The problem of exogenous subclinical hyperthyroidism.

Over the past two decades a plethora of publications and clinical practice data have established that subclinical thyroid dysfunction is a common condition occurring much more frequently than the overt expression of thyroid disease. Subclinical hypothyroidism is considered to be the most common of these entities. However, far more common and relatively less studied is exogenous sublinical hyperthyroidism (SubHyper) caused by L-thyroxine (T4) administration to thyroidectomized or hypothyroid patients or patients with simple or nodular goiter. Despite iodination, simple goiter is still prevalent and single or multiple nodules are now detected by ultrasound screening in 25-30% of adults, who are accordingly frequently given long-term T4 treatment. Approximately half of European Endocrinologists administer T4 permanently to patients with the above entities with the aim of suppressing TSH levels. Furthermore, in the USA the Colorado Study demonstrated that 40% of patients receiving thyroid hormones had abnormal [corrected] TSH levels (i.e. lower than 0.3 or higher than 5.1 mU/L); of these, 0.9% had hyperthyroidism and 20.7% subclinical hyperthyroidism [corrected] These facts render exogenous SubHyper an everyday problem for the endocrinologist. Exogenous SubHyper differs in many aspects from endogenous, its principal difference being that it is an iatrogenic thyroid disorder induced by the endocrinologist. The management of exogenous SubHyper relies on appropriate adjustment of T4 dosage taking into consideration a) individual requirements in T4, sex, age and the presence of cardiovascular disease or other co-morbidity, b) the recognition that small changes in serum FT4 have a logarithmic effect on TSH, c) the variability of FT4-TSH interactions between individuals, d) the instability of T4 preparations and its bioavailability, and e) the values of serum FT4 and FT3 that accompany a suppressed TSH. This last parameter is of importance since it is the free thyroid hormones values in the serum that generate and reflect the thyroid metabolic state of the organism rather than the degree of TSH suppression.