Administration of TSHSuppressive Doses of LThyroxine

After thyroidectomy and 131I ablation there is a need for life-long T4 replacement therapy. In patients with nonmedullary thyroid cancer the prescribed daily T4 dose is usually higher than the replacement dose in order to reach suppression and not just normalization of serum TSH values. For a number of studies have shown that TSH suppression is associated with a longer disease-free interval [4].A French study reports a longer relapse-free survival in patients with constantly suppressed TSH (all values <0.05 mU/ L) than in patients with nonsuppressed TSH (all values >1 mU/L); the degree of TSH suppression predicted relapse-free survival independently of other factors [32]. In a US cooperative study the degree of TSH suppression was an independent predictor of disease progression in high risk patients with papillary carcinoma, but not in low risk patients or when radioiodine treatment was included in the model [3]. A Finnish study reports that a nonsuppressed TSH is an independent predictor for recurrence in multivari-ate analysis [33]. A study from Taiwan suggests stratification: TSH should be suppressed in patients with active disease, but might be kept within the normal range in patients who are clinically disease free [34].

The question thus arises which degree of TSH suppression is most appropriate (<0.4, <0.1 or

Table 10.4 Role of the endocrinologist in the postsurgical postablative phase

1. Administration of TSH-suppressive doses of L-thyroxine

2. Long-term follow-up with search for residual thyroid cancer at regular intervals

3. Management plan for recurrent or metastatic thyroid cancer

4. Attention to quality of life

<0.01mU/L?) and for how long should TSH suppression be maintained. This should be discussed in the multidisciplinary team. The endocrinolo-gist seems best suited to monitor the required TSH level by adjusting the daily T4 dose. A suppressed TSH effectively means induction of subclinical hyperthyroidism, a condition with potential adverse side effects notably on the heart and the bones. It also befits the endocrinologist to evaluate these risks in the individual patient and to take preventive measures if indicated.

There is no doubt that subclinical hyperthy-roidism increases the risk of atrial fibrillation [35]. Careful investigations, however, have also shown subtle cardiac dysfunction in these patients as evident from an increased left ventricular mass, impaired ventricular relaxation, and reduced exercise performance [36]. The long-term consequences of this cardiac dysfunction are unknown, but b-blockade improves cardiac function [36,37]. If there is a clear indication for marked TSH suppression, it may be prudent to prescribe b-blockers. This may be especially worthwhile if the patient does not tolerate the high doses of thyroxine.

Subclinical hyperthyroidism is also associated with high bone turnover [38], and may induce bone loss according to meta-analyses, especially in postmenopausal women [39,40]. It has not been demonstrated that this results in a higher fracture rate [41], but again it seems prudent that the endocrinologist monitors the risk in individual patients (by taking a history with respect to the well-known risk factors for osteoporosis, and performing bone densimetry in selected cases) and takes appropriate action in high risk patients (ensuring sufficient calcium intake, and considering supplementation with vitamin D).

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