Abstract: PUB236
Severe Aplastic Anemia Due to Azathioprine in a Kidney-Pancreas Transplant Recipient
Session Information
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Chevasath, Passawee, Jefferson Einstein Philadelphia Hospital, Philadelphia, Pennsylvania, United States
- Chewaproug, Daranee, Jefferson Einstein Philadelphia Hospital, Philadelphia, Pennsylvania, United States
Introduction
Azathioprine (AZA) is a commonly used immunosuppressant in solid organ transplantation but has the potential to cause bone marrow toxicity. Cytopenias can range from isolated anemia or leukopenia to full pancytopenia and can even mimic malignancy, infection, or other marrow failure syndromes. We report a case of AZA-induced aplastic anemia (AA) in a kidney-pancreas transplant recipient.
Case Description
A 47-year-old male with a past medical history of kidney-pancreas transplant 17 years prior, type 1 diabetes mellitus, end-stage kidney disease, and monomorphic post-transplant lymphoproliferative disorder, diffuse large B-cell lymphoma type, treated with chemotherapy with complete remission 11 years prior, presented with progressive worsening fatigue of one month’s duration. His medications included tacrolimus, AZA (switched from mycophenolate mofetil three months prior due to diarrhea), and prednisone. Laboratory evaluation revealed severe pancytopenia with hemoglobin 3.8 g/dL (corrected reticulocyte count 0.2%), white blood cell count 1,200 cells/µL (absolute neutrophil count 300 cells/µL), and platelet count 27,000 cells/µL. AZA was discontinued. Workup for nutritional deficiencies and viral etiologies was negative. Given concern for malignancy, a bone marrow biopsy was performed and showed marked hypocellularity (5%) without blasts, lymphoma infiltration, or definitive dysplasia. Computed tomography of the chest, abdomen, and pelvis showed no bulky lymphadenopathy or masses. The leading diagnosis was secondary AA due to AZA-induced myelosuppression. The patient received supportive transfusions and granulocyte colony-stimulating factor (G-CSF). The pancytopenia improved and completely resolved over the course of two weeks.
Discussion
AZA-induced AA is a reversible but potentially severe complication in transplant recipients. Myelosuppression may present weeks to years after AZA initiation. Pharmacogenetic variants in TPMT and NUDT15 increase susceptibility, and pre-treatment screening allows for dose adjustment or alternative therapy. Management requires prompt drug discontinuation, supportive transfusions, and G-CSF for severe neutropenia.
AA is a rare but known adverse effect of AZA. Early recognition and discontinuation of therapy, along with supportive care, can result in rapid hematologic recovery. A high clinical suspicion is essential for timely diagnosis and management.