Chronic Myeloid Leukemia After Liver Transplantation and the Role of Immunosuppression: A Case Report

TL;DR

A rare case of chronic myeloid leukemia (CML) following liver transplantation is reported, highlighting the role of immunosuppressive drugs and the importance of monitoring for CML in transplant patients.

Contribution

This case report adds to the limited evidence on the link between immunosuppressive drugs and post-transplant CML, emphasizing clinical vigilance and management strategies.

Findings

A 43-year-old liver transplant recipient developed CML 66 months post-transplant.

Reduction of tacrolimus and initiation of Imatinib led to significant hematologic response.

The case underscores the need for routine blood monitoring and BCR::ABL1 testing in transplant patients.

Abstract

Chronic myeloid leukemia (CML) occurring after liver transplantation is uncommon and has been reported only sporadically in the literature. Long-term exposure to calcineurin inhibitors and mammalian targets of rapamycin inhibitors (mTORis) is thought to support expansion of Breakpoint cluster region-Abelson 1 (BCR::ABL1)-positive hematopoietic clones, but the clinical evidence base is still limited. We describe a case with a notably long latency between liver transplantation and the diagnosis of CML and discuss it in the context of the available literature. A 43-year-old man underwent a living-donor liver transplant in 2019 for cirrhosis secondary to metabolic dysfunction-associated steatohepatitis. In view of tacrolimus-related neurotoxicity six months post-transplant, dose reduction was undertaken, and everolimus was introduced. Sixty-six months post-transplant, he presented with high-grade fever, significant weight loss, marked fatigue, and massive splenomegaly. Laboratory testing showed leukocytosis of 304 × 10⁹/L, normocytic anemia, and mild thrombocytopenia. Abdominal CT confirmed massive splenomegaly without lymphadenopathy. Peripheral blood smear demonstrated a left shift with myelocytes and occasional blasts; bone marrow biopsy revealed hypercellularity with <5% blasts. Cytogenetic analysis identified t(9;22)(q34;q11), and quantitative polymerase chain reaction (PCR) detected BCR::ABL1 p210. Epstein-Barr virus PCR was negative. After clinical stabilization, Imatinib 400 mg daily was initiated, alongside pre-emptive reduction of tacrolimus, guided by weekly trough monitoring. The patient achieved a significant hematologic response within six weeks, maintaining excellent graft function and tolerating therapy well. Although rare, post-transplant CML warrants high clinical suspicion, routine blood count surveillance, and reflex BCR::ABL1 testing of unexplained leukocytosis. Careful adjustment of immunosuppression allows effective tyrosine kinase inhibitor therapy without compromising graft integrity, but multi-center registries are essential to refine preventative and therapeutic strategies.

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