Thyroid UK advisors have published papers showing that patients without a thyroid have lower T3 levels. A new paper jstage.jst.go.jp/article/en... shows that serum T3 levels are related to thyroid volume. Patients with little or no thyroid tissue left have lower T3 levels and so would benefit more from liothyronine.
This study is not paticularly good but is easier to follow that some of the more mathematical studies. It has two flaws: blood was taken after ingestion of levothyroxine and the patients have fT3 and fT4 levels that are a little below average suggesting they are undermedicated. i suspect that adequately medicated patients will show a greater difference in fT3 and fT4 levels but this study at least shows a trend. It clearly demonstrates that patients without a thyroid should receive T3 therapy.
My personal view is that we should look at where T3 is coming from. Does it come from type-2 deiodinase (D2) that takes place close to the cell nucleus (especially in the brain), or does it come from circulation in the blood via the thyroid and type-1 deiodinase (D1). Patients on levothyroxine monotherapy that restores blood fT3 will have a higher fT4 and lower TSH. High fT4 increases reverse T3 levels and rT3 is known to inhibit D2. Similarly, a lower TSH reduces D2 activity. I believe these mechanisms combine to reduce T3 levels at the receptors in tissues dependent upon D2 for local T3. This is a secondary consequence arising from the loss of thyroidal T3. The lower TSH and elevated fT4 necessitated by levothyroxine monotherapy produces a shift from D2 to D1 deiodinase and a resultant loss of T3 in D2 dependent organs such as the brain.
Hope I haven't lost everyone. If you have little or no thyroid tissue you will need some T3 to restore the thyroid axis back to normal.