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Increased Cerebral Iron Uptake in Wilson's Disease: A ⁵²Fe-Citrate PET Study

PET Program, Paul Scherrer Institute, Villigen, Switzerland
Department of Neurology, Technische Universität Munich, Munich, Germany

Correspondence: For correspondence or reprints contact: Matthias Bruehlmeier, MD, PET Program, Paul Scherrer Institute, CH-5232 Villigen, Switzerland.

ABSTRACT

Toxicity of abundant copper is the main cause of brain and liver tissue damage in patients with Wilson's disease (WD). However, there is also evidence of a disturbed iron metabolism in this genetically determined disorder. This PET study was undertaken to assess cerebral iron metabolism in WD patients. Methods: We used ⁵²Fe-citrate, which converts to ⁵²Fe-transferrin in blood plasma, to study basic pharmacokinetic features of the cerebral iron transport in 6 WD patients and in 16 healthy volunteers (control subjects). A 2-tissue-compartment model and multiple time graphic plotting were used to calculate ⁵²Fe-transferrin distribution volumes and transport rates. Results: Net iron uptake (Ki) from plasma into brain tissue was significantly (P < 0.001) higher in WD patients (Ki [mean ± SEM] = 15.1E-05 ± 7.13E-05 [1/min]) than in healthy volunteers (Ki = 2.66E-05 ± 0.351 E-05 [1/min]). There was no difference of tracer iron distribution in the cerebral plasma volume between patients and healthy volunteers. Iron uptake values resulting from 2 methods to model PET data of patients and healthy volunteers were highly correlated (P < 0.001). Conclusion: An abnormally increased cerebral ⁵²Fe-transferrin uptake was found in WD patients.

Key Words: ⁵²Fe • iron • brain • PET • Wilson's disease