[A case of FK 506-induced leukoencephalopathy]

Yumi Okoshi1, Masayuki Itoh, Yuri Okimoto

  • 1Department of Hematology and Oncology, Chiba Children's Hospital.

No to Shinkei = Brain and Nerve
|March 1, 2002
PubMed

Insights

A 15-year-old boy developed leukoencephalopathy after FK 506 treatment for graft versus host disease. Vascular damage, including calcification, was implicated in this FK 506-induced neurological condition.

Area of Science:

  • Neuroscience
  • Hematology
  • Toxicology

Background:

  • FK 506 (tacrolimus) is an immunosuppressant used to prevent graft-versus-host disease after stem cell transplantation.
  • Acute myelomonocytic leukemia is a type of blood cancer.
  • Leukoencephalopathy is a disease of the white matter of the brain.

Observation:

  • A 15-year-old boy with acute myelomonocytic leukemia developed seizures and altered consciousness four weeks after starting FK 506 for graft-versus-host disease.
  • High serum FK 506 levels (27.5 ng/ml) were detected.
  • Brain MRI revealed white matter lesions in the frontal and parietal lobes.

Findings:

  • Neuropathological examination showed myelin and axonal destruction in the cerebral white matter, correlating with MRI findings.
  • Calcification and mineralization of small blood vessels in the cortex and white matter were observed.
  • Osteopontin immunoreactivity in small vessel endothelial cells suggested vascular involvement.

Implications:

  • These findings suggest that vascular damage plays a role in FK 506-induced leukoencephalopathy.
  • This case highlights the potential neurotoxicity of FK 506, particularly at high serum concentrations.
  • Understanding the mechanism of FK 506 neurotoxicity is crucial for managing patients undergoing transplantation.

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