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Preserved thyroidal secretion of thyroxione in acromegalic patients with suppressed hypophyseal secretion of thyrotrophin
Author(s) -
Yoshinari Motolaka,
Tokuyama Takashi,
Kuroda Takeo,
Sato Kaori,
Okazawa Kaeko,
Mizokami Tetsuya,
Okamura Ken,
Fujishima Masatoshi
Publication year - 1992
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/j.1365-2265.1992.tb01460.x
Subject(s) - medicine , endocrinology , acromegaly , secretion , hormone , thyroid , basal (medicine) , stimulation , trh stimulation test , pituitary gland , thyrotropin releasing hormone , growth hormone , insulin
SUMMARY objective We have assessed the mechanisms which maintain euthyroidism in acromegalic patients despite the suppression of thyrotrophin (TSH) secretion materials Fourteen untreated patients with acromegaly were analysed. Ten patients were also studied after pituitary surgery methods Thyroid hormones, growth hormone (GH), Insulin‐like growth factor‐I (IGF‐I) and thyroidal uptake of radioactive iodine, thyrotrophin releasing hormone (TRH) test and basal metabolic rate (BMR) were measured before and after pituitary surgery results Nine patients had paipable goitres. The TSH response to TRH stimulation was suppressed in eight patients, who maintained normal serum levels of total T3, T4 and free T4. The patients with normal TSH response had lower levels of free and total T4 than controls. The response of TSH to TRH correlated inversely with the serum level of total and free T4, and also with the plasma level of IGF‐I ( r =–0·74, P > 0·05, n = 9). After pituitary surgery, the serum levels of total and free T4 were elevated for at least up to 6 months, with a decrease in the T3/T4 ratio and the BMR. conclusion GH may have a direct stimulatory action on the thyroid secretion of T4 possibly via increased IGF‐I, despite suppressed TSH secretion. The post‐operative elevation of serum T4 suggests the persistent secretion of T4 from the thyroid gland, in spite of instantaneous normalization of the accelerated conversion of T4 to T3, even after reduction of excess GH secretion