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Methotrexate poisoning with acute hepatorenal dysfunction.

E Goto¹, S Tomojiri, I Okamoto

¹Department of Emergency & Critical Care Medicine, School of Medicine, Fukuoka University, Japan. eiichig@msn.com

Journal of Toxicology. Clinical Toxicology

|May 1, 2001

Summary

High-dose methotrexate for osteosarcoma caused acute renal failure and liver dysfunction. Plasma exchange, hemodialysis, and continuous hemodiafiltration effectively reduced toxic methotrexate levels, preventing rebound.

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Area of Science:

Oncology
Nephrology
Pharmacology

Background:

High-dose methotrexate is a critical chemotherapy for osteosarcoma.
Complications like acute renal failure and liver dysfunction can occur.
Management of methotrexate toxicity is crucial for patient outcomes.

Observation:

A 17-year-old osteosarcoma patient developed severe methotrexate toxicity.
Acute renal failure, liver dysfunction, and coagulation disorder were observed.
Initial treatment with plasma exchange and hemodialysis reduced levels but a rebound occurred.

Findings:

Continuous hemodiafiltration (CHF) was initiated to manage rebound methotrexate concentrations.
CHF effectively lowered plasma methotrexate levels without rebound, despite low column clearance.

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The study suggests CHF can manage methotrexate toxicity rebound.

Implications:

This case highlights the potential role of CHF in managing severe methotrexate toxicity.
Effective management strategies are vital for patients undergoing high-dose methotrexate therapy.
Further research into CHF's efficacy in methotrexate clearance is warranted.