Hasil untuk "Diseases of the blood and blood-forming organs"

Hualong Bai, Zhuo Li, Alan Dardik

Background: Current models of arterial thrombus frequently rely on chemical or mechanical injury and often cause total vessel occlusion, limiting their relevance as a model of early events. To address this, we developed a reproducible mouse model of mural thrombus induced by an aortotomy. Methods: A 1-mm aortotomy was created in the mouse abdominal aorta using a 31-gauge needle, and then the site was covered with autologous adipose tissue using gentle pressure for hemostasis. Arterial mural thrombus with an arteriovenous fistula was created by using a 25-gauge needle puncturing from the mouse aorta into the inferior vena cava. Thrombus formation and vessel remodeling were assessed via histology, immunofluorescence, and scanning electron microscopy up to 90 days. We also evaluated the effect of local delivery of rapamycin and β-aminopropionitrile. Results: Acute mural thrombus formation occurred immediately after aortotomy, followed by endothelial and smooth muscle cell infiltration by day 7. Most thrombi regressed by day 21, and the vessel wall closely resembled native aorta after 6 weeks. Rapamycin and β-aminopropionitrile were associated with increased mural thrombus size. All aortotomies developed saccular aneurysms that dilated gradually over 21 days. Rapamycin was also associated with increased arterial mural thrombus size with arteriovenous fistula. Conclusion: The aortotomy model replicates mural thrombus initiation, resolution, and wall remodeling without complete vessel occlusion. This mouse model offers a robust platform for investigating mural thrombosis, vascular healing, and aneurysm biology.

M.I. Del Principe, G. Paterno, E. Buzzatti et al.

Introduction. Multiparameter flow cytometry (FC) has demonstrated superior sensitivity over conventional cytology (CC) in detecting occult central system disease (OCNSD) in adult acute lymphoblastic leukemia (ALL) patients (pts), a condition associated with a more unfavorable outcome. This has led to intensified CNS-directed therapy (CNSDT) in OCNSD pts, though its impact on relapse risk remains uncertain. Aim. To prospectively assess disease-free survival (DFS) of OCNSD pts via a multicenter, observational Campus ALL study. Methods. We recorded data on all consecutive cerebrospinal fluid (CSF) samples from adult ALL pts (since 1 June 2020) analyzed by CC and FC. Data on demographics, ALL type, biology, CSF features, intrathecal (IT) prophylaxis/therapy, FC event count, treatments, complete remission (CR), relapse (RE), and mortality were also collected. Positivity by CC was defined by standard criteria. FC used 8–10 antibodies, with at least 10 clonal and abnormal events considered positive. CSF results identified 3 groups: manifest CNS disease (MCNSD, CC+FC+), OCNSD (CC–FC+), and CNS neg (CC–FC–). Results. A total of 134 pts (median age 48, range 19–81; M/F 52%/48%) were enrolled across 14 Italian centers. Treatments followed the GIMEMA/NILG or Hyper-CVAD protocols. CNSDT intensification consisted of biweekly IT therapy until CSF blast clearance, followed by two weekly doses. A CR was achieved in 82% of pts (111/134), with a RE in 38/110 (34.5%) including one isolated CNS RE. MCNSD, OCNSD and CNS neg were found in 14 (10%), 10 (8%), and 110 (82%) pts, respectively. CNSDT was intensified in all MCNSD and in 9/10 OCNSD pts. In the OCNSD, the median of the total acquired, and the leukemic events were 4548 (60-79697) and 61 (13-2100), respectively. No significant differences were observed among groups for gender, B/T lineage, cytogenetic/genetic features. Compared with CNS neg group, OCNSD pts had more frequent WBCc >30x109/L (p=.016). The 3-year DFS in CNS neg, OCNSD and MCNSD pts did not differ: 62% (95% CI, 51.1-75), 47% (95% CI, 21.5-100) and 35% (95% CI, 12.3-100), respectively (p<0.42) (Figure). Conclusions. Our data confirm that OCNSD is uncommon. Apart from high WBC, no other predictive feature was identified, highlighting the need of routine FC in all pts. Although preliminary, our findings suggest that intensified CNSDT may improve prognosis in OCNSD pts, which could be particularly relevant as systemic chemotherapy strategies are being de-escalated.

Yoshito Ogihara, Yugo Yamashita, Takeshi Morimoto et al.

Background: The risk of recurrent venous thromboembolism (VTE) in patients with isolated distal deep vein thrombosis (IDDVT) is generally low, particularly when IDDVT is asymptomatic. However, cancer patients with IDDVT, even asymptomatic IDDVT, may be at a higher risk of recurrent VTE. Objectives: To compare the clinical outcomes of cancer patients with asymptomatic and symptomatic IDDVT. Methods: The ONCO DVT trial is a randomized clinical trial that compared 12-month versus 3-month edoxaban treatment regimens in cancer patients with IDDVT. In this post hoc analysis, 601 patients were categorized into the asymptomatic (n = 479) and symptomatic (n = 122) groups based on IDDVT-related symptoms at diagnosis. The primary outcome was the composite of symptomatic recurrent VTE or VTE-related death at 12 months, while the major secondary outcome was major bleeding at 12 months. Results: The cumulative 12-month incidence of the primary outcome was lower in the asymptomatic group than that in the symptomatic group (2.9% vs 13.4%; P < .001; hazard ratio, 0.21; 95% CI, 0.10-0.47). Among the 12 patients with symptomatic recurrent VTE in the asymptomatic group, 8 (67%) had recurrent IDDVT, and 11 (92%) experienced recurrence after discontinuing anticoagulation therapy. The cumulative 12-month incidence of major bleeding was lower in the asymptomatic group than that in the symptomatic group (7.8% and 13.2%; P = .048). Conclusion: The risk of recurrent symptomatic VTE was lower in cancer patients with asymptomatic IDDVT than in those with symptomatic IDDVT. Most recurrent VTE events were recurrent IDDVT, with the majority occurring after discontinuing anticoagulation therapy.

Besim Fazıl Ağargün, Murat Özbalak, Übeyde Ayşe Gülseren et al.

Gacser Zita, Bourke Steven, Hosszú Dalma et al.

The European Haemophilia Consortium (EHC) Think Tank was established as a platform for system change to ensure the healthcare ecosystem remains effective and relevant for people with bleeding disorders and other rare diseases. Operating alongside traditional advocacy initiatives, it comprised a series of thematic workstreams in which multiple stakeholders explored and co-designed potential solutions for specific aspects of the healthcare system. This final report from the workstreams on Access Equity and Future Care Pathways summarises recommendations for system change and the actions needed to achieve critical goals.

ECVR Cruz, LBA Lima, MT Schramm et al.

Introdução: O Sarcoma Mieloide (SM) é uma massa tumoral, que consiste em blastos mielóides acometendo sítios extramedular. A forma isolada, sem envolvimento da medula óssea, é rara, ocorrendo em menos de 1% dos casos. O diagnóstico exige biópsia tecidual. Cerca de 75%‒90% dos pacientes com SM desenvolverão leucemia mieloide aguda (LMA) com um período de latência que varia de 4‒12 meses e necessidade de tratamento sistêmico. Objetivo: Relatar um caso raro de SM primário de mediastino em pediatria e, devido à escassez de literatura sobre o tema, estimular a discussão das possíveis abordagens terapêuticas atuais. Material e métodos: Descrição do caso de paciente ALS, masculino, pré-escolar de 3 anos, previamente hígido. Iniciou quadro de dor abdominal difusa com relato de múltiplos atendimentos em pronto atendimento pediátrico sendo medicado com sintomáticos durante 1 mês. Na ocasião, evoluiu com piora da dor abdominal e desconforto respiratório. Foi realizado exames radiológicos e confirmado por tomografia de tórax a presença de massa de mediastino anterior. Evoluiu com dispneia, necessitando transferência para UTI pediátrica do Instituto Nacional do Câncer (INCA) para monitorização clínica e elucidação diagnóstica. Foi realizada biópsia percutânea guiada por USG, cujo resultado histopatológico foi de sarcoma mieloide, confirmado por estudo imuno-histoquímico com positividade de LCA, CD68, CD4, Mieloperoxidase (MPO), CD117 e negatividade para CD20 e CD3. O paciente apresentava hemograma normal. Não foi evidenciado acometimento de medula óssea, assim como também não se identificaram alterações citogenéticas ou moleculares. Resultados: Diante do diagnóstico foi iniciado tratamento quimioterápico conforme o protocolo BFM LMA 2004. O paciente apresentou redução significativa da massa mediastinal após a indução. Realizou exame PET-CT, após completar fase de intensificação, compatível com massa residual fibrosada com critérios de remissão. No momento, encontra-se na fase de manutenção em remissão completa. Não possui doador HLA compatível. Discussão: O tratamento do SM em pediatria exige uma abordagem multidisciplinar. Quimioterapia intensiva, com base em protocolos para LMA, seguida de terapia de consolidação com transplante de células-tronco hematopoiéticas tem sido a estratégia mais adotada. Diferentes abordagens têm sido exploradas em poucos relatos de casos, demonstrando a necessidade de individualização do tratamento, considerando o risco de toxicidade e complicações a longo prazo. Conclusão: O SM primário de mediastino é uma apresentação rara que exige atenção especializada para o diagnóstico e tratamento. Devido à raridade, não existem diretrizes de tratamento bem estabelecidas. É fundamental que os casos de SM em crianças sejam abordados em centros especializados e que uma colaboração multidisciplinar seja buscada para aprimorar o conhecimento e definir estratégias terapêuticas mais eficazes. A escolha do tratamento deve ser individualizada, considerando os benefícios potenciais em relação aos riscos.

Leticia O. Marani, Amanda Costa, Fernanda B. Silva et al.

Background: Despite recent advances and development of new therapeutic targets and personalized medicine, acute myeloid leukemia (AML) treatment remains defiant. Identification of residual leukemic cells (measurable residual disease -MRD) by Multiparametric Flow Cytometry has been a fast and effective tool, but disease heterogeneity makes MRD assessment a clinical challenge, especially in cases with uncommon features, needing clinical and technical expertise to be accurately performed and interpreted. Aims: To emphasize how absent CD33 expression impacts on interpreting MDR in AML. Methods: We report three clinical cases of AML with absent CD33 assessed for FLT3 and NPM1 mutation, RUNX1/RUNX1T1 and CBFB-MYH11 rearrangements, karyotype and an 8-color panel immunophenotyping (Table 1). Empty gating strategy was used to identify LAIPs (Leukemia Associated-Immunophenotype), different from normal and leukemic stem cells, compared to healthy and regenerating non-AML bone marrow (BM) from diagnosis and follow up (Figures 1 and 2). Assays were performed at the Hematology Laboratory of Ribeirão Preto the Medical School, University of São Paulo, in accordance to Local Ethical Boards. Results: Patient's demographic and clinical data are summarized on Table 2. MFC revealed completely negative CD33 from diagnosis to follow-ups. Treatment consisted of 2 induction cycles (cycle 1: 3 days of Daunorubicin 60 mg/m2 and 7 days of cytarabine 200 mg/m2; cycle 2: 6 days of cytarabine 1 g/m2 twice a day). Consolidation consisted of 1 or 2 cycles of 6 days of cytarabine 1 g/m2 twice a day. BMs were obtained at diagnosis, after 1st and 2nd induction, after 1st and 2nd Consolidation, and 3, 9, 12 and 15 months after consolidation of chemotherapy. Even with different number of follow-ups for each patient, time analysis was preserved. Complete remission (complete or incomplete) was achieved by day 30 after 1st induction and no change in the outcome was reported, even though an altered maturational phenotype persisted with complete absent CD33 expression, during and after treatment, suggesting a very rare polymorphism of CD33 receptor that mimicked MRD positivity. Since CD33 is a common myeloid antigen expressed on malignant blasts in AML, it is prominent evaluate and carefully analyze this marker, once is known that polymorphisms, for example, rs12459419 can affect CD33-antibody conjugated based therapy. CD33low blasts are associated to a more mature AML and its high expression is related to adverse landscapes in pediatric AML, highlighting the importance of CD33 evaluation. Regarding vulnerable steps of MRD assessment, Post –analytical phase must embrace a set of standards in order to prevent report errors. Here we present three cases of AML with absent CD33 from diagnosis till follow-ups visits. CD33 absence mimics positivity for MRD studies. This data emphasizes the importance of caution in MFC analysis and correlation of diagnostic and follow-ups results and interpretation, as constant training of the team.

Lai Yee Orbell, Nouf Abutheraa, Andrew S Duncombe et al.

Abstract Alleviating symptom burden in patients with myeloproliferative neoplasms (MPNs) is imperative to achieving optimal management. Research remains to elucidate the relationship between the JAK2V617F (Janus kinase 2) mutation present in many MPN patients, and the symptomatology they experience. This retrospective study analysed data collected from MPN patients included in the Myeloproliferative Neoplasms: An In‐depth Case–Control (MOSAICC) pilot study. The MPN Symptom Assessment Form was administered, and median symptom scores were compared between JAK2V617F‐positive and JAK2V617F‐negative groups. Multivariate logistic regression analysis adjusted for confounding variables. Overall, 106 MPN patients participated: 65.1% were JAK2V617F positive, 30.2% were JAK2V617F negative and 4.7% had an unknown status. Multivariate analysis revealed a low symptom burden for early satiety (p < 0.01), dizziness (p < 0.05), cough (p < 0.05) and bone pain (p < 0.01) in those receiving venesection alone. Interferon alpha was significantly associated (p < 0.05) with severe burden for 16 of the 27 symptoms. JAK2V617F‐positive females experienced a greater symptom burden than JAK2V617F‐positive males. There was no discernible relationship between the JAK2V617F mutation and symptom burden in MPN patients, unlike the therapeutic agents investigated. Larger studies are required to validate these results and identify mechanisms of symptom development and control in MPN patients.

Radosław Dziedzic, Lech Zaręba, Teresa Iwaniec et al.

Abstract Introduction Central retinal artery occlusion (CRAO) is a common cause of blindness and visual morbidity. In the majority of cases, it is related to thrombotic embolism. Nevertheless, the role of inherited or acquired thrombophilic risk factors in CRAO pathogenesis has not been comprehensively studied. Methods In 126 CRAO patients (66 [52.4%] men, median age 55 [range: 18–80] years) and 107 matched controls (56 [52.3%] men, median age 53 [range: 34–78] years) we evaluated classical atherosclerotic risk factors, including serum lipid profile and glucose level, analyzed intima-media complex thickness (IMT) of external carotid arteries, and performed transthoracic echocardiography. Furthermore, we established the prevalence of inherited and acquired thrombophilic risk factors, such as factor V Leiden (FVL) and prothrombin 20210 G/A genetic variants, plasma activity of factor (F) VIII, protein C and antithrombin activity, and free protein S levels. We also assessed the presence of antiphospholipid antibodies (APLA) and evaluated blood homocysteine in all enrolled subjects. Additionally, we estimated the occurrence of Val34Leu polymorphism of the A subunit of coagulation factor XIII (FXIII-A) in both groups as a potential thrombosis-protecting factor. Results Among traditional atherosclerotic risk components, obesity/overweight and hypercholesterolemia were the most common in the CRAO group and occurred in 103 (81.7%) and 85 (67.5%) patients, respectively. CRAO patients also had elevated IMT and altered echocardiographic parameters, indicating diastolic cardiac dysfunction. In thrombophilia investigations, at least one laboratory risk factor occurred in 72.2% (n = 91) of CRAO patients, with APLA as the most frequent, detected in 38.1% (n = 48) of them (almost seven times more frequent than in controls, p < 0.001). Deficiencies in protein C activity and free protein S levels were also common in the CRAO group, reported in 17.5% (n = 22) and 19.8% (n = 25) of patients, respectively. Interestingly, among two analyzed prothrombotic genetic variants, only the FVL was related to CRAO, with the allelic frequency 2.4 times more prevalent than in controls (p = 0.044). Finally, the CRAO group was characterized by hyperhomocysteinemia, almost twice as common as in controls (p = 0.026). Antithrombin deficiency, elevated FVIII, and FXIII-A Val34Leu polymorphism were not associated with CRAO. Conclusions Our findings suggest that thrombophilia plays a vital role in the pathogenesis of CRAO. Thus, proper laboratory screening should be considered in the primary and secondary prevention of those episodes, with implementing appropriate therapy as needed.

Piers Patten, Paul Buckley, Julie Chan et al.

Jing Liu, Qiu-Sha Huang, Xiao-Hui Zhang

Benedetta Rambaldi, Haesook T. Kim, Yohei Arihara et al.

CD6 is a co-stimulatory receptor expressed on T cells that binds activated leukocyte cell adhesion molecule (ALCAM), expressed on antigen presenting cells, epithelial and endothelial tissues. The CD6-ALCAM pathway plays an integral role in modulating T-cell activation, proliferation, and trafficking. In this study we examined expression of CD6 by reconstituting T cells in 95 patients after allogeneic cell transplantation and evaluated the effects of itolizumab, an anti- CD6 monoclonal antibody, on T-cell activation. CD6 T cells reconstituted early after transplant with CD4 regulatory T cells (Treg)-expressing lower levels of CD6 compared to conventional CD4 T cells (Tcon) and CD8 T cells. After onset of acute graft-versus-host disease (aGvHD), CD6 expression was further reduced in Treg and CD8 T cells compared to healthy donors, while no difference was observed for Tcon. ALCAM expression was highest in plasmacytoid dendritic cells (pDC), lowest in myeloid dendritic cells (mDC) and intermediate in monocytes and was generally increased after aGvHD onset. Itolizumab inhibited CD4 and CD8 T-cell activation and proliferation in preGvHD samples, but inhibition was less prominent in samples collected after aGvHD onset, especially for CD8 T cells. Functional studies showed that itolizumab did not mediate direct cytolytic activity or antibody-dependent cytotoxicity in vitro. However, itolizumab efficiently abrogated the costimulatory activity of ALCAM on T-cell proliferation, activation and maturation. Our results identify the CD6-ALCAM pathway as a potential target for aGvHD control and a phase I/II study using itolizumab as first line treatment in combination with steroids for patients with aGvHD is currently ongoing (clinicaltrials gov. Identifier: NCT03763318).

Verónica Bravo Villa, Job Romero, Eunice Rojas‐Zaldivar et al.

Abstract Introduction Apixaban, a direct factor Xa inhibitor, has been shown to be at least as safe and probably more effective than dalteparin for the treatment of cancer‐associated thrombosis (CAT) as reported in the ADAM‐VTE and Caravaggio studies, which included a low percentage of underweight patients. Lower‐weight–based dosing is supported by cancer‐specific studies such as half‐dose edoxaban in the Hokusai‐VTE cancer trial in individuals weighing <60 kg. Objective To examine apixaban plasma trough levels in low‐weight individuals with CAT, stably anticoagulated with full or half‐dose apixaban. Methods This was a cross‐sectional study of 61 routinely treated patients with active cancer and venous thromboembolism comparing three groups: patients weighing >60 kg treated with apixaban 5 mg twice daily, patients weighing ≤60 kg also receiving apixaban 5 mg twice daily, and patients weighing ≤60 kg given half‐dose apixaban (2.5 mg twice daily). Apixaban plasma steady‐state trough levels were determined on a single occasion. Results Mean apixaban plasma trough levels were similar for patients weighing >60 kg on full‐dose apixaban to those weighing ≤60 kg taking 2.5 mg twice daily (mean, 109 ng/dL; 95% confidence interval [CI], 74‐145; standard deviation [SD]: 77.6; and mean,101 ng/dL, 95% CI, 67‐135; SD: 80, respectively). Mean values for low‐weight patients (≤60 kg) on the full 5 mg twice‐daily dosing tended to be higher (mean, 136 ng/dL; 95%CI, 70‐201; SD:114), without statistical significance (P = .22). Conclusions This study supports the rationale for studying weight‐based adjustments in apixaban dosing in prospective studies evaluating safety and efficacy of dose reduction in low‐weight patients with cancer.

Francesco Saglio

D. V. Krinochkin, I. S. Bessonov, V. A. Kuznetsov et al.

Timely performed endovascular revascularization is the main modern method of treating for patients with acute myocardial infarction and elevated ST segment. In most cases, it is possible to achieve rapid recovery of coronary blood flow in the infarct related artery. Nevertheless, 10–40 % of patients manifest diminished myocardial reperfusion despite successful opening of the obstructed epicardial artery – so called the no-reflow phenomenon. The main angiographic features of hypoperfusion in the infarction zone are decrease in the degree of myocardial glow and/or blood flow by the TIMI scale. However, the use of angiographic criteria does not always allow accurate detection of developing no-reflow phenomenon. The presented case demonstrates the possibilities and potential benefits of contrast enhanced echocardiography in assessing the no-reflow phenomenon in a patient with acute myocardial infarction after revascularization.

Anna Wojtuszkiewicz, Yehuda G. Assaraf, Mirthe Hoekstra et al.

Emel Okulu, Talia İleri, Vildan Koşan Çulha et al.

Objective: To increase our understanding of the etiology of idiopathic thrombocytopenic purpura (ITP) some cytokine gene polymorphisms were analyzed for susceptibility to the disease. The aim of this study was to investigate the role of tumor necrosis factor-alpha (TNF-α) -308 G/A and transforming growth factor-beta 1 (TGF-β1) –915 G/C polymorphisms in the development and clinical progression of childhood ITP.Materials and Methods: In all, 50 pediatric patients with ITP (25 with acute ITP and 25 with chronic ITP) and 48 healthy controls were investigated via LightCycler® PCR analysis for TNF-α -308 G/A and TGF-β1 -915 G/C polymorphisms.Results: The frequency of TNF-α -308 G/A polymorphism was 20%, 16%, and 22.9% in the acute ITP patients, chronic ITP patients, and controls, respectively (p>0.05). The frequency of TGF-β1 -915 G/C polymorphism was 16%, 8%, and 8.3% in the acute ITP patients, chronic ITP patients, and controls, respectively (p>0.05). The risk of developing ITP and clinical progression were not associated with TNF-α -308 G/A (OR: 0.738, 95% CI: 0.275-1.981, and OR: 0.762, 95% CI: 0.179-3.249) or TGF-β1 -915 G/C (OR: 1.5, 95% CI: 0.396-5.685, and OR: 0.457, 95% CI: 0.076-2.755) polymorphisms. Conclusion: The frequency of TNF-α -308 G/A and TGF-β1 -915 G/C polymorphisms did not differ between pediatric ITP patients and healthy controls, and these polymorphisms were not associated with susceptibility to the development and clinical progression of the disease.

Ren'an Chen, Li Liu, Yinmin Liang

A 25-year-old man was diagnosised subcutaneous panniculitis-like T-cell lymphoma (SPTCL) through biopsy of a nodule from the anterior chest. After the treatment with prednisone 90 mg 3 weeks and tapered off in 1 month, the disease released, but relapsed together with symptions of hemophagocytic syndrome eight months after the termination of prednisone. CHOEP recipe was given but with unsatisfactory result until cyclosporine was prescribed. Cyclosporine was removed 6 months later. There is no evidence of clinical relapse 1 year later. This case suggest that cyclosporine could be a selectable treatment even in relapsed SPTCL.

Daphne de Jong, Ad Koster, Anton Hagenbeek et al.

Background The clinical behavior of follicular lymphoma is largely determined by properties of the non-malignant tumor microenvironment. The precise nature of the cell populations is still unclear and published data on their prognostic significance are highly conflicting. This may be partly due to heterogeneous composition and treatments.Design and Methods Pre-treatment biopsy samples of patients with follicular lymphoma treated in an EORTC/BNLI trial comparing fludarabine to cyclophosphamide, vincristine and prednisone (CVP) chemotherapy could be retrieved for 61 patients in five European countries. Immunohistochemical investigations were performed evaluate tumor cell characteristics, T-cell subsets, follicular dendritic cells and macrophages and associations with clinical outcome were studied.Results Some markers showed a homogeneous prognostic impact, while others had a different nd sometimes opposite effect in the treatment arms. CD69 expression on tumor cells was a poor prognostic sign and an interfollicular infiltrate of FoxP3-positive T cells was a good prognostic sign irrespective of the treatment arm. It is suggestive that a dense infiltrate of FoxP3-positive T cells, dense and interfollicular infiltrate of CD68-positive macrophages and complete follicular dendritic meshworks were associated with a favorable time to progression in CVP-treated patients, while being poor prognostic sign in fludarabine-treated patients.Conclusions Our results suggest that characteristic properties of the microenvironment in follicular lymphoma determines the responses to essentially different chemotherapeutic approaches. These data may provide an explanation for the highly conflicting results on immunohistochemical markers and the prognostic role of the microenvironment in follicular lymphoma reported thus far and lay the basis for the development of predictive assays to tailor treatment in patients with follicular lymphoma.

Vianed Marsán Suárez, Miriam Sánchez Segura, René Rivero Jiménez et al.

Se estudiaron 118 leucemias agudas en un período de 4 años. El fenotipaje celular se realizó a través del ultramicrométodo inmunocitoquímico (UMICIQ), mediante la utilización de un panel de anticuerpos monoclonales con el que se evaluó la expresión de antígenos linfoides y mieloides. La expresión de antígenos mieloides en pacientes con leucemia linfoide aguda se encontró en el 28,4 % y de antígenos linfoides en pacientes con leucemia mieloide aguda en el 56,7 %. Las leucemias agudas híbridas representaron el 16,1 % del total de pacientes estudiados: 73,7 % al inicio de la enfermedad y el 26,3 % restante en el estudio posterior al tratamiento de inducción de la remisión, lo que sugiere en estos últimos la posibilidad de cambio de linaje por la selección de variantes resistentes a drogas procedentes del clon original, o la aparición de neoplasias secundarias por el uso de drogas genotóxicas<br>118 acute leukemias were studied during 4 years. The cellular phenotyping was carried out through the immunocytochemical ultramicromethod by using a panel of monoclonal antibodies with which the expression of lymphoid and myeloid antigens was evaluated. The expression of myeloid antigens in patients with acute lymphoid leukemia was found in 28.4 %, whereas the expression of lymphoid antigens in patients suffering from acute myeloid leukemia was observed in 56.7 %. The acute hybrid leukemias accounted for 16.1 % of the total of patients studied: 73.7 % at the onset of the disease and the other 26.3 % in the study following the induction treatment of the referred patients, which suggests in the latter the possibility of changing lineage by selecting variantes resistant to drugs from the original clon, or the appearance of secondary neoplasias due to the use of genotoxic drugs