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Twenty‐four‐hour serum levels of T 4 and T 3 in relation to decreased TSH serum levels and decreased TSH response to TRH in affective disorders
Author(s) -
Undén F.,
Ljunggren JG.,
Kjellman B. F.,
BeckFriis J.,
Wetterberg L.
Publication year - 1986
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1111/j.1600-0447.1986.tb02696.x
Subject(s) - medicine , endocrinology , hormone , trh stimulation test , triiodothyronine , thyroid stimulating hormone , hypothalamic–pituitary–thyroid axis , melatonin , major depressive disorder , dexamethasone , thyrotropin releasing hormone , amygdala
The serum levels of thyroxine and triiodothyronine (T 4 and T 3 ) were investigated at 10 different time points during a 24 h period in 31 inpatients meeting the RDC criteria for acute major depressive disorder. Twenty‐three of these patients were also reinvestigated in a state of partial or complete remission. The results show that there was no significant difference in T 4 or T 3 levels during the 24 h period between depressed patients and 32 healthy controls despite significantly decreased TSH levels and TSH response to TRH administration (Δ TSH) in the patient group. No indications were obtained that the patients’ clinical presentation or depressive symptomatology as revealed by their CPRS scores, psychotropic medication, melatonin levels, or the outcome of the dexamethasone test, significantly influenced the T 4 or T 3 levels. The depressed patients who were studied longitudinally showed increased T 4 levels in the acute phase compared to remission, wheras the T 3 levels did not change. However, the levels of thyroid hormones were within the normal range in the acute phase as well as in remission. Furthermore, the changes in thyroid hormones between the state of relapse and remission were not significantly correlated to the corresponding increase in TSH levels and Δ TSH between the two assessments. The present results are consistent with the hypothesis that the mechanism behind the impaired TSH response to TRH in acute major depressive disorder is a downregulation of the pituitary TRH receptors.