Subscribe to RSS
DOI: 10.1055/s-0038-1632181
F-18-FDG-PET bei Schilddrüsen-Autonomien
F-18-FDG-PET in Autonomous GoiterPublication History
Eingegangen:
23 July 1998
in revidierter Form:
11 September 1998
Publication Date:
03 February 2018 (online)
![](https://www.thieme-connect.de/media/10.1055-s-00034924/199901/lookinside/thumbnails/10-1055-s-0038-1632181_de-1.jpg)
Zusammenfassung:
Ziel: Die Schilddrüsenautonomie im lodmangelgebiet beruht in der Mehrzahl der Fälle auf konstitutiven, funktionsaktivierenden Mutationen des Thyreotropin-(TSH-)Rezeptors. Diese Studie evaluiert F-18-Fluoro-Deoxy-Glukose-(F-18-FDG-)PET der Schilddrüse bei Patienten mit funktionell relevanter Autonomie der Schilddrüse. Methoden: 20 Patienten mit fokaler und 10 Patienten mit disseminierter Autonomie der Schilddrüse wurden am Tag vor geplanter Radioiod-Therapie mit FDG-PET untersucht. 20 Patienten mit Kopf/Halstumoren und normaler Schilddrüsenfunktion dienten als Kontrollgruppe. Ergebnisse: Die F-18-FDG-Aufnahme in die Schilddrüse war signifikant höher bei Patienten mit funktionell relevanter Autonomie im Vergleich zu den Kontrollen. Fokale Autonomien zeichneten sich ausnahmslos durch einen intensiven, fokal gesteigerten Glukose-Uptake aus, während disseminierte Autonomien ein variables Muster globaler Steigerungen des Glukose-Uptakes zeigten. Schlußfolgerung: Funktionelle Autonomien der Schilddrüse zeigen einen gleichzeitig gesteigerten Glukose- und lodstoffwechsel als Folge der konstitutiven Mutation des TSH-Rezeptors, wobei das Ausmaß beider Veränderungen positiv korreliert.
Summary
Aim: Gain-of-function mutations of the thyrotropin receptor (TSHR) gene have been invoked as one of the major causes of toxic thyroid adenomas. This study evaluates F-18-FDG-PET in these patients. Methods: Twenty patients with focal autonomous nodules and ten with disseminated autonomy were investigated the day before radioiodine therapy. Twenty patients with cancer of the head or neck and normal thyroid function served as controls. Results: F-18-FDG-Uptake was higher in patients than in controls. Focal autonomous nodules were associated with focally enhanced glucose metabolism. Disseminated autonomous goiters showed various patterns of focal or global hypermetabolism. Conclusion: Autonomous thyroid tissue caused by constitutive mutations of the TSH receptor is characterised by simultaneous increases in glucose and iodine metabolism which are correlated.
-
Literatur
- 1 Adler LP, Bloom AD. Positron emission tomography of thyroid masses. Thyroid 1993; 3: 195-200.
- 2 Als C, Listewnik M, Ritter HP, Rosler H. Scintigraphic method in the quantification of morphological and functional changes of thyroid autonomy before and after iodine radiotherapy. Schweiz Med Wochenschr 1997; 127: 102-6.
- 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) 1988; 117: 145-53.
- 4 Becker W, Börner W, Rendl J. Is a TSH screening for the diagnosis or exclusion of functional thyroid autonomy meaningful?. Nuklearmedizin 1992; 31 (04) 132-6.
- 5 Börner AR, Voth E, Wienhard K, Wagner R, Schicha H. F-18-FDG-PET der Schilddrüse bei M. Basedow. Nuklearmedizin. 1998 (in Druck).
- 6 Dai G, Levy O, Carrasco N. Cloning and characterization of the thyroid iodide transporter. Nature 1996; 379: 458-60.
- 7 Dederichs B, Otte R, Klink JE, Schicha H. Volumenreduktion der Schilddrüse nach Radioiodtherapie bei Patienten mit Schilddrüsenautonomie und M. Basedow. Nuklearmedizin 1996; 35: 164-9.
- 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 1996; 81: 1898-904.
- 9 Dietlein M, Scheidhauer K, Voth E, Theissen P, Schicha H. Diagnostische Algorithmen in der Nachsorge des differenzierten Schilddrüsenkarzinoms: Welchen Stellenwert haben FDG und Sestamibi?. Nuklearmedizin 1998; 37: 6-11.
- 10 Dietlein M, Scheidhauer K, Voth E, Theissen P, Schicha H. Fluorine-18-fluorodeoxyglucose positron emission tomography and iodine-131 whole-body scintigraphy in the follow-up of differentiated thyroid cancer. Eur J Nucl Med 1997; 24: 1341-8.
- 11 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 1991; 5: 905-10.
- 12 Feine U, Lietzenmayer R, Hanke JP, Wöhrle H, Müller-Schauenburg W. F-18-FDG-Ganzkörper-PET bei differenzierten Schilddrüsenkarzinomen. Nuklearmedizin 1995; 34: 127-34.
- 13 Field JB. Intermediary metabolism of the thyroid. In: Greep RO, Astwood EB. eds. Handbook of Physiology, Section 7: Endocrinology, Part III: Thyroid. Washington: American Physiological Society; 1974: 147-59.
- 14 Filetti S, Damante G, Foti D. Thyrotropin stimulates glucose transport in cultured rat thyroid cells. Endocrinoloy 1987; 120: 2576-81.
- 15 Flower MA, Al-Saadi A, Harmer CL, McReady VR, Ott RJ. Dose-response study on thyreotoxic patients undergoing positron emission tomography and radioiodine therapy. Eur J Nucl Med 1994; 21: 531-6.
- 16 Gerber H, Peter HJ, Ramelli F, Miloni E, König MP, Studer H, Berchthold R, Gemsenjäger E. Autonomie und Heterogenität der Follikel in der euthyreoten und hyperthyreoten menschlichen Knotenstruma: die Lösung alter Rätsel?. Schweiz Med Wschr 1983; 113: 1178-87.
- 17 Gerber H, Bürgi U, Peter HJ. Etiology and pathogenesis of thyroid nodules. Exp Clin Endocrinol 1993; 101: 97-101.
- 18 Grünwald F, Menzel C, Bender H, Palmedo H, Willkomm P, Ruhlmann J, Franckson T, Biersack HJ. Comparison of F-18-FDG-PET with 131-iodine and 99m-Tc-sestamibi scintigraphy in differentiated thyroid cancer. Thyroid 1997; 7: 327-35.
- 19 Hawkins RA, Höh CK. PET FDG studies in oncology. Nucl Med Biol 1994; 21: 739-47.
- 20 Joensuu H, Ahonen A. Imaging of metastases of thyroid carcinoma with fluorine-18 fluorodeoxyglucose. J Nucl Med 1987; 28: 910-4.
- 21 Joseph K. Diagnosis and therapy of functional autonomy. Acta Med Austriaca 1990; 17 (Suppl. 01) 47-53.
- 22 Krohn K, Fuhrer D, Holzapfel HP, Paschke R. Clonal origin of toxic thyroid nodules with constitutively activating thyrotropin receptor mutations. J Clin Endocrinol Metab 1998; 83: 130-4.
- 23 Luster M, Jacob M, Thelen MH, Michalowski U, Deutsch U, Reiners C. Reduction of thyroid volume following radioiodine therapy for functional autonomy. Nuklearmedizin 1995; 34: 57-60.
- 24 Moka D, Voth E, Schicha H. Effect of antithyroid medication on the effective halflife and uptake of 131-iodine following radioiodine therapy. Nuklearmedizin 1997; 36: 87-92.
- 25 Parma J, Duprez L, Van Sande J, Hermans J, Rocmans P, Van Vliet G, Costagliola S, Rodien P, Dumont JE, 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 1997; 82: 2695-701.
- 26 Parma J, Van Sande J, Swillens S, Tonacchera M, Dumont J, Vassart G. Somatic mutations causing constitutive activity of the thyrotropin receptor are the major cause of hyperfunctioning thyroid adenomas: identification of additional mutations activating both the cyclic adenosine 3’,5’-monophosphate and inositol phosphate-Ca2+-cascades. Mol Endocrinol 1995; 9: 725-33.
- 27 Paschke R, Ludgate M. The thyrotropin receptor in thyroid diseases. N Engl J Med 1997; 337: 1675-81.
- 28 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 1996; 104 (Suppl): 129-32.
- 29 Pinducciu C, Borgonovo G, Arezzo A, Torre GC, Giordano G, Cordera R. Toxic thyroid adenoma: absence of DNA mutations of the TSH receptor and Gs alpha. Eur J Endocrinol 1998; 138: 37-40.
- 30 Porcellini A, Fenzi G, Avvedimento EV. Mutations of thyrotropin receptor gene. J Mol Med 1997; 75: 567-75.
- 31 Reinhardt MJ, Moser E. An update on diagnostic methods in the investigation of diseases of the thyroid. Eur J Nucl Med 1996; 23: 587-94.
- 32 Russo D, Arturi F, Suarez HG, Schlumberger M, Du VJ, Crocetti U, Filetti S. Thyrotropin receptor gene alterations in thyroid hyperfunctioning adenomas. J Clin Endocrinol Metab 1996; 81: 1548-51.
- 33 Studer H, Peter HJ, Gerber H. Morphologie and functional changes in developing goiters. In: Hall R, Köbberling J. (eds). Thyroid disorders associated with iodine deficiency and excess. New York: 1985: 227-40.
- 34 Sachs L. Angewandte Statistik. 6. Aufl.. Berlin, Heidelberg, New York, Tokio: Springer-Verlag; 1984
- 35 Sanders J, Oda Y, Roberts SA, Maruyama M, Furmaniak J, Smith BR. Understanding the thyrotropin receptor function-structure relationship. Baillieres Clin Endocrinol Metab 1997; 11: 451-79.
- 36 Sasaki M, Ichiya Y, Kuwabara Y, Akashi Y, Yoshida T, Fukumura T, Masuda K. An evaluation of FDG-PET in the detection and differentiation of thyroid tumours. Nucl Med Comm 1997; 18: 957-63.
- 37 Siegel RD, Lee SL. Toxic nodular goiter. Toxic adenoma and toxic multinodular goiter. Endocrinol Metab Clin North Am 1998; 27: 151-68.
- 38 Sisson JC, Ackermann RJ, Meyer MA, Wahl RL. Uptake of 18-fluoro-2-deoxy-D-glucose by thyroid cancer: implications for diagnosis and therapy. J Clin Endocrinol Metab 1993; 77: 1090-4.
- 39 Thomson FJ, Jess TJ, Moyes C, Plevin R, Gould GW. Characterization of the intracellular signalling pathways that underlie growth-factor-stimulated glucose transport in Xenopus oocytes: evidence for ras-and rho-dependent pathways of phosphatidylinositol-3-kinase activation. Biochem J 1997; 325: 637-43.
- 40 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 1998; 83: 492-8.
- 41 Utiger RD. Thyrotropin-receptor mutations and thyroid dysfunction. N Engl J Med 1995; 332: 183-5.
- 42 Vassart G, Van Sande J, Parma J, Tonacchera M, Duprez L, Swillens S, Dumont J. Activating mutations of the TSH receptor gene cause thyroid diseases. Ann Endocrinol 1996; 57: 50-4.
- 43 Vassart G. New pathophysiological mechanisms for hyperthyroidism. Horm Res 1997; 48 (Suppl): 47-50.
- 44 Voth E, Börner AR, Theissen P, Schicha H. Positron emission tomography (PET) in benign thyroid diseases. Exp Clin Endocrinol 1994; 102 (Suppl. 03) 71-4.
- 45 Yao WJ, Hoh CK, Hawkins RA, Glaspy JA, Weil JA, Lee SJ, Maddahi J, Phelps ME. Quantitative PET imaging of bone marrow glucose metabolic response to hematopoietic cytokines. J Nucl Med 1994; 36: 794-9.
- 46 Zasadny KR, Wahl RL. Standardizes uptake values of normal tissues at PET with 2-[Fluorine-18]-Fluoro-2-deoxy-D-glucose: Variations with body weight and a method for correction. Radiology 1993; 189: 847-50.