Increased cerebral iron uptake in Wilson's disease: A 52Fe-citrate PET study

Matthias Bruehlmeier, Klaus L. Leenders, Peter Vontobel, Claudio Calonder, Angelo Antonini, Adolf Weindl

Research output: Contribution to journalArticlepeer-review


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 (Kl = 2.66E-05 (+) 0.351E-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.

Original languageEnglish
Pages (from-to)781-787
Number of pages7
JournalJournal of Nuclear Medicine
Issue number5
Publication statusPublished - May 2000


  • Fe
  • Brain
  • Iron
  • PET
  • Wilson's disease

ASJC Scopus subject areas

  • Radiological and Ultrasound Technology


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