Successful cytokine treatment of aplastic anemia following living‐related orthotopic liver transplantation for non‐A, non‐B, non‐C hepatitis

Abstract

The relationship between aplastic anemia and viral hepatitis is well recognized, and such patients usually have a high mortality. We successfully treated a case of aplastic anemia following living-related orthotopic liver transplantation (LROLT) for non-A, non-B, non-C hepatitis. A 2-yr-old boy with fulminant hepatic failure from non-A, non-B, non-C hepatitis received LROLT. Before transplantation, he had pancytopenia which was probably hepatitis associated, and viral suppression was suspected after bone marrow (BM) biopsy. After the transplantation, he developed progressive pancytopenia and a diagnosis of aplastic anemia was made via BM biopsy. With immunosuppressant agents (cyclosporine, methylprednisolone), cytokine therapy (granulocyte-colony stimulating factor (G-CSF), macrophage-colony stimulating factor (M-CSF), recombinant human erythropoietin (rhEPO)) was effectual and the patient recovered from pancytopenia. He was discharged from the hospital 57 d after the liver transplantation and remains well 1 yr after LROLT. Combined cytokine therapy with high doses of G-CSF, M-CSF and rhEPO appeared to be effective in the treatment of aplastic anemia following liver transplantation for non-A, non-B, non-C hepatitis. Since M-CSF activates macrophages, it may have contributed to the graft rejection. Careful consideration should be given to the use of high-dose M-CSF in liver transplant patients.

Immunotherapy for severe aplastic anemia following orthotopic liver transplantation in children

“…Severe aplastic anemia after liver transplantion for fulminant non‐A, non‐B, and non‐C hepatic failure is a serious and relatively common complication. Successful treatment of severe aplastic anemia following orthotopic liver transplantion with immunotherapy has been reported 6. We describe two children with severe aplastic anemia following orthotopic liver transplant successfully treated with combination therapy of anti‐thymocyte globulin, methylprednisolone, and adjustments to routine calcineurin inhibitors.…”

“…Either a matched‐related bone marrow transplant, or ATG/cyclosporine with high‐dose steriods have been reported as treatment options for acquired aplastic anemia after orthotopic liver transplantation for fulminant non‐A, non‐B, and non‐C hepatitis 3,5,6. Tacrolimus may be substituted for cyclosporine for the treatment of severe aplastic anemia in children who experience cyclosporine related undesirable side effects.…”

“…Immunosuppressive therapy is effective in treating severe aplastic anemia in patients who lack a histocompatible donor or are poor candidates for stem cell transplant. Patients with severe aplastic anemia following orthotopic liver transplantation have been successfully treated with bone marrow transplantation, if a histocompatible donor is available, or with immunotherapy alone 2,5,6. We describe two children who developed severe aplastic anemia following orthotopic liver transplantation for fulminant non‐A, non‐B, and non‐C hepatitis.…”

Fatal GvHD as a complication of liver transplantation for undetermined fulminant hepatic failure and associated aplastic anemia

“…The association of liver failure and AA has an increased mortality rate. Non‐ or partial recovery of the bone marrow after liver transplant has been described before, mostly as a secondary event after orthotopic liver transplant 2, 4–8. In this report, we describe a patient in which the AA preceded fulminant liver failure and who developed a fatal graft vs. host disease (GvHD) after liver transplantation.…”

Successful bone marrow transplantation for severe aplastic anemia following orthotopic liver transplantation: long-term follow-up and outcome

“…1,2 Full hematologic recovery following immunosuppression has been reported, however time to recovery is often on the order of several months to years. 1,2 Sato et al 4 recently described a child successfully treated with growth factors and immunosuppression for SAA which developed following living-related orthotopic liver transplantation for FHF. The patient remained well at 1-year follow-up.…”