sciencedirect.com/science/a...
This was posted in the ITT group on FB and is certainly of interest, especially the quoted part as it questions the whole concept of subclinical hyperthyroidism. Graves and TSH supression after thyroidectomy should not be seen as the same thing (we know it but some many doctors seem not to).
"Our findings contrast the thyroid-active (hyperthyroidism) and no-thyroid response to treatment (thyrotoxicosis), determined either by activation or lack of the physiological feedforward path on T3. Outcome measures cannot therefore rely on the assumption of response equivalence, which would require a consistent translation of the signalling chain from TSH to TSH receptor, FT4 and finally onto FT3. This questions the utility of TSH measurement alone as a clinical predictor in subclinical hyperthyroidism/ thyrotoxicosis, rather rendering it strongly dependent on the underlying cause and clinical entity. This is similar to the hypothyroid situation where the decision whether to treat or not to treat has been separated from the definition and diagnosis of subclinical hypothyroidism [60].
Conclusion
The present study demonstrates a biochemically heterogenous expression of hormone activities in subclinical/overt hyperthyroidism and exogenous thyrotoxicosis. From a clinical, biochemical and statistical perspective, the two conditions can and should be clearly distinguished, particularly when assessing risks in association with TSH measurement. Our findings support calls from other authors to abandon the term subclinical hyperthyroidism which refers solely to a laboratory constellation, putting stronger emphasis on etiological and clinical entities."