| The question of whether subclinical hyperthyroidism should be treated remains controversial 15,56 . To date, large, long-term randomized trials examining this question have not been carried out. Clinical manifestations of subclinical hyperthyroidism can be managed without antithyroid therapies: osteoporosis can be treated with estrogen replacement and bisphosphonates, and tachycardia with beta-blockers. However, once a persistently suppressed TSH level has been documented, the goal of specific therapy is to normalize the serum TSH using small doses of thiamazole/methimazole (MMI), carbimazole (CBI), or propylthiouracil (PTU). Definitive therapy with 131 I may be carried out, especially in patients with goiter, although large doses may be required in the setting of normal 24-hour radioactive iodine uptakes. The thyroid 131 I uptake may be enhanced by the prior administration of recombinant human TSH 57,58 . If the serum TSH is low during therapy for hypothyroidism (in non-thyroid cancer patients), the dose of L-T 4 should be decreased every 3–4 months until the serum TSH normalizes. Treatment with anti-thyroid drugs has been shown to have a beneficial effect on osteoporosis in two small studies 59,60 . Additionally, treatment of subclinical hyperthyroidism does seem to decrease the risk for atrial fibrillation 56 . Some authors 61,6 advocate aggressive treatment for subclinical hyperthyroidism, while others suggest a policy of watchful waiting, deferring treatment until the hyperthyroidism becomes overt 15,62 . Samuels suggests that good candidates for treatment include elderly patients with unexplained weight loss, women with osteopenia, and those with additional known risk factors for atrial fibrillation 9 . |
