TSH suppression in the management of autonomously functioning thyroid lesions.
TSH suppression in the management of autonomously functioning thyroid lesions.
复制标题
TSH 抑制治疗自主功能性甲状腺病变。
DOI:
10.1007/bf01655242
复制
发表时间:
1986
影响因子:
2.6
通讯作者:
Nayfeh,SN
中科院分区:
文献类型:
--
作者:
ThomasJr,CG;Tawil,M;Berman,MI;Nayfeh,SN
Solitary autonomously functioning thyroid lesions (AFTL) are discrete hyperfunctioning nodules whose growth and function do not appear to be dependent on thyroid‐stimulating hormone (TSH). Although they gradually increase in size and function over years, rarely do they progress to produce hyperthyroidism. This article presents the thesis that this “self‐limiting feature” is related to their growth and function being modulated by levels of TSH. Thyroid membranes from autonomously functioning thyroid lesions were examined in 6 patients. A nonlinear Scatchard plot was obtained with the hyperfunctioning thyroid lesion demonstrating high‐affinity, low‐capacity TSH receptor components. These exhibited a binding capacity ranging from 7 to 600 fmol/mg protein in patients with suppressed TSH levels to 1,450 in a euthyroid patient. All lesions exhibited basal adenylate cyclase activity which was stimulated 2–3‐fold by Bovine TSH. A review of the natural history of the lesion demonstrates a decremental increase in size and function with time. In 9 patients receiving thyroid hormone as suppressive therapy observed over a period of 4–14 years, the lesions partially regressed in 4 and did not progress in 5. This concept of growth and function of AFTL being modulated by TSH levels has therapeutic implications when such nodules are identified early in the course of their development. At this time, TSH suppression may be inhibitory to increase in nodule size and secretion of thyroid hormones.