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A 66-year-old woman was diagnosed with chronic lymphocytic leukemia (CLL) due to the finding of leukocytosis and started acalabrutinib and obinutuzumab (AO) therapy. After three cycles of AO therapy, she developed severe pancytopenia with hypoplastic bone marrow and was diagnosed with fulminant aplastic anemia (AA) due to neutropenia with no response to granulocyte colony-stimulating factor. One month after the onset of AA, she received HLA-haploidentical allogeneic hematopoietic stem cell transplantation (haplo-SCT) from a daughter using FluMelTBI (fludarabine 180 mg/m, melphalan 80 mg/m, total body irradiation 4 Gy) as the conditioning regimen and tacrolimus, mycophenolate mofetil, and post-transplant cyclophosphamide (PTCy) for graft-versus-host disease (GVHD) prophylaxis.
View Article and Find Full Text PDFSepsis-induced NET formation requires MYD88 but is independent of GSDMD and PAD4.
FASEB J
January 2025
Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Neutrophils are peripheral blood-circulating leukocytes that play a pivotal role in host defense against bacterial pathogens which upon activation, they release web-like chromatin structures called neutrophil extracellular traps (NETs). Here, we analyzed and compared the importance of myeloid differentiation factor 88 (MYD88), peptidyl arginine deiminase 4 (PAD4), and gasdermin D (GSDMD) for NET formation in vivo following sepsis and neutrophilia challenge. Injection of lipopolysaccharide (LPS)/E.
View Article and Find Full Text PDFHypercalcemia and co-occurring TBX1 mutation in Glycogen Storage Disease Type Ib: case report.
BMC Med Genomics
January 2025
Laboratory of Clinical Immunology, Inflammation, and Allergy (LICIA), Faculty of Medicine and Pharmacy of Casablanca, Hassan II University, Casablanca, Morocco.
Glycogen Storage Disease Type Ib (GSD-Ib) is a rare autosomal recessive metabolic disorder caused by mutations in SLC37A4, leading to a deficiency in glucose-6-phosphate translocase. This disorder is characterized by impaired glycogenolysis and gluconeogenesis, resulting in clinical and metabolic manifestations. We report a three-month-old Moroccan female patient presenting with doll-like facies, hepatomegaly, dysmorphic features, and developmental delays.
View Article and Find Full Text PDFLiterature review analysis of aortitis induced by granulocyte-colony stimulating factor.
Front Pharmacol
December 2024
Department of Clinical Pharmacy, Weifang People's Hospital, Shandong Second Medical University, Weifang, China.
Background: Recombinant human granulocyte-colony stimulating factors (G-CSF)-induced aortitis is a rare but particularly serious adverse event, commonly seen in cancer patients undergoing chemotherapy. The aim of this article is to clarify the clinical characteristics of G-CSF- induced aortitis and provide effective references for clinical diagnosis and intervention.
Methods: Case reports of adverse reactions of aortitis induced by G-CSF were collected from the relevant databases.
Granulocyte Colony-Stimulating Factor-Associated Aortitis Unveiled by 18 F-FDG PET/CT.
Clin Nucl Med
February 2025
From the Department of Nuclear Medicine, Pitié-Salpêtrière Hospital, Assistance Publique-Hôpitaux de Paris, Sorbonne University, Paris, France.
In oncology, G-CSF (granulocyte colony-stimulating factor) is often administered to counteract chemotherapy-induced neutropenia. Recent studies have highlighted a significant side effect, G-CSF-associated aortitis, with an incidence of ~0.4%.
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