The thyrotropin response to thyrotropin-releasing hormone in endogenous depression

Kirkegaard, C.

doi:10.1016/0306-4530(81)90029-9

Cited by 131 publications

(47 citation statements)

References 136 publications

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“…The first hypothesis seems to contradict our previous results, in which we saw persistance of abnormal AP responses to RH in patients during a normothymic phase of the disease [Brambilla et al, 1979]. However, it may be that, as for the flat responses of TSH to TRH [Kirkegaard et al, 1975;Whybrow and Prange, 1981] and the non-suppression of cortisol by dexamethasone [Greden et al, in press;Carroll, 1980], the presence of a neuroendocrine abnormal ity during remission of the disease in some cases is simply predictive of poor prognosis and a tendency to relapse. In other words, the persistant AP alterations might cluster a sub group of patients with both a specific biolog ical substratum and a specific course of the disease.…”

Section: Discussioncontrasting

confidence: 55%

“…In 2 PAD patients who were improving psychologically the flat TSH response to TRH stimulation persisted: 1 of them was a frequently relapsing patient, and in fact she relapsed later. It has been sug gested that flat responses tend to persist in this type of patients and may even be predic tive for a poor prognosis [Kirkegaard et al, 1975;Whybrow and Prange, 1981].…”

Section: Discussionmentioning

confidence: 99%

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Abnormal Anterior Pituitary Responsiveness to Hypothalamic Hormones in Primary Affective Disorders

Brambilla

Scarone²,

Massironi³

et al. 1982

Neuropsychobiology

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Abnormal anterior pituitary responsiveness to acute administration of thyrotropin-releasing hormone was investigated in 8 patients, 6 women and 2 men, with primary affective disorders in a depressive phase and in 2 women with schizoaffective disorders. Thyrotropin-releasing hormone, 500 µg i.v., induced a rise of plasma growth hormone levels in 1 patient suffering from primary affective disorders and in the 2 schizoaffective subjects, a rise of follicle-stimulating hormone in 1 schizoaffective patient, of luteinizing hormone in the 2 schizoaffective patients, an excessive prolactin rise in 5 patients with primary affective disorders and in 1 schizoaffective subject and a flat response of thyroid-stimulating hormone in 4 patients with primary affective disorders and in 2 schizoaffective patients. Desimipramine was given at a dose of 50–100 mg/day for 3–5 weeks. The thyrotropin-releasing hormone stimulation test was repeated when the patients were improving or after 5 weeks of treatment without improvement. The hormonal impairments tended to disappear in those patients showing symptomatic improvement and were still present in those who did not improve.

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Section: Discussioncontrasting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Abnormal Anterior Pituitary Responsiveness to Hypothalamic Hormones in Primary Affective Disorders

Brambilla

Scarone²,

Massironi³

et al. 1982

Neuropsychobiology

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“…By contrast the TRH test is unaffected by psychiatric diseases other than endogenous depression and anorexia nervosa (2). Therefore healthy subjects were used as controls for the TRH test.…”

Section: Methodsmentioning

confidence: 99%

Dexamethasone suppression test and TRH test in endogenous depression

Aggernaes

Kirkegaard

Krog-Meyer

et al. 1983

Acta Psychiatr Scand

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Dexamethasone suppression test (DST) and thyrotropin releasing hormone (TRH) stimulation test were performed in 34 patients with endogenous depression. Compared with 33 psychiatric controls (limit of discrimination for serum cortisol of 275 nmol/l = 10 micrograms/100 ml) the specificity of the DST was 91% and the sensitivity was 65%. Compared with 24 healthy subjects the sensitivity of the TRH test was 24%, and the combined sensitivity for the DST and the TRH test was 76%. In contrast to the TRH test the DST showed a significant relationship (r = 0.54, P less than 0.01) to the Hamilton Rating Score. Repeating the tests after clinical recovery parallel changes of the two tests were found in 14 of 19 patients with abnormal DST in the depressed phase. In the remaining five patients the DST normalized, while the TRH test remained unchanged. It is suggested that both the apparent higher diagnostic sensitivity and the higher rate of normalization after clinical recovery of the DST is due to the dependency of the severity of depression.

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“…The free fraction of iodothyronine was estimated by ultrafiltration as ear¬ lier described (19). Serum TSH levels were estimated by RIA (20). CSF concentrations of T4 and rT3 were measured by modifying the serum analyses.…”

Section: Methodsmentioning

confidence: 99%

Free thyroxine and 3,3',5'-triiodothyronine levels in cerebrospinal fluid in patients with endogenous depression

Kirkegaard

Faber

1991

Acta Endocrinologica

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Total and free concentrations of T4 and rT3 in serum and cerebrospinal fluid were estimated by ultrafiltration in 12 patients with unipolar endogenous depression before and after electroconvulsive treatment. Recovery from depression resulted in a decrease in CSF concentrations of free T4 (median) (26.2 to 21.4 pmol/l, p<0.02) and free rT3 (14.1 to 12.3 pmol/l, p<0.05). Concentrations of free T4 in the cerebrospinal fluid were lower than those in serum (p<0.02), the ratio being 0.6. In contrast, levels of free rT3 in the cerebrospinal fluid were considerably higher than those found in serum (p<0.01), the ratio being 25. These ratios did not change following recovery from depression. In 9 patients with nonthyroidal somatic illness, concentrations of free T4 and rT3 in the cerebrospinal fluid were similar to those found in patients with endogenous depression, whereas 4 hypothyroid patients and one hyperthyroid patient had considerably lower and higher, respectively, concentrations of both free T4 and rT3. In conclusion, levels of free T4 and free rT3 in the cerebrospinal fluid are increased during depression compared with levels after recovery, probably reflecting an increased supply of T4 from serum and an increased production of rT3 from T4 in the brain. The data also suggest that the transport of iodothyronines between serum and the cerebrospinal fluid is restricted.It is generally agreed that thyroid hormones play an important role in the development and function of the brain (1,2). In cerebral tissue, the active thy¬ roid hormone T3 is partly derived from blood and partly produced locally by 5'-deiodination of T4 (3,4). In vitro studies have shown that the activity of the T3 producing enzyme (5'-deiodinase, type 2) is inhibited by iodothyronines, rT3 being the most potent inhibitor (5-7).A relationship between thyroid function and en¬ dogenous depression has been recognized for many years. Serum free T4 levels are enhanced in untreated endogenous depression and normalize after treatment, whereas serum free T3 levels remain unaltered. Following recovery from de¬ pression, serum free rT3 levels decrease slightly within the normal range (8,9). Recently we have demonstrated that the daily thyroidal production of T4 is enhanced in untreated endogenous depres¬ sion (10). In contrast, the T3 production was unal¬ tered, suggesting reduced conversion from T4. In addition, much older studies have shown that ad¬ dition of T3 to antidepressive treatment enhanced recovery from depression (reviewed in 9), suggest¬ ing an insufficient supply of T3 to the brain. There¬ fore, a better understanding of the role of thyroid hormone metabolism in the brain during endoge¬ nous depression would be most important.Cerebrospinal fluid (CSF) concentrations of iodothyronines probably reflect the metabolism in the brain, as well as their transport in and out of this compartment. The information on the free levels of iodothyronines in human CSF is sparse and conflicting (11)(12)(13)(14)(15)(16), and concerning endoge¬ nous depression only o...

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The thyrotropin response to thyrotropin-releasing hormone in endogenous depression

Cited by 131 publications

References 136 publications

Abnormal Anterior Pituitary Responsiveness to Hypothalamic Hormones in Primary Affective Disorders

Abnormal Anterior Pituitary Responsiveness to Hypothalamic Hormones in Primary Affective Disorders

Dexamethasone suppression test and TRH test in endogenous depression

Free thyroxine and 3,3',5'-triiodothyronine levels in cerebrospinal fluid in patients with endogenous depression

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