Rituximab in thrombotic microangiopathy

Abstract

We read with interest the recent short report by Au et al (2007) on the efficacy of rituximab in post-transplantation thrombotic microangiopathy (TM). The regression of related symptoms in four out of five patients was quite suprising. As the authors stated, a relationship between ADAMTS13 levels and the presence of anti-ADAMTS13 was not evident in post-transplantation TM. Furthermore, Au et al (2007) found no change in ADAMTS13 and anti-ADAMTS13 after treatment with rituximab. The genesis of TM after transplant may be more related to endothelial damage rather than an antibody-mediated lowering of ADAMTS13 levels (Peyvandi et al, 2006). We wonder whether rituximab was really responsible for the regression of TM in this small cohort of patients, rather than possible alternative contributory factors, e.g. the replacement of ciclosporin with tacrolimus and the use of steroids, which can probably control graft-versus-host disease (a known risk factor for TM), in three out of four responding patients. Furthermore, patients received a median of 13 plasma exchanges (range 7–17), though it has been reported that, in this setting, a longer treatment is needed to obtain significant regression of TM (Zeigler et al, 1995). We think that the role of rituximab in the treatment of post-transplantation TM is at least questionable, and a stronger biological background is needed before advocating use of this expensive drug in these circumstances.