# 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.

## Key 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.