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Glucocorticoids, either endogenous in response to stress, or exogenous, are potent inhibitors
of TSH secretion (Brabant et al, 1989). Dopaminergic drugs, even at sub-pressor doses, cause
profound, rapidly reversible inhibition of TSH secretion. After cessation of a 5 ug/kg/min dopamine
infusion a rapid serum TSH increase from ‹ 0.5 mU/l to 3 mU/l was observed within 2-3 hours (Van
den Berghe et al, 1994). Dobutamine in high doses also suppresses TSH (Lee et al, 1999).
Cytokines directly affect TSH secretion. For example, infusion of interferon-a in normal volunteers resulted in a 60-70% decrease in serum TSH within 8-12 hours, prior to any significant change in serum thyroid hormone concentrations (Corssmit et al, 1995). The inverse effect, higher TSH in relation to serum free T4 is seen during longterm amiodarone therapy (fig 1), perhaps because this drug, or its active metabolite, desethylamiodarone, acts as an antagonist at thyroid hormone receptors (Wiersinga, 1996). Heavy amphetamine abuse may also result in higher than normal levels of serum TSH, according to a report of TSH-induced hyperthyroxinemia, an effect that was reproduced in monkeys (Morley et al, 1980). In general, agents that increase or decrease the basal level of serum TSH have a similar effect on the TSH response to TRH, whenever the two effects have been directly compared. Figure 1:
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