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@ARTICLE{Zeisbrich:129194,
      author       = {M. Zeisbrich and N. Becker$^*$ and A. Benner$^*$ and A.
                      Radujkovic and K. Schmitt and J. Beimler and A. D. Ho and M.
                      Zeier and P. Dreger and T. Luft},
      title        = {{T}ransplant-associated thrombotic microangiopathy is an
                      endothelial complication associated with refractoriness of
                      acute {G}v{HD}.},
      journal      = {Bone marrow transplantation},
      volume       = {52},
      number       = {10},
      issn         = {0268-3369},
      address      = {London},
      publisher    = {Nature Publishing Group55086},
      reportid     = {DKFZ-2017-05199},
      pages        = {1399-1405},
      year         = {2017},
      abstract     = {There is increasing evidence that endothelial dysfunction
                      is involved in refractoriness of acute GvHD (aGvHD). Here we
                      investigated the hypothesis that another endothelial
                      complication, transplant-associated thrombotic
                      microangiopathy (TMA), contributes to the pathogenesis of
                      aGvHD refractoriness. TMA was retrospectively assessed in
                      771 patients after allogeneic stem cell transplantation
                      (alloSCT). Incidences of TMA and refractory aGvHD were
                      correlated with biomarkers of endothelial damage obtained
                      before alloSCT for patients receiving or not receiving
                      statin-based endothelial prophylaxis (SEP). Diagnostic
                      criteria for TMA and refractory aGvHD were met by 41
                      $(5.3\%)$ and 76 $(10\%)$ patients, respectively. TMA was
                      overrepresented in patients with refractory aGvHD (45.0 vs
                      $2.3\%$ in all other patients, P<0.001). TMA independently
                      increased mortality. Elevated pretransplant suppressor of
                      tumorigenicity-2 and nitrates along with high-risk variants
                      of the thrombomodulin gene were associated with increased
                      risk of TMA. In contrast, SEP abolished the unfavorable
                      outcome predicted by pretransplant biomarkers on TMA risk.
                      Patients on SEP had a significantly lower risk of TMA
                      (P=0.001) and refractory aGvHD (P=0.055) in a multivariate
                      multistate model. Our data provide evidence that TMA
                      contributes to the pathogenesis of aGvHD refractoriness.
                      Patients with an increased TMA risk can be identified
                      pretransplant and may benefit from pharmacological
                      endothelium protection.},
      cin          = {C060},
      ddc          = {610},
      cid          = {I:(DE-He78)C060-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28650448},
      doi          = {10.1038/bmt.2017.119},
      url          = {https://inrepo02.dkfz.de/record/129194},
}