《美国血液学杂志》广泛报道了人类血液疾病和人类疾病动物模型的实验和临床特征。该杂志发表在非恶性和恶性血液病方面的原创贡献，包括止血和血栓形成、免疫学、血库和干细胞生物学的临床和基础研究。欢迎和鼓励描述诊断和治疗血液疾病的新治疗方法的临床转化报告。该杂志包括常规的原创实验室和临床研究文章、简短的研究报告、批判性评论、血液学图像、信件和信件。

The American Journal of Hematology publishes extensive research on the experimental and clinical features of human blood diseases and their animal models. The journal features original contributions on both malignant and non-malignant hematological disorders, including clinical and basic research in hemostasis and thrombosis, immunology, blood banking, and stem cell biology. We welcome and encourage clinical translational reports that describe new diagnostic and therapeutic approaches for blood diseases. The journal includes regular original laboratory and clinical research articles, brief research reports, critical reviews, hematology images, letters, and other relevant content.

《美国血液学杂志》广泛报道人类血液疾病及其动物模型的实验和临床特征。该杂志发表关于非恶性和恶性血液病的原创研究，包括止血与血栓形成、免疫学、血库和干细胞生物学的临床与基础研究。我们欢迎并鼓励临床转化报告，描述诊断和治疗血液疾病的新方法。该杂志内容包括常规的原创实验室和临床研究文章、简短研究报告、批判性评论、血液学图像、信件及其他相关内容。

American Journal of Hematology

Tingting Zhang

Yaxiao Lu

Xia Liu

Mengmeng Zhao

Jin He

Xianming Liu

Lanfang Li

Lihua Qiu

Zhengzi Qian

Shiyong Zhou

Bin Meng

Qiongli Zhai

Xiubao Ren

Huilai Zhang

Xianhuo Wang

American J Hematol

Comprehensive analysis of <scp>TP53</scp> mutation characteristics and identification of patients with inferior prognosis and enhanced immune escape in diffuse large B‐cell lymphoma

Abstract Myeloproliferative neoplasms represent a group of clonal hematopoietic disorders of which myelofibrosis (MF) is the most aggressive. In the context of myeloid neoplasms, there is a growing recognition of the dysregulation of immune response and T‐cell function as significant contributors to disease progression and immune evasion. We investigated cytotoxic T‐cell exhaustion in MF to restore immune response against malignant cells. Increased expression of inhibitory receptors like CTLA‐4 was observed on cytotoxic T cells from MF patients together with a reduced secretion of IFNɣ and TNFɑ. CTLA‐4 ligands CD80 and CD86 were increased on MF granulocytes and monocytes highlighting a possible role for myeloid cells in suppressing T‐cell activation in MF patients. Unlike healthy donors, the activation of cytotoxic T cells from MF patients was attenuated in the presence of myeloid cells and restored when T cells were cultured alone or treated with anti‐CTLA‐4. Moreover, anti‐CTLA‐4 treatment promoted elimination of neoplastic monocytes and granulocytes in a co‐culture system with cytotoxic T cells. To test CTLA‐4 inhibition in vivo , patient‐derived xenografts were generated by transplanting MF CD34+ cells and by infusing homologous T cells in NSGS mice. CTLA‐4 blockade reduced human myeloid chimerism and led to T‐cell expansion in spleen and bone marrow. Overall, these findings shed light on T‐cell dysfunction in MF and suggest that CTLA‐4 blockade can boost the cytotoxic T cell‐mediated immune response against tumor cells.

Lara Tavernari

Sebastiano Rontauroli

Ruggiero Norfo

Margherita Mirabile

Monica Maccaferri

Barbara Mora

Elena Genovese

Sandra Parenti

Chiara Carretta

Elisa Bianchi

Matteo Bertesi

Francesca Pedrazzi

Elena Tenedini

Silvia Martinelli

Maria Teresa Bochicchio

Paola Guglielmelli

Leonardo Potenza

Alessandro Lucchesi

Francesco Passamonti

Enrico Tagliafico

Mario Luppi

Alessandro Maria Vannucchi

Rossella Manfredini

Targeting exhausted cytotoxic T cells through <scp>CTLA</scp>‐4 inhibition promotes elimination of neoplastic cells in human myelofibrosis xenografts

通过<scp>CTLA</scp>‐4抑制靶向耗竭的细胞毒性T细胞促进人类骨髓纤维化异种移植中肿瘤细胞的消除

One out of ten patients with Philadelphia-negative myeloproliferative neoplasms (MPN) develop a second cancer (SC): in such patients we aimed at assessing the survival impact of SC itself and of MPN-specific therapies. Data were therefore extracted from an international nested case-control study, recruiting 798 patients with SC diagnosed concurrently or after the MPN. Overall, 2995 person-years (PYs) were accumulated and mortality rate (MR) since SC diagnosis was 5.9 (5.1-6.9) deaths for every 100 PYs. A "poor prognosis" SC (stomach, esophagus, liver, pancreas, lung, ovary, head-and-neck or nervous system, osteosarcomas, multiple myeloma, aggressive lymphoma, acute leukemia) was reported in 26.3% of the patients and was the cause of death in 65% of them (MR 11.0/100 PYs). In contrast, patients with a "non-poor prognosis" SC (NPPSC) incurred a MR of 4.6/100 PYs: 31% of the deaths were attributed to SC and 15% to MPN evolution. At multivariable analysis, death after SC diagnosis was independently predicted (HR and 95% CI) by patient age greater than 70 years (2.68; 1.88-3.81), the SC prognostic group (2.57; 1.86-3.55), SC relapse (1.53; 10.6-2.21), MPN evolution (2.72; 1.84-4.02), anemia at SC diagnosis (2.32; 1.49-3.59), exposure to hydroxyurea (1.89; 1.26-2.85) and to ruxolitinib (3.63; 1.97-6.71). Aspirin was protective for patients with a NPPSC (0.60; 0.38-0.95). In conclusion, SC is a relevant cause of death competing with MPN evolution. Prospective data are awaited to confirm the role of cytoreductive and anti-platelet drugs in modulating patient survival after the occurrence of a SC.

Monia Marchetti

Arianna Ghirardi

Arianna Masciulli

Alessandra Carobbio

Francesca Palandri

Nicola Vianelli

Elena Rossi

Silvia Betti

Ambra Di Veroli

Alessandra Iurlo

Daniele Cattaneo

Guido Finazzi

Massimiliano Bonifacio

Luigi Scaffidi

Andrea Patriarca

Elisa Rumi

Ilaria Carola Casetti

Clemency Stephenson

Elena Maria Elli

Miroslava Palova

Davide Rapezzi

Daniel Erez

Montse Gomez

Kai Wille

Manuel Perez‐Encinas

Francesca Lunghi

Anna Angona

Maria Laura Fox

Eloise Beggiato

Giulia Benevolo

Giuseppe Carli

Rossella Cacciola

Mary Frances McMullin

Alessia Tieghi

Valle Recasens

Susanne Isfort

Fabrizio Pane

Valerio De Stefano

Martin Griesshammer

Alberto Alvarez‐Larran

Alessandro Rambaldi

Tiziano Barbui

Second cancers in MPN: Survival analysis from an international study

MPN中的第二癌症：一项国际研究的生存分析

Ineffective erythropoiesis is observed in many erythroid disorders including β‐thalassemia and anemia of chronic disease in which increased production of erythroblasts that fail to mature exacerbate the underlying anemias. As loss of the transcription factor FOXO3 results in erythroblast abnormalities similar to the ones observed in ineffective erythropoiesis, we investigated the underlying mechanisms of the defective Foxo3 −/− erythroblast cell cycle and maturation. Here we show that loss of Foxo3 results in overactivation of the JAK2/AKT/mTOR signaling pathway in primary bone marrow erythroblasts partly mediated by redox modulation. We further show that hyperactivation of mTOR signaling interferes with cell cycle progression in Foxo3 mutant erythroblasts. Importantly, inhibition of mTOR signaling, in vivo or in vitro enhances significantly Foxo3 mutant erythroid cell maturation. Similarly, in vivo inhibition of mTOR remarkably improves erythroid cell maturation and anemia in a model of β‐thalassemia. Finally we show that FOXO3 and mTOR are likely part of a larger metabolic network in erythroblasts as together they control the expression of an array of metabolic genes some of which are implicated in erythroid disorders. These combined findings indicate that a metabolism‐mediated regulatory network centered by FOXO3 and mTOR control the balanced production and maturation of erythroid cells. They also highlight physiological interactions between these proteins in regulating erythroblast energy. Our results indicate that alteration in the function of this network might be implicated in the pathogenesis of ineffective erythropoiesis. Am. J. Hematol. 89:954–963, 2014. © 2014 Wiley Periodicals, Inc.

Xin Zhang

Genís Campreciós

Pauline Rimmelé

Raymond Liang

Safak Yalcin

Sathish Kumar Mungamuri

Jeffrey Barminko

Valentina D'Escamard

Margaret H. Baron

Carlo Brugnara

Dmitri Papatsenko

Stefano Rivella

Saghi Ghaffari

FOXO3‐mTOR metabolic cooperation in the regulation of erythroid cell maturation and homeostasis

FOXO3-mTOR代谢合作在调控红细胞成熟和稳态中的作用

Abstract Disease Overview The eosinophilias encompass a broad range of non‐hematologic (secondary or reactive) and hematologic (primary or clonal) disorders with the potential for end‐organ damage. Diagnosis Hypereosinophilia (HE) has generally been defined as a peripheral blood eosinophil count greater than 1.5 × 10 9 /L, and may be associated with tissue damage. After the exclusion of secondary causes of eosinophilia, diagnostic evaluation of primary eosinophilias relies on a combination of various tests. They include morphologic review of the blood and marrow, standard cytogenetics, fluorescence in situ hybridization, molecular testing and flow immunophenotyping to detect histopathologic or clonal evidence for an acute or chronic hematolymphoid neoplasm. Risk Stratification Disease prognosis relies on identifying the subtype of eosinophilia. After evaluation of secondary causes of eosinophilia, the 2022 World Health Organization and International Consensus Classification endorse a semi‐molecular classification scheme of disease subtypes. This includes the major category “myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions” (MLN‐eo‐TK), and the MPN subtype, “chronic eosinophilic leukemia” (CEL). Lymphocyte‐variant HE is an aberrant T‐cell clone‐driven reactive eosinophila, and idiopathic hypereosinophilic syndrome (HES) is a diagnosis of exclusion. Risk‐Adapted Therapy The goal of therapy is to mitigate eosinophil‐mediated organ damage. For patients with milder forms of eosinophilia (e.g., &lt;1.5 × 10 9 /L) without symptoms or signs of organ involvement, a watch and wait approach with close follow‐up may be undertaken. Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib. Pemigatinib was recently approved for patients with relapsed or refractory FGFR1 ‐rearranged neoplasms. Corticosteroids are first‐line therapy for patients with lymphocyte‐variant HE and HES. Hydroxyurea and interferon‐α have demonstrated efficacy as initial treatment and in steroid‐refractory cases of HES. Mepolizumab, an interleukin‐5 (IL‐5) antagonist monoclonal antibody, is approved by the U.S Food and Drug Administration for patients with idiopathic HES. Cytotoxic chemotherapy agents, and hematopoietic stem cell transplantation have been used for aggressive forms of HES and CEL, with outcomes reported for limited numbers of patients. Targeted therapies such as the IL‐5 receptor antibody benralizumab, IL‐5 monoclonal antibody depemokimab, and various tyrosine kinase inhibitors for MLN‐eo‐TK, are under active investigation.

William Shomali

Jason Gotlib

World Health Organization and International Consensus Classification of eosinophilic disorders: 2024 update on diagnosis, risk stratification, and management

世界卫生组织与国际共识的嗜酸性粒细胞疾病分类：2024年诊断、风险分层及管理的更新

Immune thrombocytopenia (ITP) is an autoimmune disorder associated with the production of autoantibodies directed against platelet glycoprotein complexes, resulting in both accelerated destruction of platelets and a relative reduction in platelet production. In adults, the majority of the acute cases respond to initial steroid therapy, but 50% relapse by 6 months and an additional 25% relapse beyond 1 year [1]. The non-responders and early relapsers can be difficult to manage and require additional therapies. These include intravenous immunoglobulin (IVIg), splenectomy, and rituximab, all of which can be problematic with variable and non-sustained responses, and specific thrombotic and infective risks with splenectomy [2]. Thrombopoietin receptor agonists (TPO-RA) exert their effects in ITP by increasing platelet production. Clinical trials have shown that TPO-RA are efficacious and well tolerated in chronic ITP patients, with some patients achieving a lasting response after cessation [3]. At the time, the study described in this manuscript was designed (2014), little was known about the short- and long-term response to TPO-RA in patients with newly diagnosed ITP. Hence, this study was initiated to evaluate the early- and long-term efficacy and safety of eltrombopag in adult non-splenectomized patients with steroid-unresponsive or dependent ITP within 6 months of diagnosis. Patients at six Australian centers were enrolled into this multicenter, single arm, prospective open-label study between February 2014 and February 2016. Patients were 18 years or older and with ITP diagnosed within the prior 6 months which was steroid-unresponsive or -dependent and, if used, without a sustained response to IVIg. Full inclusion and exclusion criteria can be found in the Supporting Information. The study was conducted following approval from the ethics committees of participating institutions and patients provided written informed consent. The study was registered as a clinical trial [ACTRN12613000721707]. Patients with platelets < 10 × 109/L commenced 75 mg eltrombopag daily; those with a platelet count ≥ 10 × 109/L commenced 50 mg daily. The dose was progressively increased by 25 mg increment every 2 weeks to maximum of 150 mg daily (100 mg daily if East Asian) if the platelet count remained ≤ 30 × 109/L or there was clinically significant bleeding. The dose in responding patients was maintained until the week 12 response assessment, unless the platelet count was ≥ 200 × 109/L. Subsequently, the dose was adjusted to the minimum required to maintain a platelet count > 30 × 109/L but ideally > 50 × 109/L, preferably in the absence of concomitant steroids. After 6 months and beyond, patients who achieved at least a stable partial response (PR; platelets > 50 × 109/L) had eltrombopag tapered by 25 mg each 3 weeks, with resumption of the previous therapeutic dose if the platelet count fell below 30 × 109/L. Response was assessed in all patients weekly until week 12, then at further time points to week 52 or 130 (see Study schema in Supporting Information). The primary endpoint was the overall response rate (ORR) at week 12: the composite of patients achieving a complete response (CR; platelet > 100 × 109/L), PR (platelets 50–100 × 109/L) or minor response (MR; platelet 30–49 × 109/L with ≥ 50% reduction in the dose intensity of concomitant ITP therapy compared with screening). The protocol specified if a PR or greater was reached at week 12 then the platelet count should be confirmed at week 14–16. However, after noting eight patients did not have a confirmatory platelet count the analysis was modified to allow inclusion of these patients in the response outcome assessment; this is subsequently referred to as "amended analysis." Secondary endpoints included CR, PR and MR rates at weeks 4, 8, and 26, therapeutic response at week 26 and 130, and safety profile. Although not specified in the original study design, long-term follow up of participants beyond week 130 was conducted to assess long-term responses and ITP management. Thirty-nine patients were enrolled. The median age was 52 years (range 18–82), 18 (46%) were female and the median ITP duration at enrolment was 2.2 months (range 0.3–6). Prior therapies apart from prednisolone included IVIg in 27 (69%) and azathioprine in 10 (26%) patients. The median platelet count at baseline was 21 × 109/L (range 2–94) and at week 12 was 117 × 109/L (range 20–498). Figure 1 outlines responses at each time point. The ORR per protocol and per amended analysis at week 12 was 64% (90% CI 52–77; CR 41%, PR 15%, MR 8%) and 85% (90% CI 75–94) (CR 59%, PR 18%, and MR 8%), respectively. Platelet counts at week 12 in those who achieved an MR or greater were 127 × 109/L (range 58–498) and 142 × 109/L (range 42–377). The median eltrombopag dose at weeks 12 and 27 was 50 mg, and at weeks 52, 104, and 130 it was 25 mg. Of the 29 patients who completed the study at week 130, 12 (31% of the total study population) had ceased eltrombopag and remained in CR. The median prednisolone dose at baseline was 25 mg (range, 5–100) and at week 12 was 2.25 mg (range, 0–15). Of the 23 patients who achieved a CR at week 12, 17 had ceased steroids and six remained on steroids at a median dose of 5 mg (range 5–15). Six required rescue therapies with steroids (6) and IVIg (2) for an ITP relapse throughout the study. Four of these participants subsequently came off study; the other two completed study and remained on eltrombopag with ongoing CR. With long-term follow up (median of 83.5 months from enrolment), 16 patients (41%) had stopped all ITP therapies and maintained a MR or better. Twelve (31%) remained on eltrombopag alone (≤ 50 mg daily) with ongoing PR or better. Two (5%) remained on high dose eltrombopag (150 mg daily) with additional therapies (prednisolone, hydroxychloroquine) to maintain response. The remaining nine (23%) patients stopped eltrombopag, at time points indicated in Figure 1 and required alternative therapies. A symptomatic adverse event occurred in 77% of participants. The most common were headache (28%), nausea (21%), musculoskeletal pain (15%), rash (15%), and diarrhea (15%). These were mild (grade 1–2) except for one grade 3 headache. Two patients had grade 2 transaminitis, who were on doses of 150 and 125 mg, respectively, which necessitated eltrombopag dose reduction. Serious AEs (SAEs) occurred in 9 patients (23%) of which three were considered treatment-related: one grade 3 transaminitis (while on a dose of 125 mg) which resolved with eltrombopag cessation and two venous thromboembolism (VTE)—deep venous thrombosis in a 76 year-old male, at a platelet count of 97 × 109/L receiving 125 mg eltrombopag, which was subsequently ceased, and pulmonary embolism in a 71 year-old female with concurrent ANCA-positive vasculitis, with a platelet count of 230 × 109/L receiving 50 mg eltrombopag which was continued. Bleeding occurred in 14 (36%) patients, most (9; 64%) were grade 1. Grade 2 bleeding occurred in four patients: menorrhagia; gastrointestinal bleed requiring endoscopy in a patient on aspirin with a platelet count > 100 × 109/L; haematuria; and epistaxis. There was one grade 3 gastrointestinal bleeding in a non-responding patient early in the study. Four patients had thrombocytosis (platelet count ≥ 450 × 109/L), which resolved with eltrombopag dose reductions without clinical sequelae. This study is unique in describing both the efficacy and tolerability of eltrombopag in non-splenectomized adults with steroid unresponsive or dependent ITP within 6 months of diagnosis, as well as the natural history with long-term follow up. We observed a high initial response rate with 85% of participants achieving a response at week 12, and most able to wean prednisolone completely or to small doses. Most responses were durable with over 70% maintaining response (40% off all therapy and 30% on eltrombopag) at both week 130 and with follow up at 7 years, a sustained response rate similar to that seen with eltrombopag in chronic ITP [4]. The few studies evaluating eltrombopag in newly-diagnosed ITP have reported similar outcomes but with short follow-up. A single-center study of 25 patients with steroid-nonresponsive newly-diagnosed ITP, found 76% had a sustained response to eltrombopag at 3 months [5]. Retrospective and real-world studies confirm that response to eltrombopag is similar between newly diagnosed, persistent, and chronic ITP patients [6]. It is likely that the ability to maintain sustained responses represents the natural history of ITP rather than a unique effect of TPO-RAs as similar trajectories are seen in patients responding to other therapies such as rituximab and corticosteroids [1]. Therefore the main benefit in our patients was avoiding the side-effects of other therapies, such as splenectomy or prolonged high-dose steroid use, while allowing the natural history of acute ITP to run its course. This is even more relevant now with updated guidelines recommending short-courses of steroids (< 6 weeks), whereby there should be earlier movement towards second-line therapies if there has been an inadequate response. Bleeding events in this study were infrequent in responding patients. Three patients with transaminitis resolved with drug cessation or dose reduction. Of note, these were patients all on an eltrombopag doses of > 100 mg and close monitoring of liver function should be undertaken in patients on higher doses. While the current dosing guideline of eltrombopag is the maximum dose of 75 mg, higher doses are used for other indications such as aplastic anemia. There were two cases of VTE treated with anticoagulation. The strengths of our study are the multicenter design and long-term follow up. Limitations include the lack of a control arm with which to compare the rate of response to eltrombopag. In conclusion, we found a high response rate to eltrombopag in a high-risk group of recently diagnosed steroid-refractory or dependent ITP patients, who have few other rapidly-acting treatment options. This may obviate the need for splenectomy and other more toxic therapies in a significant proportion of patients. H.T. and A.G. were the principal investigators of the study, involved in study design, protocol development, data analysis and development of the manuscript. C.D. was involved in data analysis and development of the manuscript. J.R. was the statistician for the study and was involved in study design, development of the analysis plans, development of the manuscript. R.B., T.B., S.C., and S.H. were members of the steering committee and were involved in the data interpretation and manuscript development. The authors would like to thank all the participating centers, patients and their families. The SPRITE trial received study drug and funding from Novartis Pharmaceuticals Pty Ltd (Australia) and was supported by the Thrombosis & Hemostasis Society of Australia and New Zealand (THANZ). R.B. has been a speaker at Novartis and Sobi sponsored meetings, airfare and accommodation received, honorarium declined. Investigator in clinical trials sponsored by Novartis and Sanofi. JR is a former employee of Novartis AG and holds shares in the company. H.T., C.D., T.B., S.C., C.M., S.H. and A.G. have no relevant conflicts of interest to declare. The data that support the findings of this study are available from the corresponding author upon reasonable request. Data S1 Supporting Information. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Huyen Tran

Caroline Dix

Robert Bird

Sanjeev Chunilal

Tim Brighton

John Reynolds

Simon He

Christine Mazis

Andrew Grigg

Efficacy and Long‐Term Outcomes of Eltrombopag Treatment Within 6 Months of Diagnosis in Patients With Steroid Unresponsive or Dependent Immune Thrombocytopenia

诊断后6个月内使用艾曲波帕治疗对类固醇无反应或依赖的免疫性血小板减少症患者的疗效和长期结果

ABSTRACT Chimeric antigen receptor (CAR) T‐cell therapy has revolutionized treatment of aggressive large B‐cell lymphoma (aLBCL). Patients with transformed indolent non‐Hodgkin lymphoma (tiNHL) were included in key CAR trials, but outcomes of CAR for this distinct, historically high‐risk group are poorly understood. We conducted a multicenter retrospective study of 1182 patients with aLBCL receiving standard‐of‐care CAR T between 2017 and 2022, including 338 (29%) with tiNHL. Rates of grade ≥ 3 cytokine release syndrome (CRS) were similar between tiNHL and de novo cohorts (7% vs. 8%, p = 0.6), while grade ≥ 3 immune effector cell‐associated neurotoxicity syndrome was lower in tiNHL (21% vs. 27%, p = 0.02). Overall response rate was similar in both cohorts (83% vs. 81%, p = 0.3), while complete response rate was higher in tiNHL (67% vs. 59%, p = 0.017). With a median follow‐up of 22.3 months, the progression/relapse‐free (PFS) and overall survival (OS) were similar between the tiNHL and de novo cohorts (24‐month PFS 41% [95% CI: 35%–46%] vs. 38% [95% CI: 35%–42%]; 24‐month OS 58% [95% CI: 52%–63%] vs. 52% [95% CI: 48%–56%], respectively). After adjusting for key risk factors, there was a trend toward a lower hazard of disease progression, relapse or death post‐CAR for tiNHL patients compared to de novo aLBCL patients (HR: 0.84 [95% CI: 0.69–1.0], p = 0.07). Elevated LDH, advanced stage, prior bendamustine within 12 months of CAR, receipt of bridging therapy, CNS involvement, and ≥ 3 prior lines of therapy were each associated with inferior PFS. In conclusion, CAR T therapy is highly effective with an acceptable toxicity profile in patients with tiNHL.

Swetha Kambhampati Thiruvengadam

Reid Merryman

Yan Wang

Charles Gaulin

Evandro Bezerra

Timothy Voorhees

Madhav R. Seshadri

Ayo Falade

Alma Habib

Amy A. Ayers

Megumi Bailey

Annette Brown

Neil Bailey

Krish Patel

Charalambos B. Andreadis

Adam S. Kittai

Caron Jacobson

Joycelynne Palmer

Stephen J. Forman

Loretta Nastoupil

Lihua E. Budde

Outcomes of <scp>CD19 CAR</scp> T in Transformed Indolent Lymphoma Compared to De Novo Aggressive Large B‐Cell Lymphoma

转化性惰性淋巴瘤与初治侵袭性大B细胞淋巴瘤中CD19 CAR T细胞治疗结果的比较

ABSTRACT Community‐acquired respiratory viral infections (CARV) significantly impact patients with hematological malignancies (HM), leading to high morbidity and mortality. However, large‐scale, real‐world data on CARV in these patients is limited. This study analyzed data from the EPICOVIDEHA‐EPIFLUEHA registry, focusing on patients with HM diagnosed with CARV during the 2023–2024 autumn–winter season. The study assessed epidemiology, clinical characteristics, risk factors, and outcomes. The study examined 1312 patients with HM diagnosed with CARV during the 2023–2024 autumn–winter season. Of these, 59.5% required hospitalization, with 13.5% needing ICU admission. The overall mortality rate was 10.6%, varying by virus: parainfluenza (21.3%), influenza (8.8%), metapneumovirus (7.1%), RSV (5.9%), or SARS‐CoV‐2 (5.0%). Poor outcomes were significantly associated with smoking history, severe lymphopenia, secondary bacterial infections, and ICU admission. This study highlights the severe risk CARV poses to patients with HM, especially those undergoing active treatment. The high rates of hospitalization and mortality stress the need for better prevention, early diagnosis, and targeted therapies. Given the severe outcomes with certain viruses like parainfluenza, tailored strategies are crucial to improving patient outcomes in future CARV seasons.

Jon Salmanton‐García

Francesco Marchesi

Milan Navrátil

Klára Piukovics

Maria Ilaria del Principe

Marianna Criscuolo

Yavuz M. Bilgin

Nicola S. Fracchiolla

Antonio Vena

Alessandra Romano

Iker Falces‐Romero

Nicola Sgherza

Inmaculada Heras‐Fernando

Monika M. Biernat

Verena Petzer

Pavel Žák

Barbora Weinbergerová

Michail Samarkos

Nurettin Erben

Jens van Praet

Alberto López‐García

Jorge Labrador

Tobias Lahmer

Ľuboš Drgoňa

Maria Merelli

Annarosa Cuccaro

Sonia Martín‐Pérez

Julio Dávila‐Valls

Francesca Farina

Chiara Cattaneo

László Imre Pinczés

Ferenc Magyari

Ildefonso Espigado

Caterina Buquicchio

Donald C. Vinh

Igor Stoma

Martin Čerňan

Lucia Prezioso

Mario Virgilio Papa

Gaëtan Plantefeve

Reham Abdelaziz Khedr

Josip Batinić

Gabriele Magliano

Simge Erdem

Sofya Khostelidi

Natasha Čolović

Davide Nappi

Patricia García‐Ramírez

Jakub Góra

Marta Callejas‐Charavia

Jędrzej Tłusty

Respiratory Viruses in Patients With Hematological Malignancy in Boreal Autumn/Winter 2023–2024: <scp>EPICOVIDEHA</scp>‐<scp>EPIFLUEHA</scp> Report

2023-2024年寒秋/冬季血液系统恶性肿瘤患者的呼吸道病毒：EPICOVIDEHA-EPIFLUEHA报告

Abbreviation	Am. J. Hematol.
Journal Impact	10.16
Quartiles(Global)	HEMATOLOGY(Q1)

ISSN	0361-8609, 1096-8652
h-index	130
Top Journals	Yes

Publication Information	Publisher: John Wiley and Sons Inc，Publishing cycle: Monthly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1976，Proportion of original research papers: 86.75%，Self Citation Rate:5.90%， Gold OA Rate: 29.12%
Average review cycle	网友分享经验：一般,3-6周
Average recruitment ratio	网友分享经验：较易

American Journal of Hematology

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Comprehensive analysis of TP53 mutation characteristics and identification of patients with inferior prognosis and enhanced immune escape in diffuse large B‐cell lymphoma

Targeting exhausted cytotoxic T cells through CTLA‐4 inhibition promotes elimination of neoplastic cells in human myelofibrosis xenografts

Second cancers in MPN: Survival analysis from an international study

FOXO3‐mTOR metabolic cooperation in the regulation of erythroid cell maturation and homeostasis

World Health Organization and International Consensus Classification of eosinophilic disorders: 2024 update on diagnosis, risk stratification, and management

Efficacy and Long‐Term Outcomes of Eltrombopag Treatment Within 6 Months of Diagnosis in Patients With Steroid Unresponsive or Dependent Immune Thrombocytopenia

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