Background: Patients with hematological malignancies (HM) are at high risk of mortality from SARS-CoV-2 disease 2019 (COVID-19). A better understanding of risk factors for adverse outcomes may improve clinical management in these patients. We therefore studied baseline characteristics of HM patients developing COVID-19 and analyzed predictors of mortality. Methods: The survey was supported by the Scientific Working Group Infection in Hematology of the European Hematology Association (EHA). Eligible for the analysis were adult patients with HM and laboratory-confirmed COVID-19 observed between March and December 2020. Results: The study sample includes 3801 cases, represented by lymphoproliferative (mainly non-Hodgkin lymphoma n = 1084, myeloma n = 684 and chronic lymphoid leukemia n = 474) and myeloproliferative malignancies (mainly acute myeloid leukemia n = 497 and myelodysplastic syndromes n = 279). Severe/critical COVID-19 was observed in 63.8% of patients (n = 2425). Overall, 2778 (73.1%) of the patients were hospitalized, 689 (18.1%) of whom were admitted to intensive care units (ICUs). Overall, 1185 patients (31.2%) died. The primary cause of death was COVID-19 in 688 patients (58.1%), HM in 173 patients (14.6%), and a combination of both COVID-19 and progressing HM in 155 patients (13.1%). Highest mortality was observed in acute myeloid leukemia (199/497, 40%) and myelodysplastic syndromes (118/279, 42.3%). The mortality rate significantly decreased between the first COVID-19 wave (March–May 2020) and the second wave (October–December 2020) (581/1427, 40.7% vs. 439/1773, 24.8%, p value < 0.0001). In the multivariable analysis, age, active malignancy, chronic cardiac disease, liver disease, renal impairment, smoking history, and ICU stay correlated with mortality. Acute myeloid leukemia was a higher mortality risk than lymphoproliferative diseases. Conclusions: This survey confirms that COVID-19 patients with HM are at high risk of lethal complications. However, improved COVID-19 prevention has reduced mortality despite an increase in the number of reported cases.

To date, the impact of the tumor microenvironment on the prognosis of patients with classic Hodgkin lymphoma (cHL) during anti-PD-1 therapy has been studied insufficiently. This retrospective study included 61 primary samples of lymph nodes from patients who had relapsed/refractory (r/r) cHL and were treated with nivolumab. Repeated samples were obtained in 15 patients at relapse or disease progression after immunotherapy. Median follow-up was 55 (13–63) months. The best overall response rate and progression-free survival (PFS) were analyzed depending on the expression of CD68, CD163, PD-1, LAG-3, TIM-3, CTLA-4, TIGIT, CD163/c-maf in the tumor microenvironment in primary and sequential biopsies. The combination of CD163/c-maf antibodies was used for the identification of M2 macrophages (M2). A low number of macrophages in primary samples was associated with inferior PFS during nivolumab treatment (for CD163-positive cells p = 0.0086; for CD68-positive cells p = 0.037), while a low number of M2 with higher PFS (p = 0.014). Complete response was associated with a lower level of M2 (p = 0.011). In sequential samples (before and after nivolumab therapy) an increase in PD-1 (p = 0.011) and LAG-3 (p = 0.0045) and a depletion of CD68 (p = 0.057) and CD163 (p = 0.0049)-positive cells were observed. The study expands understanding of the cHL microenvironment structure and dynamics during nivolumab therapy in patients with r/r cHL.

Invasive fungal diseases (IFD) are severe complications in patients with hematological malignancies, worsening prognosis, and increasing mortality. Despite extensive research, epidemiological data often lack temporal systematization, hindering interpretation and practical application. The objective was to assess the incidence and etiology of IFDs in oncohematological patients across different therapeutic groups using published studies. A systematic search was conducted in PubMed (Medline), Embase, and Google Scholar. Meta-analyses using primarily random-effects models were performed to estimate IFD incidence, overall etiological structure (proportions of major genera like Aspergillus, Candida, and rare pathogens), and analyze temporal trends (pre- vs. post-2010). Incidence analysis included 34 publications (47 cohorts; 91,151 participants); etiology analysis included 35 cohorts (4427 isolates). Pooled IFD incidence was significantly higher in allo-HSCT recipients (9.96 %, 95 % CI 8.24-11.83 %) compared to chemotherapy (5.22 %, 95 % CI 3.96-6.65 %) and auto-HSCT (3.39 %, 95 % CI 1.56-5.83 %). Overall, Aspergillus (44.8 %) and Candida (34.1 %) dominated IFD etiology. A numerical shift occurred over time, with Candida proportion (48.6 %) surpassing Aspergillus (38.0 %) after 2010, reversing the pattern seen before 2010 (Candida 30.0 %, Aspergillus 47.8 %). Rare pathogens collectively accounted for ∼12.9 % pre-2010 and ∼8.8 % post-2010. Despite these numerical shifts, no statistically significant overall differences in IFD incidence or the proportions of major/rare pathogen groups were found between the pre- and post-2010 periods based on subgroup difference tests (p > 0.05). Etiology varied significantly by treatment. This comprehensive meta-analysis reveals significant variability in IFD incidence and etiology based on treatment modality, with allo-HSCT conferring the highest risk. While numerical shifts in pathogen distribution occurred over time, statistically significant overall temporal trends were not detected in this dataset for major or rare pathogens. High study heterogeneity is a key limitation. The findings underscore the need for risk-stratified prophylaxis and diagnostics, informing antifungal stewardship strategies tailored to treatment settings.

Objective. To study epidemiology and impact of colonization by multidrug-resistant Gram-negative bacteria (MDRGNB) on bloodstream infections (BSI) during allogeneic hematopoietic stem cell transplantation (allo-HSCT). Materials and Methods. The retrospective study included 288 patients received the first allo-HSCT between 2018 and 2019. The median age was 32 (18–66) years, male – 53% (n = 152). The majority of patients had acute leukemia – 62% (n = 178) and received transplant from matched unrelated – 42% (n = 120) or haploidentical donor – 26% (n = 75). Relapse of underlying disease at the moment of all-HSCT was registered in 23% (n = 66) of patients. Results. Colonization of non-sterile sites before allo-HSCT by at least one MDRGNB was detected in 28% (n = 64). In most cases resistance is due to extended spectrum beta-lactamases (ESBL) – 86% (n = 55), while carbapenemases in combination with ESBL were detected in 14% (n = 9) of patients. After allo-HSCT the colonization was significantly higher than before transplantation (n = 161, 56%, p = 0.001), mainly due to carbapenemase- and ESBL-producing bacteria – 73% (n = 118) (p = 0.001). BSI in the early period after transplantation developed in 26% (n = 76), and in 56% (n = 43) was caused by MDRGNB. The etiology of BSI included K. pneumoniae – 51% in mostly cases. The etiology of BSI was the same bacteria that colonized non-sterile sites 2 weeks before the detection bacteria in bloodstream in 69% (n = 30) patients. Colonization by MDRGNB was associated with the development of BSI (p < 0.0001). The 100-day overall survival (OS) after all-HSCT was significantly lower in patients with colonization of non-sterile sites by MDRGNB compared with patients without colonization (60.6% vs 88.2%, p = 0.001). Conclusions. Colonization of MDRGNB after allo-HSCT reached 56%. K. pneumoniae was predominant etiology in both colonization and bloodstream infections. Colonization by MDRGNB was associated with the development of BSI and decreased OS after allo-HSCT.

In this single-center analysis, we evaluated the trends in 5185 hematopoietic cell transplantations performed between 1990 and 2022. The study group comprised 3237 allogeneic (alloHCT) and 1948 autologous (autoHCT) hematopoietic cell transplantations. In the multivariate analysis, there was an improvement in event-free-survival (EFS) after autoHCT (HR 0.6, 95% CI 0.4–0.7, p < 0.0001) due to reduced cumulative incidence of relapse in the last five years (56% in 2010–2014 vs. 38% in 2015–2022). An improvement in EFS after alloHCT over time was observed (HR 0.33, 95% CI 0.23–0.48, p < 0.0001), which was due to reduced non-relapse mortality. No difference in cumulative relapse incidence was observed over the last decade for allografted patients. Survival after autoHCT improved in Hodgkin’s disease (HR 0.1, 95% CI 0.1–0.3), multiple myeloma (HR 0.4, 95% CI 0.2–0.7) and solid tumors (HR 0.2, 95% CI 0.2–0.4), while after alloHCT, improvement was observed in acute myeloid leukemia (HR 0.3, 95% CI 0.1–0.5), acute lymphoblastic leukemia (HR 0.2, 95% CI 0.1–0.5), Hodgkin’s disease (HR 0.1, 95% CI 0.0–0.4), non-Hodgkin’s lymphomas and chronic lymphocytic leukemia (HR 0.2, 95% CI 0.0–0.6), inborn diseases (HR 0.2, 95% CI 0.2–0.4) and acquired aplastic anemia with matched related donors and matched unrelated donors (HR 0.3, 95% CI 0.2–0.8).