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Sensorimotor neurotoxicity associated with high-dose deferoxamine treatment
J E Levine1, A Cohen, M MacQueen
1Department of Pediatrics, New York Hospital-Cornell Medical Center, NY 10021, USA.
Journal of Pediatric Hematology/Oncology
|March 1, 1997
Summary
High-dose deferoxamine (DFO) can cause reversible sensorimotor neurotoxicity in beta-thalassemia patients. Symptoms resolved upon stopping DFO, highlighting the need for careful monitoring during iron overload treatment.
Area of Science:
- Hematology
- Neuroscience
- Pharmacology
Background:
- Iron overload is a common complication in beta-thalassemia patients.
- Deferoxamine (DFO) is a standard treatment for iron overload.
- DFO therapy can be associated with various toxicities.
Observation:
- Two beta-thalassemia patients developed sensorimotor neurotoxicity while on high-dose intravenous DFO (120 mg/kg/day).
- Neurotoxicity onset occurred after 5 and 6 months of treatment.
- Symptoms resolved upon DFO discontinuation and recurred in one patient upon re-initiation.
Findings:
- High-dose DFO can induce reversible sensorimotor neurotoxicity.
- The neurotoxicity did not correlate with serum ferritin levels or DFO dose-to-ferritin ratio.
- This adds to known auditory and visual neurotoxicities of DFO.
Implications:
- Clinicians should monitor for sensorimotor neurotoxicity in patients receiving high-dose DFO.
- Discontinuation of DFO is recommended at the onset of neurotoxicity.
- Lower DFO doses may be considered for re-initiation of therapy if necessary.
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