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Endocrine Abstracts (2019) 63 D3.1 | DOI: 10.1530/endoabs.63.D3.1

ECE2019 Debates T4 is not enough (2 abstracts)

‘Yes, T4 is not enough’

Birte Nygaard


Denmark.


Most L-T4 treated hypothyroid patients return to normal health without complaints. However, persistent symptoms such as tiredness, depression, decreased cognitive function, weight increase and musculoskeletal symptoms are described in 25% of L-T4 treated hypothyroid patients compared to 15–20% in controls. It has been assumed that all the necessary T3 could be derived from peripheral de-iodination of orally administered L-T4. Nevertheless, data has pointed towards a possible need for supplementary T3 in selected patient groups to fully restore the balance between TSH, TRH, thyroid hormones, de-iodinase and metabolism. Data show a 15–20% lower serum FT3/FT4 ratio given a stabile serum TSH after thyroidectomy than before and in thyroidectomized rats it is only possible to restore normal concentrations of FT3 in all tissues by giving a combination of L-T4 as well as L-T3. A meta-analysis in 2006 of data from more than 1200 unselected patients could not confirm an effect of L-T4/L-T3 combination therapy. However, the included studies were heterogeneous, including unselected patients. A minor study in a highly selected patient-group with Hashimoto’ disease and overt hypothyroidism as well as persistent symptoms demonstrated significant effects in seven out of eleven quality of life scores and preference for L-T3/L-T4 combination therapy in 49% compared to L-T4 monotherapy in 15% (P=0.002). A suggested explanation for a possible need for a T3 substitution as well as T4 has been related to a change in the feedback in the hypothalamic-pituitary- thyroid axis induced by high dose og T4 and a possible relative inactivation of deiodinase 2 and hereby lower values of T3. Another possible suggested explanation is polymorphisms in the deiodinase 2 gene (D2-92 Ala) or to the cellular membrane transporter (MCT10) and by this a potential decrease in the transportation of thyroid hormone from plasma to the intracellular space and a decreased deiodination of T4 to T3. However, extended research is needed to explore the exact effect of these and other polymorphisms.

Volume 63

21st European Congress of Endocrinology

Lyon, France
18 May 2019 - 21 May 2019

European Society of Endocrinology 

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