Deranged Anterior Pituitary Responsiveness to Hypothalamic Hormones in Depressed Patients

Brambilla, Frăncesca; Smeraldi, Enrico; Sacchetti, Emilio; Negri, F.; Cocchi, Daniela; Müller, Eugenio E.

doi:10.1001/archpsyc.1978.01770340081009

Cited by 117 publications

(17 citation statements)

References 33 publications

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“…1977], More recently, by evaluating the anterior pituitary (AP) responsiveness to hypotha lamic regulatory hormones (RHs) in patients with PAD, we observed that not only GH was released abnormally after TRH but also FSH and LH. and PRL and GH were released after LH-RH administration [Brambilla et al, 1978], The present study was undertaken to sec if we could observe the same profound derangement of AP responsiveness to the ad ministration of RHs in AN. a disease which has been suggested to be related psychologi cally and biochemically to depression [Cant well et al, 1977: Halmi, 1978,…”

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confidence: 86%

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Anterior Pituitary Responsiveness to Hypothalamic Hormones in Anorexia Nervosa

Brambilla¹,

Nobile²,

Müller

1981

Neuropsychobiology

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7 women and 3 men with anorexia nervosa were tested with thyrotropin-releasing hormone (TRH) and luteinizing hormone-follicle stimulating hormone-releasing hormone (LH-RH) and the growth hormone (GH), prolactin (PRL), gonadotropin (FSH-LH) and thyrotropin (TSH) responsiveness of their anterior pituitaries (AP) to the two hypothalamic neurohormones were determined. Administration of TRH (500 µg i.v.) induced rises in plasma GH in 4 patients, while in 4 patients it induced rises in plasma FSH and/or LH. LH-RH (150 µg i.v.) induced rises in plasma GH in 3 patients, increased plasma PRL in 3 patients and plasma TSH in 1 patient. Collectively, in only 1 patient, who was in a phase of initial nutritional rehabilitation, was there conventional AP responsiveness to hypothalamic neurohormones. This demonstrates that there is a profound derangement of AP responsiveness to hypothalamic neurohormones in patients with anorexia nervosa, probably reflecting a primary alteration in brain neurotransmitter function.

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confidence: 86%

“…1976], severe liver disease [Panerai et al, 1977] and primary affective disorders (PAD) [Maeda et al. 1975: Brambilla et al, 1978. It has been hypothesized that in all these diseases, except acromegaly, the cause of the abnormal GH response to TRH may reside in an altered brain monoamine metab olism [Panerai et al.…”

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confidence: 99%

Anterior Pituitary Responsiveness to Hypothalamic Hormones in Anorexia Nervosa

Brambilla¹,

Nobile²,

Müller

1981

Neuropsychobiology

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“…This effect is usually absent in healthy adult subjects [14,15] and has been ascribed to alterations in neurobiochemical mechanism regulating GH secre tion [16], such as that which occurs in some diseases characterized by disorders of cere bral amine metabolism [17,18].…”

Section: Introductionmentioning

confidence: 99%

Stimulation of Growth Hormone Release by Thyrotropin-Releasing Hormone in Elderly Subjects

Barreca¹,

Franceschini²,

Messina³

et al. 1985

Horm Res

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The effect of thyrotropin-releasing hormone (TRH) on the release of growth hormone (GH) was investigated in 16 elderly male subjects aged 74-88 years. Intravenous injection of 200 µg TRH induced a clear-cut GH rise ( ≧ 10 ng/ml) in 7 of 16 subjects. TRH administration did not raise plasma GH in 10 adult subjects aged 36-58 years. The results suggest disorders in neurobiochemical mechanisms regulating hypothalamopituitary function in elderly men.

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“…Because of their high reliability, the sleep EEG (SEEG) and the TRH stimulation test (TRHST) contin ually have been proposed for differentiating depressed from other psychiatric patients [Kupfer et al, 1978;Brambilla et al, 1978;Prange and Loosen, 1984], Previous studies have shown that as many as 40-60% of major depressives have well-defined SEEG alterations such as shortened REM latencies, high REM densities, prolonged first REM periods, and decreased delta sleep [see Kupfer and Reynolds, 1983, for a review]. In one study, a short REM latency very accurately distinguished depressed from nondepressed subjects [Gillin et al, 1979].…”

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confidence: 99%

Biological Heterogeneity of Major Depressive Disorder: Indications by Sleep EEG and TRH Stimulation Test Findings

1987

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A group of 27 patients with definite (n = 20) or probable (n = 7) RDC major depressive disorder underwent 2 sleep EEGs and 1 TRH test while in a drug-free depressive phase. A short mean REM latency (< 60 min) identified 55.5% of major depressives while added use of blunted TSH responses (delta max. < 5 µU/ml) increased that percentage by 11 %. When patients were subdivided into RDC endogenous and nonendogenous, mean REM latency and global depression scores distinguished the 2 groups, while delta TSH did not. A short mean REM latency identified endogenous depression with 80% specificity and 76% sensitivity. The combination of REM latency and delta TSH reduced the specificity to 60%, and therefore cannot be recommended for differentiating endogenous from nonendogenous depression.

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Deranged Anterior Pituitary Responsiveness to Hypothalamic Hormones in Depressed Patients

Cited by 117 publications

References 33 publications

Anterior Pituitary Responsiveness to Hypothalamic Hormones in Anorexia Nervosa

Anterior Pituitary Responsiveness to Hypothalamic Hormones in Anorexia Nervosa

Stimulation of Growth Hormone Release by Thyrotropin-Releasing Hormone in Elderly Subjects

Biological Heterogeneity of Major Depressive Disorder: Indications by Sleep EEG and TRH Stimulation Test Findings

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