Artigo Acesso aberto Revisado por pares

Treatment difficulty with acute GVHD – frequent cause of mortality after allogeneic hematopoietic stem cell transplantation

2014; AEPress; Volume: 115; Issue: 02 Linguagem: Inglês

10.4149/bll_2014_017

ISSN

1336-0345

Autores

Jozef Lukáš, Eva Bojtárová, M. Mistrik, Juraj Bujdák, Ladislav Sopko, Antónia Hatalova, M. Martisova,

Tópico(s)

Renal Transplantation Outcomes and Treatments

Resumo

Acute graft-versus-host disease (aGvHD) remains a significant cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (HSCT).In this study, we have retrospectively evaluated the major risk factors for the development of aGvHD in 100 patients who underwent allogeneic transplantation at the University Hospital in Bratislava between January 2007 and December 2011.29 patients acquired acute GvHD (Grade I - 12 patients, G II - 5 , G III - 3, G IV - 9). We proved a higher incidence of developing aGvHD in patients with unrelated donor type, TBI conditioning and cyclosporine (CsA) replacement with mycophenolate mofetil due to CsA nephrotoxicity, while other risk factors such as older patient age, the use of peripheral blood progenitor cells and donor/recipient sex mismatch were without statistical significance. The average time of onset of aGvHD has been 57 days (range 13-260) after HSCT. Corticosteroids were used as standard initial therapy with 52 % complete response (CR) rate, although the likelihood of response rapidly decreased with increasing severity of disease (G IV - 100 % refracterness). The response to primary therapy also correlated with overall survival. Patients with steroid-refractory aGvHD received a different second-line therapies (antithymocyte globulin, anti-TNFα antibody, anti CD52 antibody) with response rate 45 % (CR - 18 %, PR - 27 %).Outcome for the patients with steroid-refractory aGvHD was poor, disease very often returned or progressed with one year mortality rate 81 % , that represents an important therapeutic problem (Tab. 2, Ref. 10).

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