Premium
Homeostatic equilibria between free thyroid hormones and pituitary thyrotropin are modulated by various influences including age, body mass index and treatment
Author(s) -
Hoermann Rudolf,
Midgley John E.M.,
Giacobino Adrienne,
Eckl Walter A.,
Wahl Hans Günther,
Dietrich Johannes W.,
Larisch Rolf
Publication year - 2014
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/cen.12527
Subject(s) - medicine , endocrinology , hormone , deiodinase , body mass index , thyroid , triiodothyronine , confounding , levothyroxine
Summary Objective We examined the interrelationships of pituitary thyrotropin ( TSH ) with circulating thyroid hormones to determine whether they were expressed either invariably or conditionally and distinctively related to influences such as levothyroxine ( L ‐ T 4) treatment. Design and methods This prospective study employing 1912 consecutive patients analyses the interacting equilibria of TSH and free triiodothyronine ( FT 3) and free thyroxine ( FT 4) in the circulation. Results The complex interrelations between FT 3, FT 4 and TSH were modulated by age, body mass, thyroid volume, antibody status and L ‐ T 4 treatment. By group comparison and confirmation by more individual TSH ‐related regression, FT 3 levels were significantly lower in L ‐ T 4‐treated vs untreated nonhypothyroid autoimmune thyroiditis (median 4·6 vs 4·9 p m , P < 0·001), despite lower TSH (1·49 vs 2·93 mU/l, P < 0·001) and higher FT 4 levels (16·8 vs 13·8 p m , P < 0·001) in the treated group. Compared with disease‐free controls, the FT 3‐ TSH relationship was significantly displaced in treated patients with carcinoma, with median TSH of 0·21 vs 1·63 ( P < 0·001) at a comparable FT 3 of 5·0 p m in the groups. Disparities were reflected by calculated deiodinase activity and remained significant even after accounting for confounding influences in a multivariable model. Conclusions TSH , FT 4 and FT 3 each have their individual, but also interlocking roles to play in defining the overall patterns of thyroidal expression, regulation and metabolic activity. Equilibria typical of the healthy state are not invariant, but profoundly altered, for example, by L ‐ T 4 treatment. Consequently, this suggests the revisitation of strategies for treatment optimization.