Abstract
ABSTRACTAplastic anemia (AA) is a rare and life-threatening bone marrow failure (BMF) that results in peripheral blood cytopenia and reduced bone marrow hematopoietic cell proliferation. The symptoms are similar to myelofibrosis, myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) making diagnosis of AA complicated. The pathogenesis of AA is complex and its mechanism needs to be deciphered on an individualized basis. This review summarizes several contributions made in trying to understand AA pathogenesis in recent years which may be helpful for the development of personalized therapies for AA.
Highlights
Aplastic anemia (AA) is a rare, life-threatening and heterogeneous disorder of the blood
Aplastic anemia (AA) is a rare and life-threatening bone marrow failure (BMF) that results in peripheral blood cytopenia and reduced bone marrow hematopoietic cell proliferation
It is hypothesized that AA is characterized by a loss or dysfunction of hematopoietic stem and progenitor cells (HSPCs). It involves both the quantitative loss of stem cell numbers and the qualitative abnormalities in stem cell function [8,9]. This was demonstrated by Maciejewski et al where they showed a decrease in number and function of HSPCs using long-term culture initiating cell (LTC-IC) assays [8]
Summary
Aplastic anemia (AA) is a rare, life-threatening and heterogeneous disorder of the blood. This was demonstrated by Maciejewski et al where they showed a decrease in number and function of HSPCs using long-term culture initiating cell (LTC-IC) assays [8] External factors such as viruses, radiation and chemotherapeutic drugs affect HSC homeostasis, differentiation and self-renewal, making individuals vulnerable to AA [10]. Z.H.Shao et al using flow cytometry examined 15 newly diagnosed SAA patients (9 males and 6 females) They found an increased level of apoptosis in bone marrow hematopoietic cells in SAA patients and concluded apoptosis was induced by the recognition of Fas expression antigen by FasL expressing cytotoxic T lymphocytes (CTL) [12]. The above data suggests the involvement of Fas/FasL in the apoptosis of HSC and demonstrates a possible mechanism for dysfunction of bone marrow hematopoietic cells in SAA patients
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