# Case Report: Sorafenib-induced rhabdomyolysis in a post-transplant patient with acute myeloid leukemia

**Authors:** Liuxian Ke, Lingjuan Cao, Shang Li, Zijian Zhou, Ping Zheng

PMC · DOI: 10.3389/fonc.2026.1728530 · Frontiers in Oncology · 2026-02-17

## TL;DR

A patient with acute myeloid leukemia developed severe muscle damage (rhabdomyolysis) after taking sorafenib, a drug used to prevent cancer relapse.

## Contribution

This case report identifies sorafenib as a rare but serious cause of rhabdomyolysis in post-transplant patients.

## Key findings

- A 31-year-old female developed rhabdomyolysis during sorafenib treatment after a stem cell transplant for AML.
- Discontinuation of sorafenib and supportive care led to recovery of muscle enzyme levels and symptoms.
- Neuromuscular biopsy confirmed rhabdomyolysis and immune-mediated necrotizing myopathy.

## Abstract

Rhabdomyolysis is a clinical acute syndrome characterized by acute injury or necrosis of skeletal muscle cells and may be life-threatening. We report a rare case of rhabdomyolysis caused by sorafenib.

This case report presents a 31-year-old female patient who experienced rhabdomyolysis during sorafenib treatment following allogeneic hematopoietic stem cell transplantation. The patient underwent the transplantation due to acute myeloid leukemia (AML) and subsequently received sorafenib as maintenance therapy to prevent leukemia relapse. During treatment, she developed bilateral lower limb weakness, a significant increase in creatine kinase (CK) levels, and hypokalemia. After discontinuing sorafenib and initiating supportive treatments, her CK levels gradually decreased. Neuromuscular biopsy results showed rhabdomyolysis and immune-mediated necrotizing myopathy.The patient was followed up in the outpatient clinic after discharge, and the symptoms of myasthenia in both lower limbs have improved. On the 38th day after discharge, laboratory tests showed that the levels of α-hydroxybutyrate dehydrogenase, creatine kinase, lactate dehydrogenase, and electrolytes had returned to normal.

This case highlights that sorafenib may cause rare but severe adverse reactions, such as rhabdomyolysis. Clinicians should be vigilant about these potential adverse effects when using sorafenib and enhance patient monitoring and management.

## Linked entities

- **Chemicals:** sorafenib (PubChem CID 216239)
- **Diseases:** acute myeloid leukemia (MONDO:0015667), rhabdomyolysis (MONDO:0005290), immune-mediated necrotizing myopathy (MONDO:0016098)

## Full-text entities

- **Genes:** VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, RET (ret proto-oncogene) [NCBI Gene 5979] {aka CDHF12, CDHR16, HSCR1, MEN2A, MEN2B, MTC1}, BRAF (B-Raf proto-oncogene, serine/threonine kinase) [NCBI Gene 673] {aka B-RAF1, B-raf, BRAF-1, BRAF1, NS7, RAFB1}, MB (myoglobin) [NCBI Gene 4151] {aka MYOSB, PVALB}, FLT3 (fms related receptor tyrosine kinase 3) [NCBI Gene 2322] {aka CD135, FLK-2, FLK2, STK1}, TPO (thyroid peroxidase) [NCBI Gene 7173] {aka MSA, TDH2A, TPX}, ZHX2 (zinc fingers and homeoboxes 2) [NCBI Gene 22882] {aka AFR1, RAF}, KDR (kinase insert domain receptor) [NCBI Gene 3791] {aka CD309, FLK1, VEGFR, VEGFR2}, TG (thyroglobulin) [NCBI Gene 7038] {aka AITD3, TGN}, CMPK1 (cytidine/uridine monophosphate kinase 1) [NCBI Gene 51727] {aka CK, CMK, CMPK, UMK, UMP-CMPK, UMPK}, FLT4 (fms related receptor tyrosine kinase 4) [NCBI Gene 2324] {aka CHTD7, FLT-4, FLT41, LMPH1A, LMPHM1, PCL}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, PDGFRB (platelet derived growth factor receptor beta) [NCBI Gene 5159] {aka CD140B, IBGC4, IMF1, JTK12, KOGS, OPDKD}, KIT (KIT proto-oncogene, receptor tyrosine kinase) [NCBI Gene 3815] {aka C-Kit, CD117, MASTC, PBT, SCFR}
- **Diseases:** metabolic disorders (MESH:D008659), inherited disorders (MESH:D030342), AML (MESH:D015470), muscle ischemia (MESH:D007511), inflammatory myopathy (MESH:D009220), fatigue (MESH:D005221), diarrhea (MESH:D003967), desquamation (MESH:D017490), rash (MESH:D005076), alopecia (MESH:D000505), organ dysfunction (MESH:D009102), GVHD (MESH:D006086), swelling (MESH:D004487), anorexia (MESH:D000855), cancer (MESH:D009369), limb weakness (MESH:D018908), hand-foot skin reaction (MESH:D060831), pain (MESH:D010146), stiff hand muscles (MESH:D019042), myasthenia (MESH:D020294), injury (MESH:D014947), RCC (MESH:D002292), HCC (MESH:D006528), necrosis (MESH:D009336), myopathy (MESH:D009135), Hypokalemia (MESH:D007008), tenderness (MESH:D063806), renal impairment (MESH:D007674), ADR (MESH:D064420), numbness (MESH:D006987), infection (MESH:D007239), hypothyroid (MESH:D007037), leukemia (MESH:D007938), Rhabdomyolysis (MESH:D012206)
- **Chemicals:** Sorafenib (MESH:D000077157), nucleotide (MESH:D009711), sodium chloride (MESH:D012965), Mg (MESH:D008274), creatinine (MESH:D003404), glucose (MESH:D005947), Ca (MESH:D002118), calcitriol (MESH:D002117), potassium magnesium aspartate (MESH:D011195), potassium chloride (MESH:D011189), T3 (MESH:D014284), ATP (MESH:D000255), entecavir (MESH:C413685), K (MESH:D011188), sodium phosphate (MESH:C018279), Cyclosporine (MESH:D016572), T4 (MESH:D013974), FT3 (-), H&amp;E (MESH:D006371)
- **Species:** Hepatitis B virus (no rank) [taxon 10407], Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** NIH 3T3 fibroblasts — Mus musculus (Mouse), Transformed cell line (CVCL_L992)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12953118/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12953118/full.md

## References

17 references — full list in the complete paper: https://tomesphere.com/paper/PMC12953118/full.md

---
Source: https://tomesphere.com/paper/PMC12953118