Objective: To describe the case of a child who presented hemophagocytic lymphohistiocytosis (HLH) associated with acute monocytic leukemia after chemotherapy, with hemophagocytosis caused by leukemic cells.
Case Description: In a university hospital in Southern Brazil, a 3-year-old female was diagnosed with acute monocytic leukemia with normal karyotype. The chemotherapy regimen was initiated, and she achieved complete remission six months later, relapsing after four months with a complex karyotype involving chromosomes 8p and 16q. The bone marrow showed vacuolated blasts with a monocytic aspect and evidence of hemophagocytosis. The child presented progressive clinical deterioration and died two months after the relapse.
Comments: HLH is a rare and aggressive inflammatory condition characterized by cytopenias, hepatosplenomegaly, fever, and hemophagocytosis in the bone marrow, lymph nodes, spleen, and liver. Although rare, malignancy-associated HLH (M-HLH) is fatal. The patient in this case report met five out of the eight established criteria for HLH. The evolution of the patient's karyotype, regardless of the diagnostic profile, seemed secondary to the treatment for acute monocytic leukemia. In this case, the cytogenetic instability might have influenced the abnormal behavior of leukemic cells. This is a rare case of HLH in a child with acute monocytic leukemia.
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http://dx.doi.org/10.1590/1984-0462/2021/39/2019290 | DOI Listing |
Biomedicines
December 2024
Department of Cardiology, West China Hospital, Sichuan University, Chengdu 610041, China.
Coronary obstruction following plaque rupture is a critical pathophysiological change in the progression of stable angina (SAP) to acute coronary syndrome (ACS). The accumulation of platelets and various inflammatory cells on apoptotic endothelial cells is a key factor in arterial obstruction after plaque rupture. Through single-cell sequencing analysis (scRNA-seq) of plaques from SAP and ACS patients, we identified significant changes in the annexin V and P-selectin glycoprotein ligand 1 pathways.
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January 2025
Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
Background: For the treatment of liver fibrosis, several novel cell therapies have been proposed. Autologous macrophage therapy has been reported as one of the promising treatments. So far, most studies have used colony-stimulating factor 1 (CSF-1) to induce the differentiation of macrophage progenitor cells.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Shanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Acute myocardial infarction (AMI) is associated with well-established metabolic risk factors, especially hyperlipidemia and obesity. Myocardial ischemia-reperfusion injury (mIRI) significantly offsets the therapeutic efficacy of revascularization. Previous studies indicated that disrupted lipid homeostasis can lead to lipid peroxidation damage and inflammation, yet the underlying mechanisms remain unclear.
View Article and Find Full Text PDFJ Exp Med
March 2025
Division of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.
Lysosomal stress due to the accumulation of nucleic acids (NAs) activates endosomal TLRs in macrophages. Here, we show that lysosomal RNA stress, caused by the lack of RNase T2, induces macrophage accumulation in multiple organs such as the spleen and liver through TLR13 activation by microbiota-derived ribosomal RNAs. TLR13 triggered emergency myelopoiesis, increasing the number of myeloid progenitors in the bone marrow and spleen.
View Article and Find Full Text PDFFront Immunol
January 2025
Neuroimmunology Unit, Santa Lucia Foundation IRCCS, Rome, Italy.
Introduction: Acute COVID-19 infection causes significant alterations in the innate and adaptive immune systems. While most individuals recover naturally, some develop long COVID (LC) syndrome, marked by persistent or new symptoms weeks to months after SARS-CoV-2 infection. Despite its prevalence, there are no clinical tests to distinguish LC patients from those fully recovered.
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