The aim of this study was to determine the time to positivity (TTP) of neonatal blood cultures, to investigate differences between early onset versus late-onset sepsis, and non-proven versus proven sepsis, and to examine differences in TTP by organism type using a retrospective observational study at the

The CellaVision Advanced RBC Software Application is an easy-to-use software that helps to detect most RBC morphological abnormalities in a sensitive and specific way without increasing work load, provided the proper cut-offs are chosen. However, evaluation of the images by an experienced observer remains necessary.

The recent study of Boettcher et al 1 describes 5 cases of donor-engrafted clonal hematopoiesis (CH), one of which progressed into myelodysplastic syndrome (MDS) in both donor and recipient. We share our experience with 4 additional cases of donor-engrafted CH in which all recipients evolved into a donor cell-derived hematologic neoplasm (DCHN). All patients had received an allogeneic stem cell transplant from an HLA-identical sibling resulting in long-term complete remission and full donor chimerism.Case 1. A 43-year-old female patient with MDS with excess blasts-2 (MDS-EB2) received a peripheral blood stem cell (PBSC) transplant from her 45-year-old sister. A second PBSC transplant from the same donor was performed for a relapse of the original disease 20 months after the first transplant. As reported previously, 2 the discovery of JAK2 p.(V617F) mutations led to the retrospective analysis of both donor and recipient samples, as the donor had a history of a portal venous thrombosis before the first PBSC donation. We identified a JAK2 p.(V617F) mutation in pretransplant donor samples and posttransplant donor and recipient samples. Twenty years posttransplant, the recipient exhibited an exponential increase in JAK2 p.(V617F) mutational burden with clinical progression toward a myeloproliferative neoplasm (MPN)-type polycythemia vera with secondary myelofibrosis.Treatment was needed with phlebotomies, hydroxyurea, and ruxolitinib. In contrast, the donor so far remained untreated as no further myeloproliferative features were observed, despite a gradual increase in JAK2 p.(V617F) mutational burden as high as 100% (Figure 1). Interestingly, we performed shallow whole-genome sequencing analysis and observed an identical del(20)(q11q13) in recent blood samples from both donor and recipient (supplemental Data), suggesting donorengrafted CH with both a JAK2 p.(V617F) and del(20q) abnormality.Case 2. A 68-year-old man with MDS with multilineage dysplasia received a PBSC transplant from his 63-year-old-brother. Three and a half years later, the patient developed a donor cell leukemia with 21% myeloblasts in the bone marrow aspirate and full donor chimerism. Next-generation sequencing (NGS) analysis revealed 3 pathogenic variants: SFRS2 p.(P95H), DNMT3A p.(W314*), and RUNX1 p.(R346Afs*248). Sequencing of the healthy donor's peripheral blood showed identical SFRS2 and DNMT3A variants, although at a lower variant allele frequency (VAF) (Figure 2).Case 3. A 30-year-old man with acute myeloid leukemia with maturation (AML FAB M2, not otherwise specified) received a PBSC transplant from his 35-year-old brother. Seventeen years later, the patient developed acute monoblastic leukemia with full donor chimerism. NGS analysis revealed 5 pathogenic variants: ASXL1 p.(G646Wfs*12), EZH2 p.(E745K), FLT3 p.(I836del), SETBP1 p.(D868N), and TET2 p.(Q219*). Sequencing of the healthy donor's bone marrow at the time of the DCHN showed an identical EZH2 variant (Figure 2). Morphological evaluation of the peripheral blood and bone marrow reveal...

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Introduction: Myeloid sarcoma (MS), previously known as granulocytic sarcoma or chloroma, is a rare neoplastic condition defined as a tumor mass consisting of myeloblasts or immature myeloid cells occurring at an extramedullary site. Clinical presentation is diverse and determined by a tumor mass effect or local organ dysfunction. Case Report: We report the case of a 25-year-old previously healthy male with rapidly progressive shortness of breath. A chest CT scan demonstrated a heterogenous anterosuperior mediastinal mass with pleural and pericardial invasion. A diagnosis of MS with both myeloid and lymphoid characteristics was made by pathologic, morphologic, and immunophenotypic investigation. Next generation analysis revealed a pathogenic TP53 mutation (c.1035_1036insCT, p.Glu346Leufs*25). After 4 cycles of chemotherapy only a partial metabolic response and tumor size reduction was obtained. A pretransplant bone marrow biopsy revealed the progression of disease to acute myeloid leukemia. Cytogenetic analysis demonstrated a t(10; 11)(p12;q21). Fluorescence in situ hybridization confirmed the presence of a PICALM-MLLT10 fusion gene. Conclusion: MS with a mediastinal localization is rare and often misdiagnosed as malignant lymphoma. Acute leukemia harboring a PICALM-MLLT10 fusion gene is characterized by a mixed T cell and myeloid phenotype. The rearrangement is a rare recurrent translocation associated with specific clinical features, as illustrated in this case report.