Thyroid Suppression

Ld, Hill; Hg, Beebe; Hipp, R.; Jones, Harry C.

doi:10.1001/archsurg.1974.01350280011003

Cited by 41 publications

(5 citation statements)

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“…Crile [15], Hill et al [29] and Mazzaferri and their associates [30] have reported that some thyroid cancers also regress. Hill et al [29] found that in 2 of 16 patients (13%) with papillary carcinoma and in 2 of 6 patients (33%) with follicular carcinoma there was significant regression in the size of the thyroid lesion in response to treatment with thyroid hormone, whereas patients with medullary and undifferentiated thyroid cancer failed to respond. Mazzaferri et al [30] also found that in 11 of 83 patients (13%) with thyroid nodules subsequently proven to be papillary carcinoma there was a decrease in size of the lesions with TSH suppressive therapy.…”

Section: Tsh and Thyroid Cancermentioning

confidence: 97%

TSH suppression in the management of thyroid nodules and thyroid cancer

Clark

1981

World j. surg.

109

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Clinical and experimental data concerning TSH suppression, by giving exogenous thyroid hormone, in patients with goiter and in patients with thyroid cancer show a beneficial effect. In the goiter patients, TSH suppressive therapy seems most effective in young patients with diffuse or newly discovered goiters, in hypothyroid patients, and in patients with chronic lymphocytic thyroiditis or compensatory thyroid hypertrophy after partial thyroidectomy. With TSH suppressive therapy about 2/3 of thyroid nodules become smaller, but only about 5% to 10% disappear. In patients with differentiated thyroid cancer (papillary, mixed papillary‐follicular, and follicular), tumor recurrence, tumor progression, and long‐term survival all seem to be influenced favorably by TSH suppressive therapy. Experimental investigations demonstrate that both benign thyroid adenomas and differentiated thyroid carcinomas have TSH receptors situated on the plasma membranes. These TSH receptors appear to be coupled to the activation of adenylate cyclase in a one‐to‐one relationship. Experimental and clinical studies strongly support the use of thyroid hormone both for the treatment of patients after thyroidectomy for thyroid cancer and as prophylaxis to prevent the development of thyroid cancer in high‐risk irradiated patients. The dose of thyroxine recommended for adequate TSH suppression is the lowest dose of thyroxine that will completely block the TSH response to TRH (usually 0.2 to 0.25 mg).

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Section: Tsh and Thyroid Cancermentioning

confidence: 97%

TSH suppression in the management of thyroid nodules and thyroid cancer

Clark

1981

World j. surg.

109

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“…Numerous clinical studies have demonstrated that treatment of patients with benign thyroid tumors with thyroid hormone causes about two-thirds of these tumors to decrease significantly in size [1][2][3]. Other studies have demonstrated that some differentiated thyroid cancers will decrease in size in response to treatment with thyroid hormone [4][5][6][7][8] and that recurrent thyroid cancer is less common [8] and survival is better [9]. The higher death rate from thyroid cancer in areas of endemic goiter also suggests an important relationship between increased TSH levels and thyroid cancer growth [10].…”

mentioning

confidence: 99%

“…Clinically, thyroid tumor stimulation (growth or increased thyroglobulin secretion) in response to increased blood TSH levels as well as the regression or disappearance of primary and meta- static thyroid tumors in response to treatment with thyroid hormone is well documented [4,5,11]. Unfortunately, this does not occur in all patients [7,8]. TSH receptor and AC studies [13][14][15][16][17][18][19] and metabolic studies [20] also support the important role TSH has concerning the growth and function of thyroid neoplasms.…”

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confidence: 99%

Mechanisms for increased adenylate cyclase responsiveness to TSH in neoplastic human thyroid tissue

1984

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We have previously examined TSH receptors and adenyiate cyclase (AC) activity in normal and neoplastic human thyroid tissue. We found only minor differences in the affinity and capacity of the TSH receptor between the normal and neoplastic tissue, and yet there was a five-fold greater AC responsiveness in the neoplastic thyroid tissue. To determine why there was a greater AC responsiveness to TSH in most differentiated thyroid neoplasms, we probed the receptor-cyclase unit which consists of at least 3 classes of components: the receptor (R), the guanyl nucleotide regulatory unit (G), and the catalytic unit (C). The G unit binds GTP and forms a link between R and C. We studied the effects of TSH, Gpp(NH)p (a non-hydrolyzable GTP analog) and sodium fluoride (NaF) (which act on G), and forskolin (which acts on C) on the receptor-cyclase unit. The results of these studies demonstrate that: (a) there was a greater AC response to TSH (5/6), Gpp(NH)p (3/5), and NaF (5/6) in T than N; (b) the AC response to forskolin was comparable in T and N in 5/6 patients and higher in T in 1 patient; (c) Gpp(NH)p, NaF, and forskolin all had an additive or synergistic effect when added to TSH in both N and T; (d) NaF and forskolin also had an additive or synergistic effect on AC, whereas Gpp(NH)p and forskolin together in N and Gpp(NH)p and NaF together in T caused a considerably less than additive AC response.These studies demonstrate that Gpp(NH)p, NaF, and forskolin at optimal concentrations have an additive effect on

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“…1980). Accordingly, TSH suppression by thyroid hormones is used in the medical management of DTC to prevent tumour recurrence and to suppress tumour growth (Crile, 1966;Hill et al, 1974;Staunton & Greenings, 1976 Klee & Hay, 1987). L-Thyroxine is usually preferred to triiodothyronine for complete TSH suppression (Larsen, 1982) with mean suppressive daily doses ranging from 150 to 300 jtg (Hoffman, 1977; Lamberg et al, 1979; Edmonds et al.…”

Section: Discussionmentioning

confidence: 99%

TSH suppression by octreotide in differentiated thyroid carcinoma

Maini¹,

Sciuto²,

Tofani³

1994

Clinical Endocrinology

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OBJECTIVE This study evaluates the addition of octreotide and L-thyroxine to shorten the perlod of exposure to unduly elevated TSH levels in patients with differentiated thyroid carcinoma undergoing total body scan with '% DESIGN Fourteen thyroldectomized patients were studied after total body scan and the restarting of dlfferent doses of thyroxlne. After one year a second total body scan and a schedule of the same dose of thyroxine combined with octreotide were performed In each subject. PATIENTS Patients were divided into four groups according to the treatment seven patients recelved initlaily 100 pg of L-thyroxine (Group 1) and after 1 year 100 pg of L-thyroxine plus 300 pg of octreotidelday (Group 3): the other seven received lnitiaily 150 pg of L-thyroxine (Group 2) and then 150 pg of L-thyroxine plus 300 pg of octreotldel day (Group 4).MEASUREMENTS Serum TSH, T3 and T4 were measured on the day of radlolodine administration (day 0) and after 14,21,30,45,60 and 90 days.

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Thyroid Suppression

Cited by 41 publications

References 0 publications

TSH suppression in the management of thyroid nodules and thyroid cancer

TSH suppression in the management of thyroid nodules and thyroid cancer

Mechanisms for increased adenylate cyclase responsiveness to TSH in neoplastic human thyroid tissue

TSH suppression by octreotide in differentiated thyroid carcinoma

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