Hematologic abnormalities in children and young adults receiving tacrolimus‐based immunosuppression following cardiothoracic transplantation

Abstract: To define the incidence, course, and etiology of hematologic abnormalities in children on tacrolimus‐based immunosuppression, we reviewed records of 106 transplant patients (70 heart, 16 heart and lung, 20 double lung), 0–21 yr of age, who were transplanted at the Children's Hospital of Pittsburgh from 1989 to 1997. Fifty‐four of the 106 patients (51%) developed 65 abnormal hematologic episodes (32 anemia, nine neutropenia, nine thrombocytopenia, 15 simultaneous anemia and neutropenia with or without thrombocytopenia). Common etiologies included: infections, post‐transplant lymphoproliferative disease, and medications. Eleven episodes (seven anemia, one neutropenia, and three simultaneous anemia and neutropenia) had unclear etiologies and process of elimination suggested an association with tacrolimus. Interventions included filgrastim (effective in 15 of 15 patients, with resolution of neutropenia in a median of 5 days) and epoetin alfa (effective in five of 16 patients, including four of four patients with anemia possibly related to tacrolimus). Five patients (two with neutropenia and three with simultaneous neutropenia and anemia) were switched to cyclosporin A (CsA); rapid resolution occured in four of the five patients, suggesting a possible association of the hematologic abnormalities with tacrolimus. In summary, hematologic abnormalities are common in children on tacrolimus‐based immunosuppression. Most of these hematologic abnormalities are caused by common etiologies; however, a sub‐population exists where tacrolimus may be the etiologic agent. Anemia and neutropenia respond to treatment with epoetin alfa and filgrastim. After thorough investigation, a trial switch to CsA may be warranted.

[1]  S. Nathan,et al.  Successful use of cyclosporine in a lung transplant recipient with tacrolimus-associated hemolytic uremic syndrome. , 1999, The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation.

[2]  P. Suter,et al.  Tacrolimus (FK 506)-induced hemolytic uremic syndrome after heart transplantation. , 1998, The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation.

[3]  R. Busuttil,et al.  Red cell aplasia in children on tacrolimus after liver transplantation. , 1998, Transplantation.

[4]  N. Embleton,et al.  High prevalence of anemia after cardiac transplantation in children. , 1997, Transplantation.

[5]  H. Antunes,et al.  Early signs and risk factors for the increased incidence of Epstein-Barr virus-related posttransplant lymphoproliferative diseases in pediatric liver transplant recipients treated with tacrolimus. , 1997, Transplantation.

[6]  R. Marugán,et al.  Tacrolimus-induced bone marrow suppression , 1997, The Lancet.

[7]  B. Griffith,et al.  Posttransplantation lymphoproliferative disorders in pediatric thoracic organ recipients. , 1997, The Journal of pediatrics.

[8]  S. Webber,et al.  Experience of FK506 immune suppression in pediatric heart transplantation: a study of long-term adverse effects. , 1996, The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation.

[9]  S. Suzuki,et al.  Pure red cell aplasia induced by FK506. , 1996, Transplantation.

[10]  S. Boggs,et al.  Short-term myeloid reconstitution following TBI is not adversely affected by doses of FK506 that abrogate lethal GVHD. , 1994, Bone marrow transplantation.

[11]  T. Starzl,et al.  Acute hemolytic anemia in liver and bone marrow transplant patients under FK 506 therapy. , 1991, Transplantation proceedings.