Similar prevalence of somatic TSH receptor and Gsα mutations in toxic thyroid nodules in geographical regions with different iodine supply in Turkey
HI Gozu, R Bircan, K Krohn, S Müller… - European journal of …, 2006 - academic.oup.com
HI Gozu, R Bircan, K Krohn, S Müller, S Vural, C Gezen, H Sargin, D Yavuzer, M Sargin…
European journal of endocrinology, 2006•academic.oup.comObjective Differences in iodine intake could account for the variable prevalences reported
for somatic TSH receptor (TSHR) mutations in toxic thyroid nodules (TTNs). However, this
question has not been settled, since no study has yet determined the TSHR mutation
prevalence in regions with different iodine supplies in the same population using the same
methodology. Therefore, we studied the prevalence of somatic TSHR mutations in TTNs
from patients living in iodine-deficient or-sufficient regions in Turkey. Design and methods …
for somatic TSH receptor (TSHR) mutations in toxic thyroid nodules (TTNs). However, this
question has not been settled, since no study has yet determined the TSHR mutation
prevalence in regions with different iodine supplies in the same population using the same
methodology. Therefore, we studied the prevalence of somatic TSHR mutations in TTNs
from patients living in iodine-deficient or-sufficient regions in Turkey. Design and methods …
Objective
Differences in iodine intake could account for the variable prevalences reported for somatic TSH receptor (TSHR) mutations in toxic thyroid nodules (TTNs). However, this question has not been settled, since no study has yet determined the TSHR mutation prevalence in regions with different iodine supplies in the same population using the same methodology. Therefore, we studied the prevalence of somatic TSHR mutations in TTNs from patients living in iodine-deficient or -sufficient regions in Turkey.
Design and methods: We screened 74 TTNs for somatic TSHR mutations. Exons 9 and 10 of the TSHR and 7 and 8 of the Gsα were screened by denaturing gradient gel electrophoresis. Determination of X-chromosome inactivation was used for clonality analysis.
Results
TSHR mutations were identified in 52 (70.2%) of 74 TTNs. A Gsα mutation was identified in one TTN. Three new TSHR mutations were detected (A627V, I640K, I486N). No significant difference between frequencies of TSHR mutations in iodine deficient/sufficient regions was found. The frequency of non-random X-chromosome inactivation was similar in iodine-sufficient or -deficient regions and in TSHR mutation positive or negative hot nodules.
Conclusions
These findings suggest that TTNs in iodine deficient/sufficient areas predominantly arise from aberrant growth of a single cell. Our results suggest that neither the prevalence of TSHR mutations nor that of monoclonal TTNs is related to iodine supply.
Oxford University Press