Background: Tuberculosis (TB) is a rare but potentially devastating complication in hematopoietic stem cell transplantation (HSCT) recipients. Myelosuppression-related antibiotics should be used cautiously in patients with hematological malignancies, especially those undergoing bone marrow transplantation and receiving bone marrow suppression therapy. Although linezolid has become the recommended drug for severe TB, its hematological toxicity is still an obstacle to its clinical application. Contezolid is a new representative of oxazolidinones in clinical development, showing superior anti-infection efficacy, but there have been no reports on the treatment of post-HSCT TB.
Case Presentation: We reported a patient with acute lymphoblastic leukemia suffered from pulmonary TB infection after HSCT. During anti-TB treatment, the patient had a poor response to linezolid-containing regimen, and developed side effects such as gingival bleeding and thrombocytopenia, so the administration was switched to contezolid. After 15 days of continuous treatment, the patient's platelet increased to 58×10/L, and he was discharged in stable condition. During subsequent anti-TB treatment with contezolid for more than 7 months, the platelets remained stable, and no hematological adverse reactions and no symptoms of peripheral neuropathy were observed. Moreover, repeat imaging showed that the bilateral lung lesions were significantly reduced, indicating a good outcome for the patient.
Conclusion: This was the first successful case of post-HSCT TB patients treated with contezolid-containing antibiotic management strategies, which exhibited remarkable efficacy and good safety in this deadly disease.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10614019 | PMC |
http://dx.doi.org/10.3389/fcimb.2023.1258561 | DOI Listing |
Stem Cell Rev Rep
January 2025
Institute for Cellular and Molecular Medicine, Department of Immunology, SAMRC Extramural Unit for Stem Cell Research and Therapy, University of Pretoria, Pretoria, 0084, South Africa.
J Mol Med (Berl)
January 2025
Department of Hematology and Oncology, Children's Hospital of Nanjing Medical University, 72 Guangzhou Road, Nanjing, 210008, Jiangsu Province, China.
Glucose phosphate isomerase (GPI) deficiency caused by GPI gene mutations is a rare heterogenous condition that causes hereditary non-spherocytic hemolytic anemia (HNSHA). Patients who suffer from severe anemia may need more effective treatment. Here, clinical data and genetic testing results of two cases of HNSHA with GPI mutations treated with allogeneic hematopoietic stem cell transplantation (allo-HSCT) were retrospectively analyzed.
View Article and Find Full Text PDFAnn Hematol
January 2025
Hematology and Hematopoietic Stem Cell Transplant Center, Department of Medicine and Surgery, University of Naples Federico II, Via S. Pansini 5, Naples, 80131, Italy.
Splenomegaly is a quite common clinical feature of Philadelphia (Ph) negative chronic myeloproliferative neoplasms (MPNs) and its presence may, in some cases, drives treatment decision. Most importantly, palpable splenomegaly is a minor criterion for both pre-fibrotic/early primary myelofibrosis and primary myelofibrosis (PMF) diagnosis, even if clinical assessment by physical examination is poorly reliable and accurate. On the other hand, despite the International Working Group-Myeloproliferative Neoplasms Research and Treatment and European LeukemiaNet guidelines defined spleen response criteria by palpation, they also recognized the highly subjective nature of spleen size assessment by physical examination, and recommended objective confirmation of volume reduction via computed tomography or magnetic resonance imaging (MRI).
View Article and Find Full Text PDFJ Exp Med
March 2025
Department of Hematology, The Second Affiliated Hospital of Chongqing Medical University, School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China.
Hematopoietic stem cells (HSCs) are susceptible to replication stress, which is a major contributor to HSC defects in Fanconi anemia (FA). Here, we report that HSCs relax the global chromatin by downregulating the expression of a chromatin architectural protein, DEK, in response to replication stress. DEK is abnormally accumulated in bone marrow (BM) CD34+ cells from patients with FA and in Fancd2-deficient HSCs.
View Article and Find Full Text PDFFront Oncol
January 2025
Department of Medical Oncology and Hematology, University of Zurich and University Hospital Zurich, Zurich, Switzerland.
Introduction: -rearrangements define a subclass of acute leukemias characterized by a distinct gene expression signature linked to the dysfunctional oncogenic fusion proteins arising from various chromosomal translocations involving the (also known as ) gene. Research on the disease pathomechanism in -rearranged acute leukemias has mainly focused on the upregulation of the stemness-related genes of the -family and their co-factor .
Results: Here we report the and fusion gene-dependent downregulation of , a TGF-β signaling axis transcription factor.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!