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Dual control of pituitary thyroid stimulating hormone secretion by thyroxine and triiodothyronine in athyreotic patients.
Ther Adv Endocrinol Metab 2017; 8(6):83-95TA

Abstract

BACKGROUND

Patient responses to levothyroxine (LT4) monotherapy vary considerably. We sought to differentiate contributions of FT4 and FT3 in controlling pituitary thyroid stimulating hormone (TSH) secretion.

METHODS

We retrospectively assessed the relationships between TSH and thyroid hormones in 319 patients with thyroid carcinoma through 2914 visits on various LT4 doses during follow-up for 5.5 years (median, IQR 4.2, 6.9). We also associated patient complaints with the relationships.

RESULTS

Under varying dose requirements (median 1.84 µg/kg, IQR 1.62, 2.11), patients reached TSH targets below 0.4, 0.1 or 0.01 mIU/l at 73%, 54% and 27% of visits. While intercept, slope and fit of linearity of the relationships between lnTSH and FT4/FT3 varied between individuals, gender, age, LT4 dose and deiodinase activity influenced the relationships in the cohort (all p < 0.001). Deiodinase activity impaired by LT4 dose significantly affected the lnTSH-FT4 relationship. Dose increase and reduced conversion efficiency displaced FT3-TSH equilibria. In LT4-treated patients, FT4 and FT3 contributed on average 52% versus 38%, and by interaction 10% towards TSH suppression. Symptomatic presentations (11%) accompanied reduced FT3 concentrations (-0.23 pmol/l, p = 0.001) adjusted for gender, age and BMI, their relationships being shifted towards higher TSH values at comparable FT3/FT4 levels.

CONCLUSIONS

Variation in deiodinase activity and resulting FT3 levels shape the TSH-FT4 relationship in LT4-treated athyreotic patients, suggesting cascade control of pituitary TSH production by the two hormones. Consequently, measurement of FT3 and calculation of conversion efficiency may identify patients with impaired biochemistry and a resulting lack of symptomatic control.

Authors+Show Affiliations

Department of Nuclear Medicine, Klinikum Lüdenscheid, Paulmannshoeher Str 14, D-58515 Luedenscheid, Germany.North Lakes Clinical, Ilkley, UK.Medical Department I, Endocrinology and Diabetology, Bergmannsheil University Hospitals, Ruhr University of Bochum, Bochum, Germany.Department of Nuclear Medicine, Klinikum Lüdenscheid, Lüdenscheid, Germany.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28794850

Citation

Hoermann, Rudolf, et al. "Dual Control of Pituitary Thyroid Stimulating Hormone Secretion By Thyroxine and Triiodothyronine in Athyreotic Patients." Therapeutic Advances in Endocrinology and Metabolism, vol. 8, no. 6, 2017, pp. 83-95.
Hoermann R, Midgley JEM, Dietrich JW, et al. Dual control of pituitary thyroid stimulating hormone secretion by thyroxine and triiodothyronine in athyreotic patients. Ther Adv Endocrinol Metab. 2017;8(6):83-95.
Hoermann, R., Midgley, J. E. M., Dietrich, J. W., & Larisch, R. (2017). Dual control of pituitary thyroid stimulating hormone secretion by thyroxine and triiodothyronine in athyreotic patients. Therapeutic Advances in Endocrinology and Metabolism, 8(6), pp. 83-95. doi:10.1177/2042018817716401.
Hoermann R, et al. Dual Control of Pituitary Thyroid Stimulating Hormone Secretion By Thyroxine and Triiodothyronine in Athyreotic Patients. Ther Adv Endocrinol Metab. 2017;8(6):83-95. PubMed PMID: 28794850.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dual control of pituitary thyroid stimulating hormone secretion by thyroxine and triiodothyronine in athyreotic patients. AU - Hoermann,Rudolf, AU - Midgley,John E M, AU - Dietrich,Johannes W, AU - Larisch,Rolf, Y1 - 2017/07/13/ PY - 2017/03/20/received PY - 2017/05/29/accepted PY - 2017/8/11/entrez PY - 2017/8/11/pubmed PY - 2017/8/11/medline KW - TSH feedback control KW - deiodinase KW - levothyroxine treatment KW - set point KW - thyroid homeostasis KW - triiodothyronine SP - 83 EP - 95 JF - Therapeutic advances in endocrinology and metabolism JO - Ther Adv Endocrinol Metab VL - 8 IS - 6 N2 - BACKGROUND: Patient responses to levothyroxine (LT4) monotherapy vary considerably. We sought to differentiate contributions of FT4 and FT3 in controlling pituitary thyroid stimulating hormone (TSH) secretion. METHODS: We retrospectively assessed the relationships between TSH and thyroid hormones in 319 patients with thyroid carcinoma through 2914 visits on various LT4 doses during follow-up for 5.5 years (median, IQR 4.2, 6.9). We also associated patient complaints with the relationships. RESULTS: Under varying dose requirements (median 1.84 µg/kg, IQR 1.62, 2.11), patients reached TSH targets below 0.4, 0.1 or 0.01 mIU/l at 73%, 54% and 27% of visits. While intercept, slope and fit of linearity of the relationships between lnTSH and FT4/FT3 varied between individuals, gender, age, LT4 dose and deiodinase activity influenced the relationships in the cohort (all p < 0.001). Deiodinase activity impaired by LT4 dose significantly affected the lnTSH-FT4 relationship. Dose increase and reduced conversion efficiency displaced FT3-TSH equilibria. In LT4-treated patients, FT4 and FT3 contributed on average 52% versus 38%, and by interaction 10% towards TSH suppression. Symptomatic presentations (11%) accompanied reduced FT3 concentrations (-0.23 pmol/l, p = 0.001) adjusted for gender, age and BMI, their relationships being shifted towards higher TSH values at comparable FT3/FT4 levels. CONCLUSIONS: Variation in deiodinase activity and resulting FT3 levels shape the TSH-FT4 relationship in LT4-treated athyreotic patients, suggesting cascade control of pituitary TSH production by the two hormones. Consequently, measurement of FT3 and calculation of conversion efficiency may identify patients with impaired biochemistry and a resulting lack of symptomatic control. SN - 2042-0188 UR - https://www.unboundmedicine.com/medline/citation/28794850/Dual_control_of_pituitary_thyroid_stimulating_hormone_secretion_by_thyroxine_and_triiodothyronine_in_athyreotic_patients_ L2 - http://journals.sagepub.com/doi/full/10.1177/2042018817716401?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -