A male with myelodysplastic syndrome (MDS) following aplastic anemia is reported. The patient had been diagnosed as aplastic anemia at 8 years of age, and treated with blood transfusions, anabolic and glucocorticoid steroid hormones. Over a period of subsequent twelve years, he had remission and deterioration. At the age of 21, the patient developed a sudden progression of severe anemia, when his bone marrow showed hyperplasia with prominent dyshematopoiesis and excess of blasts, compatible with MDS by the definition of FAB classification. He received low dose Ara-C therapy, which was ineffective. Nine months later he developed acute monocytic leukemia (M5b) and died. Chromosomal analysis revealed 46, XY at the onset of aplastic anemia, 46, XY, del (6) (q21 q27) at the MDS and 46, XY, -7, +21, 6q-/47, XY, +Y, -7, +21, 6q- at the acute leukemic stage.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Adverse drug events (ADEs) risk signal mining related to eculizumab based on the FARES database.
Front Pharmacol
January 2025
The First Department of Specialty Medicine, Inner Mongolia Corps Hospital of The Chinese People's Armed Police Force, Hohhot, China.
Introduction: Eculizumab is a C5 complement inhibitor approved by the FDA for the targeted treatment of four rare diseases, paroxysmal nocturnal hemoglobinuria (PNH), atypical hemolytic uremic syndrome (aHUS), generalized myasthenia gravis (gMG), and aquaporin-4 immunoglobulin G-positive optic neuromyelitis optica spectrum disorders (AQP4-IgG+NMOSD). The current study was conducted to assess real-world adverse events (AEs) associated with eculizumab through data mining of the FDA Adverse Event Reporting System (FAERS).
Methods: Disproportionality analyses, including Reporting Ratio Ratio (ROR), Proportional Reporting Ratio (PRR), Bayesian Confidence Propagation Neural Network (BCPNN), and Multi-Item Gamma Poisson Shrinker (MGPS) algorithms were used to quantify the signals of eculizumab-associated AEs.
Clinical utility of hematological parameters in aplastic anemia.
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 PDFEfficacy of Poloxamer 188 in Carboplatin-Induced Aplastic Anemia Model in CBA Mice.
Dokl Biol Sci
January 2025
Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry Branch, Russian Academy of Sciences, Pushchino, Russia.
Poloxamer 188 (P188) was tested for effect on medullary hematopoiesis in aplastic anemia. P188 was administered to CBA mice with developing anemia via oral gavage at doses of 10, 100, and 500 mg/kg. A dose-dependent effect was observed, including an increase in erythrocyte count, hemoglobin, and reticulocyte count.
View Article and Find Full Text PDFCase Report: A Novel Homozygous Variant in the Gene Causes Fanconi Anemia.
Genet Test Mol Biomarkers
January 2025
Department of Biology, University of Sistan and Baluchestan, Zahedan, Iran.
Fanconi anemia (FA) is a rare genetic disorder that affects multiple systems in the body and is the most prevalent congenital syndrome, leading to bone marrow failure. Twenty-two genes have been identified as contributors to the disease. Significant advancements have been made in the past 2 decades in understanding the genetic and pathophysiological processes involved.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!