Mechanisms and therapies of thrombocytopenia in myelodysplastic syndrome
- VernacularTitle:骨髓增生异常综合征合并血小板减少症的 原因及治疗策略
- Author:
Hua-quan WANG
1
;
Jia-xi LIU
Author Information
1. Department of Hematology, Tianjin Medical University General Hospital, Tianjin 300052, China
- Publication Type:Journal Article
- Keywords:
骨髓增生异常综合征；血小板减少；血小板生成素；巨核细胞
- From:
Tianjin Medical Journal
2018;46(8):789-794
- CountryChina
- Language:Chinese
-
Abstract:
Myelodysplastic syndromes (MDS) is a kind of bone marrow failure disease. Thrombocytopenia in patients
with MDS is a frequent causes of mortality in MDS with 37% to 67% incidence. Thrombocytopenia in MDS is an independent
factor predicting worse prognosis associated with increased risk of acute leukemic transformation (AML) and reduces overall
survival. In addition, thrombocytopenia in MDS limits the therapeutic efficacy of disease-modifying therapies, such as
azacitidine or lenalidomide. Mechanisms of thrombocytopenia in MDS are complicated, involving suppression of
megakaryocytic differentiation, enhanced apoptosis, and increased platelet destruction. Platelet transfusion is still the
standard treatment option for MDS combined with thrombocytopenia. Recently, novel thrombopoietin (TPO) receptor agonists
have showed curative effect in MDS patients in many clinical trials, including reducing bleeding events, decreasing
dependency on platelet transfusions and increasing clinical benefits of disease-modifying therapies. Several clinical trials
are ongoing to assess the efficacy and safety of novel TPO receptor agonists; the results would further help guide treatment for
thrombocytopenia in MDS.
