Thyroid Hormone Therapy

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TSH Suppression

The idea that TSH stimulates both the iodine transport and growth of thyroid carcinoma (only DTC) is the basis for the wide use of T4 in treating this disease. Like normal thyroid tissue, most PTCs and FTCs have functional TSH receptors, but whether postoperative T4 alone improves survival is less certain. Although there have been no prospective randomized trials of this question, there is evidence that TSH stimulates tumor growth [168]. PTC in patients with Graves' disease may be more aggressive, presumably as a result of stimulatory effects of circulating TSH receptor antibodies [82]. Rapid tumor growth sometimes follows T4 withdrawal [169] or the use of rhTSH in preparation for 131I therapy [168]. Moreover, T4 given as an adjuvant to surgical and 131I therapy is effective [122,170]. After 30 years' follow-up, we found that there were significantly fewer recurrences in patients treated with T4 as compared with no adjunctive therapy (P < 0.01) and there were fewer cancer deaths in the T4 group (6% versus 12%, P < 0.001) [19].

Potential Adverse Effects of T4 Therapy

Patients with thyroid cancer are usually treated with T4 to lower TSH secretion below normal, thereby deliberately causing subclinical if not overt thyrotoxicosis. One potential consequence of this is bone mineral loss, even in children [79], but especially in postmenopausal women with thyroid carcinoma [171-173]. This may be prevented by estrogen or bisphosphonate therapy. More importantly, using the smallest T4 dose necessary to suppress TSH has no significant effects on bone metabolism and bone mass in men or women with thyroid cancer [174].

Cardiovascular abnormalities occur in patients taking suppressive doses of T4 and may be ameliorated by beta-adrenergic blockade. Subclinical thyrotoxicosis causes an increased risk of atrial fibrillation [175], a higher 24-hour heart rate, more atrial premature contractions, increased cardiac contractility and ventricular hypertrophy, systolic and diastolic dysfunction, and increased cardiovascular mortality [176-179], especially when the TSH is <0.1mIU/L.

Thyroxine (T4) Dosage

Patients with thyroid cancer who have undergone total thyroid ablation require more T4 than those with spontaneously occurring primary hypothyroidism. In one study, for example, the average dose of T4 that resulted in an unde-tectable basal serum TSH concentration and no increase in serum TSH after thyrotropin-releasing hormone (TRH) was 2.7 ± 0.4 (SD) mg/kg/day [180].Younger patients needed larger T4 doses than older patients did and TSH suppression was more likely when the therapy had been prolonged. In a study of patients with thyroid cancer and other forms of hypothy-roidism, the dose of T4 needed to bring serum

TSH concentrations to normal was 2.11 and 1.62 mg/Kg/day, respectively [181].

One study found that a constantly suppressed TSH (<0.05mIU/L) was associated with a longer relapse-free survival than when serum TSH levels were always 1 mIU/L or higher, and that the degree of TSH suppression was an independent predictor of recurrence [182]. Another large study found that disease stage, patient age, and 131I therapy independently predicted disease progression, but that the degree of TSH suppression did not [183].

The most appropriate amount of T4 for most patients with thyroid cancer reduces the serum TSH concentration to just below the lower limit of normal or the low normal range (e.g. 0.3 or 0.4mIU/L) if careful follow-up examinations show the patient is free of tumor. Some prefer greater suppression, lowering TSH levels to between 0.05 and 0.1mIU/L in low risk patients and to less than 0.01 mIU/L in high risk patients [171]. However, there is no published evidence that maintaining serum TSH levels lower than 0.01mIU/L has benefits and it does have some risks.

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