![]() ![]() All but one (male subject with pubic hair development no greater than Tanner stage II) were considered to be in prepuberty development, and all boys' present plasma testosterone was less than 20 ng/mL. 1) Control subjects consisted of four healthy subjects(one girl and three boys) with constitutional delay (24)(24-h GH greater than 3 μg/L), without endocrinologic abnormalities. Twelve children were investigated and divided in three groups according to the 24-h serum GH, GH stimulation tests, and growth velocity. The purpose of the current study was to characterize pulsatile and circadian TSH and PRL release, examine the nocturnal secretion pattern of TSH and PRL in GHD, and evaluate the relationships among thyroid hormone, GH, PRL, and TSH secretion in children with GH deficiency. (23) assessed the nocturnal TSH surge in GHD children during the afternoon and night periods, but to our knowledge the analysis of a circadian and pulsatile secretion of serum TSH during the 24-h period in GHD has not been previously reported. In experimental animals hypothalamic deafferentation abolishes the circadian TSH rhythm (21), explaining the absence of the nocturnal surge of TSH (22) in hypothalamic (central) hypothyroidism. The increased basal TSH levels and exaggerated TSH response to TRH could result from decreased inhibition of TSH release due to a reduction in somatostatin and/or dopamine tone associated with growth hormone deficiency (19, 20). Due to these abnormal responses, such patients have been diagnosed as having pituitary hypothyroidism (hyporesponsiveness) or hypothalamic hypothyroidism (delayed, prolonged, and/or exaggerated TSH response to TRH). Abnormal basal serum TSH concentrations and altered response of TSH to TRH in patients suffering from GHD have been reported (16– 19). Although neither the neuroendocrine mechanisms governing the pulsatile release of TSH nor its circadian rhythm in man is established, considerable evidence indicates that the dopaminergic system, timing of sleep, serum cortisol, and somatostatin tone inhibit TSH secretion (8– 15). It is now well established that TSH release is pulsatile in nature and has a circadian periodicity, characterized by a nocturnal surge that begins in the late afternoon and reaches a peak around midnight, remains relatively stable for several hours, and declines thereafter (1– 7). These data suggest that GHD and NSD are associated with an increase in pulsatile TSH secretion due to an increase in pulse amplitude and interpulse valley mean. Cosinor analysis of the 24-h TSH and PRL data revealed clear circadian rhythmicity in all groups of subjects. This increase was accounted for by increases in PRL peak amplitude, area in the control group, and peak area, amplitude, and interpulse valley mean in the GHD and NSD groups. The nighttime mean PRL concentrations in the control, GHD, and NSD subjects were higher than those found during the day. Although there were no day versus night differences in TSH pulse frequency in either group, peak amplitude, area, and interpulse valley means were increased during the night in the control group, and peak area, duration, and amplitude mean in the NSD group. When the 24 h data sets were divided into day (0800-2000 h) and night (2000-0800 h), the mean nighttime TSH concentration was higher than the daytime concentration in the control, GHD, and NSD groups. No differences in mean PRL concentration or characteristics of PRL pulses were found between the control and GHD and NSD subjects. This augmentation reflects TSH pulses of large amplitude and area, and a higher interpulse valley mean rather than a difference in peak number or peak duration. With regard to TSH, the mean serum concentration in the GHD and NSD group were higher than that of the control subjects. ![]() The mean 24-h concentration of GH in the control subjects was significantly higher than that obtained in the GHD and NSD groups. Circadian rhythmicity of TSH and PRL was assessed using cosinor analysis. Pulse analysis of TSH and PRL was undertaken using the Cluster pulse detection algorithm. Blood samples were obtained at 20-min intervals for 24 h. ![]() We have measured mean concentrations and have appraised the pulsatile nature of thyrotropin (TSH) and prolactin (PRL) release in children with classical GH deficiency (GHD n = 4) and neurosecretory GH dysfunction (NSD n = 4) and have compared the results with those obtained in children with constitutional delay (control n = 4). ![]()
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