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Several reports have been presented over the last few years, indicating
that many toxic nodules harbour somatic mutations in the TSH receptor gene
or the gene of the a-polypeptide of the coupled G protein. These two different
types of mutations lead to constitutive stimulation of the cAMP system
resulting in autonomous growth and overproduction of thyroid hormone.
Porcellini et al., Naples and AlbanoLaziale, Italy, show preliminary results that at least 25% of thyroid hyperfunctioning adenomas are indeed caused by this type of mutations at different locations in the gene. In contrast to this publication Nagayama, Tokyo, Japan, searched for such mutations in 45 autonomous functioning nodules and in only 1 sample a somatic mutation was found, however that could not explain autonomous function. The authors conclude that mutations in the gene of the TSH receptor, causing autonomous adenomas, should be rare in Japanese patients. |
