Nonlethal, attenuated, transfusion-associated graft-versus-host disease in an immunocompromised child: case report and review of the literature
Article first published online: 29 OCT 2010
© 2010 American Association of Blood Banks
Volume 50, Issue 11, pages 2484–2488, November 2010
How to Cite
Neves, J. F., Marques, A., Valente, R. and Barata, D. (2010), Nonlethal, attenuated, transfusion-associated graft-versus-host disease in an immunocompromised child: case report and review of the literature. Transfusion, 50: 2484–2488. doi: 10.1111/j.1537-2995.2010.02705.x
- Issue published online: 29 OCT 2010
- Article first published online: 29 OCT 2010
- Received for publication January 25, 2010; revision received March 23, 2010, and accepted March 24, 2010.
BACKGROUND: Transfusion-associated graft-versus-host disease (TA-GVHD) is a rare complication of transfusion of nonirradiated blood components. It usually affects children in high-risk groups, including those who have primary immunodeficiencies (PIDs). It usually presents with skin, hepatic, digestive, and hematologic involvement and is normally fatal.
CASE REPORT: We report the case of a nonlethal, attenuated, TA-GVHD in a 7-month-old boy. The disease was marked by the presence of a severe rash but lacked all the other usual manifestations. We speculate that the unusually benign course of this disease, which has normally a fulminant course, was due to the fact that this child was under high-dose corticotherapy at the time of the engraftment. This fortunate coincidence led to the survival of this child and allowed the diagnosis of a combined immunodeficiency.
CONCLUSION: A high index of suspicion is required for the diagnosis and proper management of PID. The administration of nonirradiated blood components in the first year of life, sometimes before the clinical suspicion of a PID, is of great concern. TA-GVHD may be more prevalent than reported in the literature and it is possibly a nonidentified cause of death in recipients with unexplained death and nondiagnosed PID.