Chronic myeloid leukemia following heart transplantation and immunosuppression with tacrolimus.

Chronic myeloid leukemia (CML) rarely develops following organ transplantation. Chronic immunosuppressive therapy is believed to be responsible for secondary malignancies, mainly the tumors of the lymphoid tissue and skin neoplasms.1-3 The known mechanisms involved in the development of secondary malignancies include decreased immunosurveillance due to chronic immunosuppression and direct tumorigenic effect of the immunosuppressive medications. Little is known yet of the factors that may predispose transplant recipients to secondary myeloproliferative disorders. Epstein-Barr virus reactivation, which plays a key role in post-transplant lymphoproliferative disorders (PTLD), has no known impact on secondary CML. Similarly, whereas the association between the more prevalent PTLD and the type of an immunosuppressive regimen used has been well established, the factors involved in secondary CML are yet to be identified. There are different ways to achieve immunosuppression to prevent organ rejection, and tacrolimus has recently emerged as the favorite immunosuppressive medications. Yet, little is known about the long-term effects of tacrolimus on immune surveillance. Here we present the first reported case of CML, which developed post–heart transplantation in a patient treated with tacrolimus and mycophenolate mofetil.