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(HOME) J Nucl Med 2000 May;41(5):781-7
Increased cerebral iron uptake in Wilson's disease: a 52Fe-citrate PET study.
Bruehlmeier M, Leenders KL, Vontobel P, Calonder C, Antonini A, Weindl A
PET Program, Paul Scherrer Institute, Villigen, Switzerland.
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 +/- 0.351E-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.
PMID: 10809192, UI: 20267189
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