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[F-18-FDG PET in autonomous goiter]
A R Börner1, E Voth, K Wienhard
1Klinik und Poliklinik für Nuklearmedizin, Universität zu Köln, Deutschland. a.r.boerner@fz-juelich.de
Nuklearmedizin. Nuclear Medicine
|February 13, 1999
Summary
Gain-of-function mutations in the thyrotropin receptor (TSHR) gene cause toxic thyroid adenomas. F-18-FDG-PET imaging reveals increased glucose metabolism in autonomous thyroid tissue, correlating with iodine uptake.
Area of Science:
- Endocrinology
- Nuclear Medicine
- Molecular Genetics
Background:
- Gain-of-function mutations in the thyrotropin receptor (TSHR) gene are implicated in toxic thyroid adenomas.
- Assessing metabolic activity in autonomous thyroid nodules is crucial for diagnosis and treatment planning.
Purpose of the Study:
- To evaluate the utility of F-18-FDG-PET in patients with toxic thyroid adenomas caused by TSHR mutations.
- To investigate the correlation between glucose metabolism and iodine uptake in autonomous thyroid tissue.
Main Methods:
- F-18-FDG-PET imaging was performed on 20 patients with focal autonomous nodules and 10 with disseminated autonomy before radioiodine therapy.
- A control group of 20 patients with head or neck cancer and normal thyroid function was included.
Main Results:
- F-18-FDG uptake was significantly higher in patients with autonomous thyroid tissue compared to controls.
- Focal autonomous nodules demonstrated focally enhanced glucose metabolism.
- Disseminated autonomous goiters exhibited variable patterns of focal or global hypermetabolism.
Conclusions:
- Autonomous thyroid tissue resulting from constitutive TSHR mutations exhibits increased glucose metabolism.
- There is a positive correlation between increased glucose metabolism and iodine metabolism in these tissues.