Aplastic anemia successfully treated with rituximab: the possible role of aplastic anemia-associated autoantibodies as a marker for response
Aplastic anemia successfully treated with rituximab: the possible role of aplastic anemia-associated autoantibodies as a marker for response
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利妥昔单抗成功治疗再生障碍性贫血：再生障碍性贫血相关自身抗体作为反应标志物的可能作用
DOI：
10.1111/j.1600-0609.2011.01612.x
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发表时间：
2011
期刊：
影响因子：
3.1
通讯作者：
Nakao S
中科院分区：
文献类型：
--
作者：
Takamatsu H.;Yagasaki H.;Takahashi Y.;Hama A.;Saikawa Y.;Yachie A.;Koizumi S.;Kojima S.;Nakao S
一名1岁的日本男婴患有肝炎相关性再生障碍性贫血（AA），使用抗胸腺细胞球蛋白（ATG）加环孢素A （CsA）治疗无明显效果。治疗前对患者血清的实验室检查显示，除了抗DRS - 1抗体和抗moesin抗体外，还有各种自身抗体，如PA - IgG、抗血小板、抗单链DNA （ssDNA）和抗双链DNA （dsDNA）抗体（Abs），已知约40%的AA患者可检测到这两种抗体。因此，在ATG/CsA治疗5.5个月后，他接受17.5 mg/kg/d的利妥昔单抗治疗。此后，同样的利妥昔单抗治疗重复三次，每月一次。他的中性粒细胞计数在第一次利妥昔单抗治疗后50 d开始增加，在最后一次利妥昔单抗治疗后16个月完全缓解。所有的自身抗体，包括抗ssDNA、dsDNA、DRS - 1和moesin，在患者达到缓解期后都检测不到。抗CD20单克隆抗体治疗可能对部分以自身抗体存在为特征的AA患者有效。
A 1‐yr‐old Japanese male infant developed hepatitis‐associated aplastic anemia (AA), and anti‐thymocyte globulin (ATG) plus cyclosporine A (CsA) was administered without any appreciable effects. Laboratory examination of the patient’s serum obtained before therapy revealed various autoantibodies, such as PA‐IgG, anti‐platelets, anti‐single‐stranded DNA (ssDNA), and anti‐double‐stranded DNA (dsDNA) antibodies (Abs) in addition to anti‐DRS‐1 Abs and anti‐moesin Abs, both of which are known to be detectable in approximately 40% of all patients presenting with AA. He was therefore treated with 17.5 mg/kg/d rituximab 5.5 months after ATG/CsA therapy. The same rituximab therapy was repeated three times once a month thereafter. His neutrophil counts started to increase 50 d after the first rituximab therapy and he achieved a complete remission at 16 months after the last rituximab administration. All of the autoantibodies including anti‐ssDNA, dsDNA, DRS‐1, and moesin became undetectable when he attained the remission. Anti‐CD20 monoclonal antibody therapy may be effective in a subset of patients with AA characterized by the presence of autoantibodies.