Download PDF
Exp Clin Endocrinol Diabetes 2000; Vol. 108(3): 191-196
DOI: 10.1055/s-2000-7743
Articles

© Johann Ambrosius Barth

Glucose metabolism of the thyroid in autonomous goiter measured by F-18-FDG-PET[*]

A. R. Boerner 1 , E. Voth 1 , P. Theissen 1 , K. Wienhard 2 , R. Wagner 2 , H. Schicha 1
  • 1 Department of Nuclear Medicine, University of Cologne, Germany
  • 2 Max-Planck-Institute of Neurological Research, Cologne, Germany
Further Information

Publication History

Publication Date:
31 December 2000 (online)

Also available at
    Permissions and Reprints

Summary:

The radiolabeled glucose analogue F-18-Fluoro-Deoxyglucose (F-18-FDG) and Positron Emission Tomography (PET) were used to measure glucose metabolism of the thyroid in vivo. We evaluated patients with autonomous goitre before therapy with radioiodine in comparison to patients with normal thyroids.

30 patients with autonomous goitre underwent scanning the day before radioiodine therapy. 19 patients with head or brain tumours and normal thyroids were the controls. Overall F-18-FDG uptake was determined for all thyroids and proved to be significantly higher in autonomy patients compared to controls and in disseminated autonomous goitre slightly but not significantly higher than in focal autonomy. In autonomy patients F-18-FDG uptake increased with increasing radioiodine uptake and shorter radioiodine half-life.

These results indicate that glucose metabolism is enhanced in the thyroids of patients with focal and disseminated autonomy. The negative correlation of radioiodine half-life and glucose metabolism as well as the positive correlation of radioiodine uptake and glucose metabolism suggest connections of glucose metabolism and iodine-dependent hormone synthesis in thyroid cells.

Abbreviations: F-18-FDG, F-18-Fluoro-Deoxyglucose; PET, Positron Emission Tomography.

Key words:

Thyroid - autonomy - glucose metabolism - positron emission tomography

1 * Dedicated to Prof. Dr. D. Emrich on the occasion of his 70th birthday.

References

  • 1 Adler L P, Bloom A D. Positron emission tomography of thyroid masses.  Thyroid. 3 195-200 1993; 
    PubMedGoogle Scholar
  • 2 Als C, Listewnik M, Ritter H P, Rösler H. Scintigraphic method in the quantification of morphological and functional changes of thyroid autonomy before and after iodine radiotherapy.  Schweiz Med Wochenschr. 127 102-106 1997; 
    PubMedGoogle Scholar
  • 3 Bähre M, Hilgers R, Lindemann C, Emrich D. Thyroid autonomy: sensitive detection in vivo and estimation of its functional relevance using quantified high-resolution scintigraphy.  Acta Endocrinol (Copenh). 117 145-153 1988; 
    PubMedGoogle Scholar
  • 4 Boerner A R, Voth E, Wienhard K, Wagner R, Schicha H. Glucose Metabolism of the Thyroid in Graves' Disease Measured by F-18-Fluoro-Deoxyglucose Positron Emission Tomography.  Thyroid. 8 765-772 1998; 
    PubMedGoogle Scholar
  • 5 Burke G. Effects of iodotyrosines on basal and stimulated glucose oxidation and phospholipogenesis in sheep thyroid slices.  Endocrinology. 83 495-500 1968; 
    PubMedGoogle Scholar
  • 6 Dai G, Levy O, Carrasco N. Cloning and characterization of the thyroid iodide transporter.  Natue. 379 458-460 1996; 
    CrossrefPubMedGoogle Scholar
  • 7 Dederichs B, Otte R, Klink J E, Schicha H. Volumenreduktion der Schilddrüse nach Radioiodtherapie bei Patienten mit Schilddrüsenautonomie und M. Basedow.  Nuklearmedizin. 35 164-169 1996; 
    PubMedGoogle Scholar
  • 8 Derwahl M, Hamacher C, Russo D, Broecker M, Manole D, Schatz H, Kopp P, Filetti S. Constitutive activation of the Gs alpha protein-adenylate cyclase pathway may not be sufficient to generate toxic thyroid adenomas.  J Clin Endocrinol Metab. 81 1898-1904 1996; 
    CrossrefPubMedGoogle Scholar
  • 9 Endo T, Shimura H, Saito T, Ikeda M, Ohmori M, Onaya T. Thyreotropin stimulates glucose regulated protein (GRP78) gene expression in rat functional thyroid epithelial cells, FRTL.  Mol Endocrinol. 5 905-910 1991; 
    PubMedGoogle Scholar
  • 10 Feine U, Lietzenmayer R, Hanke J P, Wöhrle H, Müller-Schauenburg W. 18FDG-Ganzkörper-PET bei differenzierten Schilddrüsenkarzinomen.  Nuklearmedizin. 34 127-134 1995; 
    PubMedGoogle Scholar
  • 11 Filetti S, Damante G, Foti D. Thyrotropin stimulates glucose transport in cultured rat thyroid cells.  Endocrinology. 120 2576-2581 1987; 
    PubMedGoogle Scholar
  • 12 Gerber H, Bürgi U, Peter H J. Morphological, immunohistochemical and autoradiographic studies of thyroid autonomy.  Exp Clin Endocrinol Diabetes 106 (Suppl 4) 1-3 1998; 
    PubMedGoogle Scholar
  • 13 Haraguchi K, Rani C S, Field J B. Effects of thyrotropin, carbachol, and protein kinase-C stimulators on glucose transport and glucose oxidation by primary cultures of dog thyroid cells.  Endocrinology. 123 1288-1295 1988; 
    CrossrefPubMedGoogle Scholar
  • 14 Joensuu H, Ahonen A. Imaging of metastases of thyroid carcinoma with fluorine-18 fluorodeoxyglucose.  J Nucl Med. 28 910-914 1987; 
    PubMedGoogle Scholar
  • 15 Krohn K, Führer D, Holzapfel H P, Paschke R. Clonal origin of toxic thyroid nodules with constitutively activating thyrotropin receptor mutations.  J Clin Endocrinol Metab. 83 130-134 1998; 
    CrossrefPubMedGoogle Scholar
  • 16 Luster M, Jacob M, Thelen M H, Michalowski U, Deutsch U, Reiners C. Reduction of thyroid volume following radioiodine therapy for functional autonomy.  Nuklearmedizin. 34 57-60 1995; 
    PubMedGoogle Scholar
  • 17 Parma J, Duprez L, Van Sande J, Hermans J, Rocmans P, Van Vliet G, Costagliola S, Rodien P, Dumont J E, Vassart G. Diversity and prevalence of somatic mutations in the thyrotropin receptor and Gs alpha genes as a cause of toxic thyroid adenomas.  J Clin Endocrinol Metab. 82 2695-2701 1997; 
    CrossrefPubMedGoogle Scholar
  • 18 Paschke R. Constitutively activating TSH receptor mutations as the cause of toxic thyroid adenoma, multinodular toxic goiter and autosomal dominant non autoimmune hyperthyroidism.  Exp Clin Endocrinol Diabetes 104 (Suppl) 129-132 1996; 
    PubMedGoogle Scholar
  • 19 Paschke R, Ludgate M. The thyrotropin receptor in thyroid diseases.  N Engl J Med. 337 1675-1681 1997; 
    CrossrefPubMedGoogle Scholar
  • 20 Pinducciu C, Borgonovo G, Arezzo A, Torre G C, Giordano G, Cordera R. Toxic thyroid adenoma: absence of DNA mutations of the TSH receptor and Gs alpha.  Eur J Endocrinol. 138 37-40 1998; 
    CrossrefPubMedGoogle Scholar
  • 21 Reinhardt M J, Moser E. An update on diagnostic methods in the investigation of diseases of the thyroid.  Eur J Nucl Med. 23 598-594 1996; 
    PubMedGoogle Scholar
  • 22 Russo D, Arturi F, Suarez H G, Schlumberger M, Du V J, Crocetti U, Filetti S. Thyrotropin receptor gene alterations in thyroid hyperfunctioning adenomas.  J Clin Endocrinol Metab. 81 1548-1551 1996; 
    CrossrefPubMedGoogle Scholar
  • 23 Sanders J, Oda Y, Roberts S A, Maruyama M, Furmaniak J, Smith B R. Understanding the thyrotropin receptor function-structure relationship.  Baillieres Clin Endocrinol Metab. 11 451-479 1997; 
    CrossrefPubMedGoogle Scholar
  • 24 Siegel R D, Lee S L. Toxic nodular goiter. Toxic adenoma and toxic multinodular goiter.  Endocrinol Metab Clin North Am. 27 151-168 1998; 
    CrossrefPubMedGoogle Scholar
  • 25 Thomson F J, Jess T J, Moyes C, Plevin R, Gould G W. Characterization of the intracellular signalling pathways that underlie growth-factor-stimulated glucose transport in Xenopus oocytes: evidence for ras- and rho-dependent pathways ofphosphatidylinositol 3-kinase activation.  Biochem J. 325 637-643 1997; 
    PubMedGoogle Scholar
  • 26 Tonacchera M, Chiovato L, Pinchera A, Agretti P, Fiore E, Cetani F, Rocchi R, Viacava P, Miccoli P, Vitti P. Hyperfunctioning thyroid nodules in toxic multinodular goiter share activating thyrotropin receptor mutations with solitary toxic adenoma.  J Clin Endocrinol Metab. 83 492-498 1998; 
    CrossrefPubMedGoogle Scholar
  • 27 Vassart G. New pathophysiological mechanisms for hyperthyroidism.  Horm Res 48 (Suppl) 47-50 1997; 
    PubMedGoogle Scholar
  • 28 Voth E, Boerner A R, Theissen P, Schicha H. Positron emission tomography (PET) in benign thyroid diseases.  Exp Clin Endocrinol 102 (Suppl 3) 71-74 1994; 
    PubMedGoogle Scholar
  • 29 Yao W J, Hoh C K, Hawkins R A, Glaspy J A, Weil J A, Lee S J, Maddahi J, Phelps M E. Quantitative PET imaging of bone marrow glucose metabolic response to hematopoietic cytokines.  J Nucl Med. 36 794-799 1994; 
    PubMedGoogle Scholar
  • 30 Yasuda S, Shohtsu A, Ide M, Takagi S, Takahashi S, Suzuki Y, Horiuchi M. Chronic thyroiditis: diffuse uptake of FDG at PET.  Radiology. 207 775-778 1998; 
    PubMedGoogle Scholar

1 * Dedicated to Prof. Dr. D. Emrich on the occasion of his 70th birthday.

2 p-value: * Wilcoxon-Mann-Whitney-test, ** Kruskal-Wallis test, *** Chi-square-analysis; normal ranges: fT3 3.07-7.68 pmol/l, fT4 10.3-30.0 pmol/l, TSH 0.5-3.5 mU/l

Dr. med. Anne R. Boerner

Dept. of Nuclear Medicine

Medical School Hannover

Carl-Neuberg-Str. 1

D-30625 Hannover, Germany

Phone: +49-5 11-5 32-25 77

Fax: +49-5 11-5 32-37 61

Email: Boerner.Anne-Rose@mh-hannover.de