Serum thyrotropin concentrations and bioactivity during sleep deprivation in depression

Citation
Dn. Orth et al., Serum thyrotropin concentrations and bioactivity during sleep deprivation in depression, ARCH G PSYC, 58(1), 2001, pp. 77-83
Citations number
69
Categorie Soggetti
Psychiatry,"Clinical Psycology & Psychiatry","Neurosciences & Behavoir
Journal title
ARCHIVES OF GENERAL PSYCHIATRY
ISSN journal
0003990X → ACNP
Volume
58
Issue
1
Year of publication
2001
Pages
77 - 83
Database
ISI
SICI code
0003-990X(200101)58:1<77:STCABD>2.0.ZU;2-K
Abstract
Background: One night of sleep deprivation induces a brief remission in abo ut half of depressed patients. Subclinical hypothyroidism may be associated with depression, and changes in hypothalamic-pituitary-thyroid function ma y affect the mood response to sleep deprivation. We wished to define precis ely the status of the hypothalamic-pituitary-thyroid axis of depressed pati ents during sleep deprivation and the possible relationship of hypothalamic -pituitary-thyroid function to the mood response. Methods: We studied 18 patients with major depressive disorder and 10 norma l volunteers. We assessed mood before and after sleep. We measured serum th yrotropin every 15 minutes during the night of sleep deprivation, thyrotrop in bioactivity, the thyrotropin response to protirelin the next afternoon, and other indexes of hypothalamic-pituitary-thyroid function. To determine if the changes were limited to the hypothalamic-pituitary-thyroid axis, we measured serum cortisol, which also has a circadian secretory pattern. Results: Nocturnal serum thyrotropin concentrations were consistently highe r in responders, entirely because of elevated levels in the women reponders . Responders had exaggerated responses to protirelin the next afternoon. Th e bioactivity of thyrotropin in nonresponders was significantly greater tha n in responders (F-1,F-8.99=7.52; P=.02). Other thyroid indexes and serum c ortisol concentrations were similar among groups. Conclusions: Depressed patients have mild compensated thyroid resistance to thyrotropin action, not subclinical autoimmune primary hypothyroidism. Sle ep deprivation responders compensate by secreting more thyrotropin with nor mal bioactivity; nonresponders compensate by secreting thyrotropin with inc reased bioactivity.