Endocrine Abstracts

Subclinical thyrotoxicosis, defined as a low serum thyrotrophin (TSH) and normal serum free T4 and T3 concentrations, has been found in up to 3.2% of adults in cross-sectional surveys of thyroid function, of whom 75% have serum TSH concentrations of 0.1 to 0.4 mU/L. If the diagnosis is limited to only those with a serum TSH lower than 0.1 mU/L, the prevalence decreases to 0.7%, with 20% being treated with thyroxine.

Thyrotoxicosis is considered overt only when the T4 or T3 concentrations are high. Few persons with a serum TSH between 0.1 to 0.45 mU/l progress to overt hyperthyroidism, whereas 1–2% per year of those with serum TSH lower than 0.1 mU/L develop overt hyperthyroidism. Serum TSH normalises in many individuals with subclinical thyrotoxicosis over time due to resolution of Graves’ disease, silent thyroiditis or a non-thyroidal illness.

The symptoms and other manifestations of subtle thyroid hormone excess are very non-specific and there is little evidence of either disability or benefit of therapy. Any potential benefits of therapy for subclinical thyrotoxicosis must be weighed against the significant morbidity associated with the treatment of hyperthyroidism with radioiodine, surgery or anti-thyroid drugs. Epidemiological studies have suggested an association with atrial fibrillation in older persons but there is no evidence that intervention to normalise serum TSH reduces the risk of arterial embolism or cardiovascular mortality. There is no evidence that treatment of subclinical thyrotoxicosis improves pregnancy outcome, and treatment could potentially adversely affect fetal outcome. Prevention of progression to overt thyroid dysfunction is not indicated in view of the high rates of spontaneous normalisation of serum TSH values. Making a diagnosis and adopting a conservative approach with regular surveillance of thyroid function and intervention only when overtly thyrotoxic is the correct strategy.