Thyroid Hormone Suppression Therapy

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The rationale for thyroid-suppressive therapy in DTC is based on many studies showing that TSH, by bind

Figure 2-16. Patient with follicular thyroid carcinoma post-total thyroidectomy in whom an asymptomatic solitary left frontal bone metastasis was detected on low-dose 131I diagnostic scan (not shown). A, Total-body scan performed 72 hours after high-dose (200 mCi) radioactive iodine (131I) therapy showing avid 131I uptake (arrowheads) in the left frontal bone and a lesser degree of 131I in the thyroid remnant (arrow). B, A second dose of 200 mCi 131I was administered 6 months later. Post-therapy scan now showed minimal 131I uptake in the left frontal bone (arrowheads) as well as the thyroid remnant (arrow), indicating dramatic treatment response. C, Further diagnostic scan performed 6 months later showed no 131I uptake in the skull or thyroid bed, indicating complete treatment response (outline of the patient's head and clavicles represented by the surface marker). Courtesy of E. S. Ang, MD, Department of Nuclear Medicine, Singapore General Hospital, Singapore.

Figure 2-16. Patient with follicular thyroid carcinoma post-total thyroidectomy in whom an asymptomatic solitary left frontal bone metastasis was detected on low-dose 131I diagnostic scan (not shown). A, Total-body scan performed 72 hours after high-dose (200 mCi) radioactive iodine (131I) therapy showing avid 131I uptake (arrowheads) in the left frontal bone and a lesser degree of 131I in the thyroid remnant (arrow). B, A second dose of 200 mCi 131I was administered 6 months later. Post-therapy scan now showed minimal 131I uptake in the left frontal bone (arrowheads) as well as the thyroid remnant (arrow), indicating dramatic treatment response. C, Further diagnostic scan performed 6 months later showed no 131I uptake in the skull or thyroid bed, indicating complete treatment response (outline of the patient's head and clavicles represented by the surface marker). Courtesy of E. S. Ang, MD, Department of Nuclear Medicine, Singapore General Hospital, Singapore.

ing to TSH receptors that are present in most tumors, exerts a trophic influence on thyroid tumor tissue. Traditionally, the goal of T4 therapy has been complete suppression of pituitary secretion of TSH, as indicated by undetectable levels of serum TSH. With the increasing availability of the sensitive assays of TSH, meticulous titration of the level of TSH suppression has become possible. A basal serum TSH level of < 0.1 mIU/L has typically been considered equivalent to a nonresponse of TSH in a thyrotropin-releasing hormone (TRH) test, previously considered the hallmark for adequate TSH suppression in DTC. Recent studies have also addressed the concerns of accelerated bone turnover and cardiovascular abnormalities associated with long-term thyroid hormone suppression therapy.21 Therefore, considerable debate has emerged on what is the acceptable degree of TSH suppression and whether the same degree of suppression is adequate for different patients.

Although controlled clinical studies are necessary to resolve the above controversy, experts generally agree that the goal of TSH suppression is <0.1 mIU/L (closer to 0.01 mIU/L using third- or fourth-generation TSH assays) in patients deemed at risk for recurrence or mortality. Conversely, the degree of TSH suppression may be less stringent in the low-risk category, especially for PTC patients, with the goal for basal serum TSH within the 0.1 to 0.4 mIU/L range.1617

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