days for four cycles. Patients achieving a remission received interferon alfa-2c (1F) 15 micrograms s.c. three times a week for 1 year. RESULTS: All 10 patients responded to 2-CdA (100%; 95% confidence interval, 68-100%), with one complete (CR) and eight partial responders (PR): one patient had only one 2-CdA cycle and showed a minor improvement (MR). Patients tolerated the treatment well. Despite considerable immunosuppression, an infection occurred in only two patients. After a median observation period of 57 weeks, three patients had shown progression, including one who died of lymphoma. CONCLUSION: 2-CdA induction and IF maintenance is a well-tolerated therapy for symptomatic untreated patients with advanced Waldenström's disease and offers excellent palliation.

Adult↗
PubMed1996

Autoimmune reactions in patients with silicone breast implants.

Silicone breast implants have been surgical routine for over 30 years. An association between silicone augmentation and immune related diseases has been reported in approximately 100 cases. In a retrospective single center study we investigated 36 non-selected women with silicone breast implants and 36 sex- and age-matched controls. Autoimmune reactions were evaluated by measuring antinuclear antibodies (ANA), rheumatoid factor (RF) and thyroid gland antibodies (TMS), along with angiotensin-converting enzyme (ACE), C-reactive protein (CRP) and other immunological and laboratory parameters. In the controls only 3 (8%) women had an elevated ANA titer and 1 demonstrated thyroid autoantibodies (microsomal), giving a total of 4 (11%) women with detectable autoantibodies. By contrast, 12 (33%) of the 36 women with silicone augmentation had raised ANA titers (> or = 1 : 80), a significantly higher percentage than in the control group (p < 0.02). Of the 12 women, 1 showed antismooth muscle antibodies (ASMA; titer 1 : 40) and 2 of the patients displayed antineutrophilic cytoplasm antibodies (ANCA; 1 : 320 and 1 : 40, respectively), one of the latter also being positive for rheumatoid factor. 2 further women demonstrated thyroid autoantibodies (microsomal), giving a total of 14 (39%) women in whom significant autoantibodies were detectable. Clinical symptoms (musculoskeletal) were present in 1 patient. Most of the observed autoantibodies were organ-unspecific, with a predominance of elevated ANA titers of the heterogeneous type and not related to a distinct clinical entity. However, none of the investigated women with silicone breast implants showed clinical symptoms or signs of connective tissue disease according to ARA criteria.

Acute-Phase Proteins↗
PubMed1996

Potentiation of granulocyte colony-stimulating factor-induced mobilization of circulating progenitor cells by seven-day pretreatment with interleukin-3.

Granulocyte colony-stimulating factor (G-CSF) as a single agent is increasingly used for the mobilization of peripheral blood progenitor cells (PBPCs) for stem cell transplantation. In patients with perturbed hematopoiesis the mobilizing capacity of G-CSF alone may be inadequate. We have shown in rhesus monkeys that interleukin-3 (IL-3) pretreatment markedly potentiated the increase in PBPC numbers by subsequent administration of granulocyte/macrophage-CSF (GM-CSF). Here we studied the effect of IL-3 pretreatment on G-CSF-induced mobilization of PBPCs in 6 patients with Hodgkin's disease (n = 5) or non-Hodgkin's lymphoma (n = 1) who had low progenitor cell numbers because of previous chemotherapy. Patients were treated in cycle 1 with G-CSF at a dose of 5 microgram/kg/d for 5 days and, after a treatment-free interval, received cycle 2 consisting of 5 microgram/kg/d of IL-3 for 7 days followed by G-CSF again at a dose of 5 microgram/kg/d for 5 days. G-CSF alone increased the mean number of circulating colony-forming units-GM (CFU-GM) by 21-fold, the number of burst-forming units-erythroid (BFU-E) by 9-fold, and the number of CFU-mix by 24-fold over pretreatment values. Treatment with 5 microgram/kg/d of IL-3 for 7 days did not mobilize by itself but significantly potentiated G-CSF-induced mobilization of all progenitor cell types leading to a 56-, 15-, and 46-fold increase over baseline of CFU-GM, BFU-E, and CFU-mix numbers, respectively. In 2 patients in whom leukapheresis was performed after G-CSF alone the target number of 2 x 10(6)/kg CD34+ cells was not reached. However, leukapheresis after the IL-3/G-CSF combination obtained > or =2 x 10(6)/kg CD34+ cells in 3 of 6 patients, including both patients who had inadequate collection after G-CSF alone. In one patient adequate function of mobilized progenitors could be shown by the demonstration of rapid trilineage engraftment after infusion of progenitors after myeloablative chemotherapy. Seven-day pretreatment with IL-3 may be a useful mean to augment mobilization of circulating progenitors by G-CSF. The combination of IL-3 and G-CSF seems to allow the procurement of sufficient numbers of PBPCs in some patients who cannot be mobilized adequately by G-CSF alone.

Adult↗
PubMed1996

Metabolic responses after laparoscopic or open hernia repair.

BACKGROUND: The purpose of a prospective randomized study was to compare the surgical trauma in patients undergoing laparoscopic or open hernia repair. METHODS: Postoperative pain, analgesic consumption, and metabolic response to surgery were assessed in 30 patients undergoing laparoscopic (group 1; n = 15) or open (group II; n = 15; Shouldice repair) unilateral inguinal hernia repair. Both groups were comparable with respect to age, sex, and type and size of inguinal hernia. RESULTS: Postoperative visual analogue scales (VAS) for pain were reduced on mobilization for patients of group I with a significant difference (P = 0.02) on the operative day, whereas pain scores at rest and analgesic requirements were similar for both groups. No differences between groups I and II were found in postoperative levels of interleukin-1, interleukin-6, tumor necrosis factor alpha, C-reactive protein, fibrinogen, transferrin, alpha-1-antitrypsin, and white blood cells. Postoperative polymorphonuclear (PMN) elastase concentrations remained within normal range in group II but showed a significant increase in patients operated laparoscopically for postoperative days 1 and 2. CONCLUSIONS: No major surgical trauma was found after herniorraphy compared to open hernia repair.

Acute-Phase Proteins↗
PubMed1996

Immunophenotypic analysis of HL-60 cells during basophilic differentiation.

Differentiation along specific myeloid lineages may be accompanied by characteristic cell surface marker changes. We have examined leukemic HL-60 cell changes under conditions which induce basophilic differentiation. An increased surface expression of CD35, CD11b, and decreased expression of CD15 was found by flow cytometry during the 5-day induction period. Further investigation revealed two cell populations after 5 days in vitro: (i) a CD35-positive population (61% of cells present) containing a significant number of CD15-negative cells, and (ii) a CD15-positive/CD35-negative population. The CD35-positive subset appears to account for the majority of the basophilic cells induced under these conditions, as measured by histamine content and metachromatic staining. In addition, this subset contains a small number of early monocytic cells (CD14 and CD23 positive). The expression of CD11b is variably found on the CD15-positive/ CD35-negative subset of induced cells. These results suggest that CD35 and CD15 surface immunophenotyping can be used to map steps involved in myeloid development. A role for CD35 and CD15 in early basophil differentiation is proposed.

Antigens, CD↗
PubMed1996

Mast cell-lineage versus basophil lineage involvement in myeloproliferative and myelodysplastic syndromes: diagnostic role of cell-immunophenotyping.

Mast cells and blood basophils are distinct hemopoietic cells. They can be distinguished from each other and from all other lymphohemopoietic cells using antibodies against surface receptors or stored cytoplasmic molecules. In patients with myelodysplastic syndromes (MDS) or myeloproliferative syndromes (MPS), an elevation of metachromatically granulated cells (MCS) is frequently seen. These cells can be classified as basophils or mast cells using monoclonal antibodies (mAbs) against leukocyte antigens, including mast cell tryptase, c-kit (= mast cell growth factor [MGF] receptor), interleukin-3 receptor alpha chain (IL-3R alpha = CD123), and CD11b (C3biR). In a stable phase of MDS or MPS, the circulating MCS usually are basophils (histamine+, tryptase-, c-kit-, IL-3R alpha +, CD11b+). In an accelerated or terminal phase of disease, however, mast cell lineage involvement and circulating mast cell precursors (histamine+, tryptase+, c-kit+, IL-3R alpha-, CD11b-) are found in a subset of patients. The use of mAbs against mast cell antigens and granulocyte antigens is diagnostic in these patients.

Basophils↗
PubMed1996

Factors influencing the timing of peripheral blood stem cell collection (PBSC).

High-dose conditioning regimens followed by autologous peripheral blood stem cell rescue are frequently used for the treatment of solid tumors and hematological malignancies. In 24 patients up to four peripheral stem cell collections (PBSC) were performed after priming with various chemotherapies and G-CSF (300 micrograms s.c. per day). In 16 patients (group A) more than 2 x 10(6) CD 34 positive cells per kg bodyweight could be collected; fewer were harvested in the remaining eight patients (group B). The amount of collected CD 34 positive cells correlated with the median number of these cells in the peripheral blood at the start of PBSC. The two groups differed both in recovery time after priming-induced cytopenia (4 vs 6 days from nadir) and in the number of WBC (21 x 10(6) mL-1 vs 6.1 x 10(6) mL-1) and platelets (133 x 10(6) mL-1 vs 58 x 10(6) mL-1) reached at first day of PBSC. No difference between the two groups was seen according to age, duration of disease or disease status. However, the intensity of prior treatment was significantly greater in group B than in group A. These observations indicate that the toxicity of previous chemotherapy is the most important factor for the mobilization of sufficient CD 34 positive cells into the peripheral blood.

Adolescent↗
PubMed1995

Effect of interleukin-3 pretreatment on granulocyte/macrophage colony-stimulating factor induced mobilization of circulating haemopoietic progenitor cells.

Recombinant human colony stimulating factors (CSFs) as single agents are increasingly used for mobilizing peripheral blood progenitor cells (PBPCs) for stem cell transplantation. We have shown in rhesus monkeys that interleukin-3 (IL-3) pretreatment markedly potentiated the increase in PBPC numbers of subsequent administration of granulocyte/macrophage-CSF (GM-CSF). Here we studied the effect of IL-3 pretreatment on GM-CSF-induced mobilization of PB progenitors in patients who were potential candidates for autologous stem cell transplantation (n = 16). Patients were treated with GM-CSF at a dose of 5 micrograms/kg/d for 5 d and after a treatment free interval received another cycle of GM-CSF immediately following pretreatment with IL-3 at different doses and duration: 2.5 micrograms/kg/d (n = 4), 5 micrograms/kg/d (n = 3) and 10 micrograms/kg/d (n = 3) for 3 d, 5 micrograms/kg/d for 7 d (n = 4) and 5 micrograms/kg/d for 14 d (n = 2), respectively. Only 7 d pretreatment with IL-3 showed consistent effects. Although IL-3 did not mobilize by itself, pretreatment with 5 micrograms/kg/d of IL-3 for 7 d significantly potentiated GM-CSF-induced mobilization of PB CFU-GM numbers, leading to a mean increase in PB CFU-GM numbers over baseline by 18.5 +/- 5.2 (SEM) fold by IL-3/GM-CSF as compared to a 4.7 +/- 1.7-fold increase by GM-CSF alone. A significant enhancement by the 7 d IL-3 pretreatment was also observed for erythroid (BFU-E) and multipotential progenitor cells (CFU-mix) which were 3.3 +/- 1.3- and 3.4 +/- 0.9-fold, respectively, mobilized by GM-CSF alone, as compared to 8.5 +/- 2.3- and 19.2 +/- 3.4-fold, respectively, by the IL-3/GM-CSF combination. Our results suggest that 7 d pretreatment with IL-3 may be a useful mean to augment mobilization of circulating progenitors by more lineage-restricted CSFs. These findings may be important for the design of mobilization strategies that use growth factors without preceding chemotherapy.

Adolescent↗
PubMed1994

High efficacy of the German multicenter ALL (GMALL) protocol for treatment of adult acute lymphoblastic leukemia (ALL)--a single-institution study.

Sixty-one consecutive patients with acute lymphoblastic leukemia (ALL) (B-ALL excluded) were treated with the protocol described by Hoelzer et al. [15]. The complete remission (CR) rate was 85% (52/61 patients). Three patients died during induction therapy; six patients were refractory to treatment. The median duration of continuous complete remission (CCR), disease-free survival (DFS), and overall survival was 41.5, 41.4, and 40.8 months, respectively. At 5 years the probability of CCR was 49%, of DFS 43.5%, and of overall survival 41.6%. In the univariate analysis older age (> 35 years, p = 0.01), bcr-abl positivity (p = 0.007), and time to CR (> 4 weeks, p = 0.05) were significantly unfavorable prognostic factors. In the multivariate analysis only age (p = 0.006) and time to CR (p = 0.02) remained significant. Thus, our data confirm the high efficacy of this treatment regimen with regard to CR rate and remission duration.

Adolescent↗
PubMed1994

Comparison of the effects of aprotinin and tranexamic acid on blood loss and related variables after cardiopulmonary bypass.

Aprotinin reduces blood loss after cardiopulmonary bypass, but may sensitize recipients and is expensive. Tranexamic acid, a synthetic antifibrinolytic, has less disadvantages, but opinions differ regarding its efficacy. We studied three groups of patients undergoing cardiopulmonary bypass for coronary disease: recipients of aprotinin (total dose 4.2 x 10(6) kallikrein inhibiting units, n = 14), recipients of tranexamic acid (total dose 20 mg/kg body weight, n = 15), and nonmedicated controls (n = 14) during 24 hours after cardiopulmonary bypass. Compared with controls, aprotinin reduced blood loss, the number of patients requiring transfusions, and the mean number of transfused red cell units (all with p < 0.05), whereas the recipients of tranexamic acid did not differ either from aprotinin recipients or from controls. Aprotinin and tranexamic acid both mitigated the early postoperative reduction of adenosine diphosphate-induced platelet aggregation seen in the controls (p < 0.05). Postoperative increases of plasma concentrations of the prothrombin activation fragment F1 + 2 and the thrombin-antithrombin III complex showed an activation of intravascular coagulation, without any intergroup differences. The balance between concentrations of tissue plasminogen activator and the type 1 plasminogen activator inhibitor disclosed an activation of fibrinolysis, without differences between the groups. The concentrations of D-dimer, a breakdown product of cross-linked fibrin, remained at baseline in the recipients of aprotinin and tranexamic acid but tripled in the controls (p < 0.05). By contrast, the plasma antiplasmin activity was equally depressed in the tranexamic acid and the control groups but decreased less in the recipients of aprotinin (p < 0.05). This discrepancy may reflect the different modes of action of the two agents, which may make aprotinin more efficacious than tranexamic acid in the "nonfibrinolytic" act of protecting platelet function against attack by plasmin during cardiopulmonary bypass.

Aged↗
PubMed1993

Transforming growth factor-beta 1 interferes with the proliferation-inducing activity of stem cell factor in myelogenous leukemia blasts through functional down-regulation of the c-kit proto-oncogene product.

Blast cells, obtained from patients with acute myelogenous leukemia (AML), that express surface binding sites for human stem cell factor (SCF) respond proliferatively upon exposure to this molecule. In the presence of human transforming growth factor-beta 1 (TGF-beta 1) the capacity of SCF to augment the proliferative state of AML blasts was, however, almost completely abolished. This inhibitory action of TGF-beta 1 could be reversed by a neutralizing anti-TGF-beta 1 antibody. Studies on the mechanism of TGF-beta 1 inhibition of SCF-induced proliferation of AML blasts revealed that TGF-beta 1 treatment of these cells was associated with down-regulation of SCF receptor surface expression, as detected with a specific monoclonal antibody, which appeared to be preferentially due to an acceleration of decay of mRNA for the c-kit proto-oncogene encoding the SCF receptor, without an effect on the overall transcriptional activity of the c-kit gene. Direct evidence to prove the importance of c-kit down-regulation in the inhibitory effect of TGF-beta 1 on AML growth came also from experiments demonstrating that signal transduction of SCF could be significantly diminished in the presence of TGF-beta 1, as demonstrated by measuring c-kit kinase-associated phosphorylation of target proteins.

Cell Division↗
PubMed1993

Granulocyte colony-stimulating factor (G-CSF) as an adjunct to induction chemotherapy of adult acute lymphoblastic leukemia (ALL).

Our purpose was to evaluate the ability of recombinant human granulocyte colony-stimulating factor (r-metHuG-CSF) as an adjunct to induction chemotherapy of acute lymphoblastic leukemia (ALL) to ameliorate chemotherapy-induced neutropenia and thus allow patients to receive full doses of chemotherapy on time. Sixteen consecutive patients with adult ALL (13 de novo, three relapsed) were treated with induction chemotherapy according to the BMFT protocol and received in addition r-metHuG-CSF (200 micrograms/m2/day). Patients who were treated with the same induction chemotherapy but without G-CSF between 1982 and 1990 served as controls. Fifteen of the 16 patients achieved complete hematological remission. One patient died because of fungal septicemia. Compared with historical controls, G-CSF-treated patients had a significantly faster neutrophil recovery in phase I, resulting in neutrophil counts > 1000/microliters at day 17 vs day 26 (in median) in controls. In phase II, the onset of severe leukocytopenia (< 1500/microliters) was significantly (p = 0.01) delayed and the degree of leukocytopenia less pronounced (mean nadir 3300/microliters) in G-CSF-treated patients compared with controls (1880/microliters). The number of days of febrile neutropenia was not different in phase I. In phase II it was lower in study patients (0 vs 1.1 days), but the difference did not reach statistical significance (p = 0.09). Full doses of chemotherapy could be given on time to 11/13 (85%) G-CSF patients but to only 7/30 (23%) controls. These data indicate that (a) G-CSF can be given along with chemotherapy in induction treatment of ALL without compromising efficacy; (b) the duration of neutropenia in phase I is markedly shortened and the degree of leukocytopenia in phase II ameliorated; (c) these beneficial effects allow patients to receive full doses of chemotherapy on time.

Adolescent↗
PubMed1993

High-dose versus intermediate dose cytosine arabinoside combined with mitoxantrone for the treatment of relapsed and refractory acute myeloid leukemia: results of an age adjusted randomized comparison.

193 patients with relapsed or refractory acute myeloid leukemia (AML) were entered into a prospective randomized comparison of high-dose versus intermediate dose cytosine arabinoside (AraC) both combined with mitoxantrone (mitox) according to the previously established sequential HD-AraC/mitox regimen (S-HAM). AraC was administered by 3 hr inf. q 12 hrs on days 1, 2, and 8, 9 at randomly assigned doses of either 3.0 versus 1.0 g/m2 in pts. < 60 years of age or 1.0 versus 0.5 g/m2 in older pts. Mitox was given to all cases at a dose of 10 mg/m2/d on days 3, 4, and 10, 11. Randomization was stratified for primary refractoriness against induction therapy and the length of first remission in relapsed cases (< 6 mths., 6-18 mths., > 18 mths.). From 151 presently evaluable cases 72 pts (48%) achieved a complete remission (CR), 38 cases (25%) were non-responders (NR) and 41 pts. (27%) died within the first 6 weeks after the start of treatment (early death = ED). No significant differences were found in CR rates being 52% and 44% for the 3.0 versus 1.0 g/m2 AraC regimens in pts. < 60 years and 48% and 45% after 1.0 versus 0.5 g/m2 AraC in older pts. No differences between the respective regimens emerged either for the time to CR (median 46 days) nor remission duration (median 4.5 mths). Analysis of treatment failures, however, demonstrated a significantly higher rate of NR after the lower dose regimens in both age groups of 41% and 32% versus 11% and 14% in pts. receiving AraC at higher doses (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗