The circadian and pulsatile TSH secretion profiles were investigated in 5 females at the time of menstruation and 21 healthy males by sampling blood every 10 min for 24 h. Computer-assisted analysis, i.e. the Cluster and Desade programs, revealed means of 9.9 +/- 1.7 (Cluster) and 11.4 +/- 3.9 (Desade) pulses/24 h. More than 50% of the TSH pulses were detected between 2000-0400 h. Male and female subjects showed no significant difference in the basal mean and pulsatile secretion of TSH or in the TSH response to TRH (200 micrograms). Repetition of the TSH secretion analysis in 4 healthy subjects after 1, 2, and 6 months (2 subjects) revealed a significantly better cross-correlation within than between individuals (P less than 0.0001). We modulate the circadian TSH secretion pattern by acute sleep withdrawal or prolonged sleep after a night of sleep withdrawal in six healthy male volunteers. Sleep withdrawal augmented the nightly TSH secretion (mean serum TSH, 2.1 +/- 1.3 mU/L; mean TSH in sleep, 1.3 +/- 0.5 mU/L; P less than 0.05), whereas sleep after sleep withdrawal almost completely suppressed the circadian variation (mean TSH, 1.1 +/- 0.7 mU/L; P less than 0.01). This modulation is due to a significant decrease in pulse amplitude, but not to an alteration in the frequency or temporal distribution of TSH pulses.

Abstract. The potentially inhibitory action of endogenous or exogenous synthetic glucocorticoids on TSH secretion was investigated. Pulsatile and circadian TSH and cortisol rhythms were measured in healthy subjects (12 rhythms), but no correlation between the hormones could be detected. Acute stimulation of endogenous cortisol secretion by CRH tests (1 μg/kg of ovine CRH) at 20.00 h in 9 healthy volunteers did not significantly alter the nightly increase in TSH. Chronic elevation of endogenous cortisol serum levels in patients with Cushing's disease revealed a heterogeneous pattern. In 2 patients serum TSH and thyroid hormone levels showed a normal 24-h rhythm, whereas the other 2 patients had low TSH serum levels. Acute treatment of 9 healthy volunteers with 0.5, 1 or 2 mg dexamethasone po at 23.00 h resulted in a significant dose-dependent suppression of mean basal TSH levels 9 h later. Treatment with 30mg of prednisone for 1 week in 7 patients with Crohn's disease did not influence basal TSH. The TSH response to TRH was only temporarily suppressed on day 3, but not on day 7 of treatment. The results suggest that under physiological conditions glucocorticoids have no regulatory influence on pulsatile and circadian TSH secretion.