[Different effects of tricyclic (clomipramine and amitriptyline) and tetracyclic (maprotiline) antidepressors on the release of thyroid stimulating hormone, prolactin and growth hormone to thyrostimulating releasing hormone in patients with psychoaffective disorders (author's transl)]

Abstract

The hormonal alterations induced by tricyclic and tetracyclic antidepressors (AD) were studied in patients with psychoaffective disorders (PAD) to ascertain the role of certain biogenic amines in the regulation of thyroid stimulating hormone (TSH), prolactin (PRL) and growth hormone (GH). The responsiveness of plasma TSH, PRL and GH to synthetic thyrostimulating release hormone (TRH; 250 microgram i.v.) was determined in 57 patients distributed in 5 groups according to the treatment: 10 non treated patients, 16 tricyclic (clomipramine and amitriptyline) treated patients, 6 patients treated by clomipramine in association with lithium, 6 tetracyclic (maprotiline) treated patients and 19 patients treated by major neuroleptics. Results of untreated patients were compared to those observed in 10 age and sex matched normal subjects. Basal plasma levels of TSH were normal in all the patients. The TSH response to TRH (delta TSH) was blunted in non treated patients. delta TSH was normal in the patients treated by maprotiline or neuroleptics and increased in the group treated by tricyclic AD in association with lithium. Basal plasma levels of PRL and PRL response to TRH (delta PRL) were decreased in the women treated by tricyclic AD, but remained normal under maprotiline. They were markedly increased in the neuroleptic group. No inadequate response of GH to TRH was noted in our series of patients. The different hormonal effects induced by AD--dissociation between delta TSH and delta PRL under tricyclics and normal or increased delta TSH under maprotiline--may be logically explained by the various ways of action of these AD on the brain monoamines. delta TSH decrease and tendency to an increased delta PRL observed with clomipramine argue for a serotoninergic regulation of these two hormones, whereas the normalisation of delta TSH under maprotiline argues for a noradrenergic regulation of this hormone. Effectively, tricyclic AD inhibits mainly the serotonin recaptation and tetracyclic inhibits rather norepinephrine recaptation. The persistent delta TSH increase observed in the group treated by the association clomipramine-lithium demonstrates that the tricyclics do not interact with the hypophyso-thyroid positive feedback.