Lymphocyte subsets were enumerated in a group of 31 patients with aplastic anemia. Abnormal numbers of immunoregulatory T-cells were found in some patients: 26% of them showed a reversed helper/suppressor ratio. Seven of 18 patients showed significantly decreased proliferation in response to PWM; this hyporesponsiveness was present in 75% of patients with a reversed helper/suppressor ratio and in 10% of those with a normal helper/suppressor ratio (R = 0.66, P = 0.008). Eight of 18 patients showed suppressor activity over PWM-induced allogeneic cell proliferation. This suppressive activity did not correlate with T-cell phenotype. Of the patients with a low number of T-cells, 73% had responded to treatment, whereas of those patients with a normal number of T-cells, 26% had responded (P = 0.016). The results are consistent with abnormal immune response in selected patients with aplastic anemia, and suggest a possible influence of T-cells on disease process.
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http://dx.doi.org/10.1002/ajh.2830160308 | DOI Listing |
Sci Rep
January 2025
Department of Laboratory Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, 030032, China.
Hematological parameters available on automated hematology analyzers have been shown to be useful indicators for hematological disorders. However, extensive studies especially in aplastic anemia for these indices are sparse. Our aim was to investigate the clinical utility of hematological parameters in aplastic anemia.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Hematology and Transplantology, Medical University of Gdansk, Gdansk, Poland.
Background: Paroxysmal nocturnal hemoglobinuria (PNH) is a rare complement-driven acquired hemolytic anemia with specific presentations of hemoglobinuria, abdominal pain, fatigue, and thrombosis.
Objective: To review the current therapeutic strategies for PNH, including anti-complement therapy and allogeneic hematopoietic cell transplantation (alloHCT), focusing on the tailoring of the approach to the disease subtype.
Results: The outcome of alloHCT varies depending on disease severity, thrombotic history, and response to prior therapies.
Front Oncol
January 2025
Department of Thyroid Surgery, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Background: It is uncommon to come across instances of aplastic anemia in individuals suffering from papillary thyroid carcinoma complicated by Hashimoto's thyroiditis. Here, a unique case is presented.
Case Presentation: A 23-year-old male was admitted to the hospital for "a lump in his right neck".
Br J Haematol
January 2025
Division of Hematology-Oncology, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Acquired aplastic anaemia (AA) is an autoimmune bone marrow failure disease resulting from a cytotoxic T-cell-mediated attack on haematopoietic stem and progenitor cells (HSPCs). Despite significant progress in understanding the T-cell repertoire alterations in AA, identifying specific pathogenic T cells in AA patients has remained elusive, primarily due to the unknown antigenic targets of the autoimmune attack. In this review, we will synthesize findings from several decades of research to critically evaluate the current knowledge on T-cell repertoires in AA.
View Article and Find Full Text PDFZhongguo Dang Dai Er Ke Za Zhi
January 2025
, Department of Pediatrics, Third Xiangya Hospital, Central South University Changsha 410013 China.
To guide clinical blood transfusion practices for pediatric patients, the National Health Commission has issued the health standard "Guideline for pediatric transfusion" (WS/T 795-2022). Blood transfusion is one of the most commonly used supportive treatments for children with hematological diseases. This guideline provides guidance and recommendations for blood transfusions in children with aplastic anemia, thalassemia, autoimmune hemolytic anemia, glucose-6-phosphate dehydrogenase deficiency, acute leukemia, myelodysplastic syndromes, immune thrombocytopenic purpura, and thrombotic thrombocytopenic purpura.
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