Pediatric Pure Red Cell Aplasia Caused by Tacrolimus After Living-Donor Liver Transplant.

Pure red cell aplasia is a relatively rare disease characterized by selective suppression of erythroid precursors in the bone marrow. This disease can also develop secondary to several other diseases and as a side effect of certain drugs. Tacrolimus, a potent immunosuppressant, is widely used in organ transplant. Several cases of pure red cell aplasia due to tacrolimus administration in organ transplant recipients have been reported.Here, we report a case of reversible pure red cell aplasia that developed during tacrolimus therapy following living-donor liver transplant. The patient, a 1-year-old girl diagnosed with progressive familial intrahepatic cholestasis type II, underwent living-donor liver transplant when she was 10 months old. She was started on 3 immunosuppressants posttransplant: tacrolimus (0.1 mg/kg/day twice daily), mycophenolate mofetil, and prednisolone (0.2 mg/kg/day). One year after transplant, she developed severe progressive anemia. Her hemoglobin concentration was extremely low (5.4 g/dL). A bone marrow biopsy revealed severe hypoplasia of the erythroblasts with no abnormality of other myelocytes. These findings were suggestive of pure red cell aplasia; we suspected that tacrolimus had caused this based on similar previous cases of tacrolimus-associated pure red cell aplasia. Accordingly, tacrolimus was switched to cyclosporine after this diagnosis. One week after this switch, the patient's red blood cell counts, reticulocytes, and hemoglobin concentration increased. Although tacrolimus is considered to have no significant potential for myelosuppression, cases of tacrolimus-related pure red cell aplasia have occurred. In patients who develop pure red cell aplasia during tacrolimus treatment following living-donor liver transplant, clinicians should consider switching from tacrolimus to another immunosuppressant.