Endothelial cell activation and injury is common after hematopoietic stem cell transplant (HSCT) and is associated with many post-transplant complications. An underexplored mechanism of endothelial cell damage in this population is the infusion of normal saline (NS, 0.9 % sodium chloride) and other crystalloids, as NS use is associated with adverse outcomes in other patient populations. We hypothesized that the infusion of unbalanced crystalloids during HSCT may lead to changes in biomarkers commonly associated with red blood cell (RBC) hemolysis in patients before and after infusion, and that markers of endothelial and end-organ damage during admission may be associated with markers of hemolysis and total crystalloid use. Samples were collected from 97 patients. From pre-fluid infusion to post-fluid infusion, mean haptoglobin decreased (11.7 ug/ml vs 8.4 ug/ml; p < 0.0001), hemopexin decreased (549 vs 512 μg/ml; p = 0.005), and red cell distribution width (RDW) decreased (15.7 vs 15.6; p = 0.0009). During admission (mean 19.4 days, SD 9.9), all markers of tissue and organ damage, including mean creatinine, lactate dehydrogenase (LDH), blood urea nitrogen (BUN), total bilirubin, AST, and ALT, increased from admission to peak levels (p < 0.0001). On linear regression, fluid volume (ml/kg) of crystalloid infusion positively predicted post-fluid infusion cell-free hemoglobin (r(96) = 0.34, p < 0.0001), free heme (r(96) = 0.36, p < 0.0001), and peak LDH during admission (r(75) = 0.23, p = 0.041), and negatively predicted post-fluid infusion hemopexin (r(96) = - 0.34, p < 0.0001). Unbalanced crystalloids may contribute to hemolysis and endothelial damage in HSCT patients. Alternatives such as buffered crystalloid solutions (PlasmaLyte, Lactated Ringer's) may be worth investigating in this population.
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http://dx.doi.org/10.1016/j.transci.2023.103641 | DOI Listing |
Cureus
December 2024
Radiodiagnosis, Malla Reddy Medical College for Women, Hyderabad, IND.
Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell disorders commonly characterized by excessive production of blood cell lineages. The JAK2 V617F mutation plays a crucial role in the pathogenesis of these conditions, often leading to thrombotic complications. Here, we present the case of a 21-year-old man who presented with acute abdominal pain and was found to have portal vein thrombosis with splenomegaly.
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January 2025
Department of Hematology, The Sixth Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, China.
CD7-targeted chimeric antigen receptor-T (CAR-T) cell therapy has shown great promise in the treatment of relapsed/refractory T-cell acute lymphoblastic leukemia (T-ALL). In this study, we reported a case of a 34-year-old male patient with T-ALL who finally developed multi-line drug resistance and refractoriness after multiple lines of high-intensity chemotherapy. After physician evaluation, this patient received allogeneic hematopoietic stem cell transplantation (allo-HSCT).
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January 2025
Department of Hematology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
B-cell acute lymphoblastic leukemia (B-ALL) with the fusion gene has a poor prognosis, and the mortality rate exceeds 90%, particularly in cases of extramedullary relapse (EMR). Herein, we present a case of a 46-year-old male patient who developed relapsed B-ALL with . The patient initially achieved a complete remission (CR) after induction therapy and underwent haploidentical hematopoietic stem cell transplantation.
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January 2025
Department of Hematology, Jiangdu People's Hospital, Yangzhou, China.
Introduction: Acute myeloid leukemia (AML), a highly heterogeneous hematological malignancy, remains a major challenge in adult oncology. Stem cell research has highlighted the crucial role of long noncoding RNA (lncRNA) in regulating cellular differentiation and self-renewal processes, which are pivotal in AML pathogenesis and therapy resistance.
Methods: This study explores the relationship between cuproptosis-related lncRNAs and AML prognosis, providing novel insights into their impact on hematopoietic stem and progenitor cells.
Eur J Haematol
January 2025
Hematology, St. Paul's Hospital and The University of British Columbia, Vancouver, British Columbia, Canada.
Introduction: Iron overload (IOL) accumulates in myelodysplastic syndromes (MDS) from expanded erythropoiesis and transfusions. Somatic mutations (SM) are frequent in MDS and stratify patient risk. MDS treatments reversing or limiting transfusion dependence are limited.
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