Exp Clin Endocrinol Diabetes 1998; 106(3): 234-236
DOI: 10.1055/s-0029-1211982
Short Communication

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Thyroid hyperfunctioning adenomas with and without Gsp/TSH receptor mutations show similar clinical features

F. Arturi, C. Capula, E. Chiefari, S. Filetti, D. Russo
  • Cattedra di Endocrinologia, Dipartimento di Medicina Sperimentale e Clinica; Cattedra di Farmacologia, Facoltà di Farmacia (D.R.), Università di Reggio Calabria, Via T. Campanella, Catanzaro, Italy
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Publication History

Publication Date:
14 July 2009 (online)

Summary

Activating mutations of Gsoc protein (gsp) and TSH receptor (TSH-R) identified in autonomously hyperfunctioning thyroid adenomas have been proposed as the primary event responsible for this disease. Since mutations have not been detected in 100% (ranging from less than 10% to 90%) of the patients, we evaluated whether the presence of gsp and TSH-R mutations cause differences in the clinical and biochemical parameters of the affected patients. Fifteen consecutive patients (11 women and 4 men) with autonomously hyperfunctioning thyroid adenomas who underwent thyroidectomy, previously examined for the presence of gsp or TSH-R mutations, were investigated. In all of the patients we examined plasma free T3, free T4, TSH levels and ultrasound volume of the nodules. The patients with mutations in gsp or TSH-R were similar to the patients without mutations for clinical presentation, sex distribution and mean age. Furthermore, basal serum FT3, TSH and tumor volume in the patients with mutations were not significantly different from the group without mutations. Our preliminary data demonstrate that no significant differences are present in the two groups of patients examined, suggesting that factors other than gsp or TSH-R mutations play a role in the clinical presentation of the disease.

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