High-dose chemotherapy followed by autologous stem cell transplantation (ASCT) remains the standard of care for multiple myeloma (MM) patients. Although outpatient ASCT has been shown to be safe and feasible, the procedure is overall rare with most patients in the US undergoing inpatient ASCT. Furthermore, hospitalization rates for patients that undergo outpatient ASCT remain high. Adequate markers that predict hospitalization during outpatient ASCT are lacking, yet would be of great clinical value to select patients that are suited to outpatient ASCT. In this study we aimed to elucidate differences between planned outpatient and inpatient ASCT and further evaluated clinical characteristics that are significantly associated with hospitalization during planned outpatient hospitalization. Factors that were significantly associated with a planned inpatient ASCT included an advanced MM disease stage, worse performance status as well as non-Caucasian race, while low albumin levels and female gender were significantly associated with hospitalization during outpatient ASCT. The results of this analysis provide crucial knowledge of factors that are associated with planned inpatient ASCT and hospitalization during outpatient ASCT and could guide the treating physician in decision-making and further facilitate outpatient transplantation.

Sickle cell disease (SCD) is a prevalent genetic disorder caused by a mutation in the beta-globin gene. Hyperhemolysis (HS) is a severe complication involving the rapid destruction of both transfused and endogenous red blood cells, commonly found in SCD. This literature review explores the clinical presentation, diagnosis, pathogenesis, and management of HS in SCD. HS can manifest acutely or in a delayed manner, complicating diagnosis due to overlapping symptoms and varying reticulocyte responses. Immunohematological assessments often reveal delayed positivity in direct antiglobulin tests and antibody screens. HS typically presents severe anemia, jaundice, hemoglobinuria, and hemodynamic instability. Diagnostic markers include elevated bilirubin and lactate dehydrogenase levels alongside a reduced reticulocyte count. The management of HS is primarily empirical, with no clinical trials to support standardized treatment protocols. First-line treatments involve steroids and intravenous immunoglobulins (IVIG), which modulate immune responses and mitigate hemolysis. Refractory cases may require additional agents such as rituximab, eculizumab, tocilizumab, and, in some instances, plasma exchange or erythropoietin-stimulating agents. Novel therapeutic approaches, including bortezomib and Hemopure, have shown promise but require further investigation. Current management strategies are empirical, underscoring the need for robust clinical trials to establish effective treatment protocols that ultimately improve outcomes for SCD patients experiencing HS.

Myelodysplastic syndromes (MDSs), either primary or secondary, are a heterogeneous group of clonal hematological neoplasms characterized by bone marrow dyshematopoiesis, peripheral blood cytopenia, and the potential risk of acute myeloid leukemia (AML) transformation. The clinical heterogeneity in MDS is a reflection of the underlying multitude of genetic defects playing a role in the pathogenesis. Recent advances in the clinicopathological, immunophenotypic, and molecular landscape in understanding the pathophysiology of MDS lead to evolving and refined classification systems with newer entities. Evolving MDS therapies will target the disease’s core mechanisms, allowing for personalized treatment based on individual patient’s genes and leading to better outcomes. This review provides an overview of MDS pathogenesis to enhance comprehension of its various subgroups. Additionally, we examine the updated classification systems of the World Health Organization (WHO) and the International Consensus Classification (ICC) pertaining to MDS, along with relevant therapeutic approaches.

Chimeric antigen receptor T-cell (CART) therapy is a novel therapeutic modality utilized for managing relapsed/refractory hematologic cancers. This approach entails the genetic modification of either autologous or allogeneic T-cells to incorporate chimeric antigen receptor (CAR) proteins, enabling them to target specific proteins present on the surface of cancer cells and causing cytotoxicity. Despite its promising therapeutic outcomes, there is a notable drawback wherein these modified cells may also attack normal tissue cells expressing similar surface proteins. This phenomenon of cross-reactivity often leads to adverse events (AEs), resulting in significant mortality and morbidity. This chapter focuses on the assessment and management of CART therapy-related toxicities.