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Human herpesvirus 6‐related pure red cell aplasia, secondary graft failure, and clinical severe immune suppression after allogeneic hematopoietic cell transplantation successfully treated with foscarnet
Author(s) -
Lagadinou E.D.,
Marangos M.,
Liga M.,
Panos G.,
Tzouvara E.,
Dimitroulia E.,
Tiniakou M.,
Tsakris A.,
Zoumbos N.,
Spyridonidis A.
Publication year - 2010
Publication title -
transplant infectious disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.69
H-Index - 67
eISSN - 1399-3062
pISSN - 1398-2273
DOI - 10.1111/j.1399-3062.2010.00515.x
Subject(s) - medicine , foscarnet , viremia , pancytopenia , human herpesvirus 6 , transplantation , aplasia , immunology , pure red cell aplasia , viral load , immunosuppression , asymptomatic , bone marrow failure , hematopoietic stem cell transplantation , bone marrow , herpesviridae , haematopoiesis , viral disease , virus , stem cell , biology , genetics
E.D. Lagadinou, M. Marangos, M. Liga, G. Panos, E. Tzouvara, E. Dimitroulia, M. Tiniakou, A. Tsakris, N. Zoumbos, A. Spyridonidis. Human herpesvirus 6‐related pure red cell aplasia, secondary graft failure, and clinical severe immune suppression after allogeneic hematopoietic cell transplantation successfully treated with foscarnet.
Transpl Infect Dis 2010: 12: 437–440. All rights reserved. Abstract: Human herpesvirus 6 (HHV‐6) is frequently detected after allogeneic hematopoietic cell transplantation (allo‐HCT); however, the clinical interpretation of HHV‐6 viremia in a transplant patient is challenging as it may signify asymptomatic reactivation, chromosomal integration of the virus genome in the donor or recipient with no clinical significance, or severe HHV‐6 disease. Here we present a case of HHV‐6 disease after allo‐HCT presenting as pure red cell aplasia, secondary graft failure, and severe immunosuppression causing multiple severe bacterial super‐infections. Examination of pre‐transplant patient and donor samples as well as serial determination of HHV‐6 DNA copy numbers after transplantation were necessary to definitively interpret HHV‐6 viremia as active HHV‐6 infection with a causative role in pancytopenia and immune suppression. Foscarnet treatment resulted both in viral load decline and disappearance of HHV‐6‐related bone marrow suppression and predisposition to severe infections. Clinicians should be aware of the wide array of clinical manifestations and the diagnostic pitfalls of post‐transplant HHV‐6 disease. These issues are extremely challenging, as they may result either in dangerous underestimation of HHV‐6 disease or in the institution of unnecessary antiviral therapy. Late bone marrow aplasia and late severe infections after allo‐HCT without other obvious causes may be HHV‐6 related.