Whereas overt thyrotoxicosis clearly requires therapy, the question of whether early, subclinical hyperthyroidism should be treated remains controversial (76,77). To date, large, long-term randomized trials examining this question have not been carried out. Clinical manifestations of subclinical hyperthyroidism, if present, can be managed without antithyroid therapies: osteoporosis can be treated with estrogen replacement and bisphosphonates and tachycardia with P-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 MMI or PTU. Definitive therapy with 131I may be carried out, especially in patients with goiter, although large doses may be required in the setting of a normal 24-h RAIU. The thyroid 131I uptake may be enhanced by the prior administration of recombinant human TSH (78,79). Early therapy may be especially beneficial for patients with multinodular goiter, given an expected progression to overt hyperthyroidism (80). Treatment with antithyroid drugs has been shown to have a beneficial effect on osteoporosis in two small studies (81,82). Additionally, treatment of subclinical hyperthyroidism does seem to decrease the risk for atrial fibrillation (77). Some authors (16,35) advocate aggressive treatment for subclinical hyperthyroidism, whereas others suggest a policy of watchful waiting, deferring treatment until the hyperthyroidism becomes overt (76,83). Samuels (2) 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. Regardless of whether one opts to treat patients with subclinical hyperthyroidism, the diagnosis mandates close follow-up to prevent the deleterious effects of overt thyrotoxicosis.
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