Henri Brauman

Thyrotrophin response to thyrotrophin-releasing hormone in unipolar and bipolar affective illness

The plasma levels of thyrotrophin (TSH) and the response of this hormone to 200 microgram of thyrotrophin-releasing hormone (TRH) were studied in 27 unipolar and 24 bipolar depressive patients before and after amitriptyline treatment as well as in 42 normal controls. There was no significant difference in basal TSH levels between any of the groups studied according to diagnosis, menopausal status and antidepressant treatment. Before treatment, the TSH response to TRH was significantly lower in the unipolar and bipolar depressive patients than in normal controls. The TSH response to TRH did not differ significantly between the unipolar and bipolar depressives. When menopausal status was taken into account, the TSH response to TRH was significantly blunted in the unipolar postmenopausal patients when compared to postmenopausal controls. In the bipolar group, the premenopausal depressive patients had a significantly lower TSH response to TRH than premenopausal controls. After amitriptyline treatment, the TSH response to TRH, which was impaired before treatment in the bipolar premenopausal patients, improved significantly. However, no significant difference in the TSH response to TRH could be demonstrated after treatment in the unipolar postmenopausal patients in whom the TSH response was blunted before treatment. Our findings suggest that the differential TSH response to TRH in unipolar and bipolar patients may constitute biological markers of endocrine dysfunction in clinical subgroups of affective disorders.

Violent suicidal behavior and the thyrotropin-releasing hormone-thyroid-stimulating hormone test: a clinical outcome study.

A relation between abnormal response of thyroid-stimulating hormone (TSH) to thyrotropin-releasing hormone (TRH) and a personal history of violent suicidal behavior was observed in a sample of 60 depressive women. Patients with a blunted TSH response to TRH were also at greater risk for subsequent suicide. There was no relationship between TSH response to TRH and age, severity of depression and polarity of the illness.

The growth hormone response to insulin induced hypoglycaemia in anorexia nervosa and control underweight or normal subjects.

Summary. Hypoglycaemic stimulation of growth hormone (GH) secretion has been measured in 12 anorexia nervosa patients, 11 adolescents approximately matched for weight and age, 14 underweight adults with no history of anorexia nervosa and 27 normal patients. The results showed a high proportion of blunted growth hormone responses among the anorexia nervosa patients as compared to normal subjects, underweight adolescents or adults. In the group of underweight adults, diminished growth hormone responses were most frequently seen in patients with depressive illness. The complex pathogenesis of the diminished growth hormone response in anorexia nervosa involves many factors; undernutrition itself, possible hypothalamic insufficiency related to the psychopathological background and other endocrine abnormalities like hypogonadism, relative hypercorticism and hypothyroidism. The interference of the nutritional, psychological and endocrine factors could not be dissociated in our investigation or from the review of the literature on this subject. It is suggested that hypothalamic insufficiency plays a prominent role in the growth hormone hyporesponsiveness in anorexia nervosa. Although diminished, the stimulated growth hormone response remains higher in anorexia nervosa than in true hypopituitarism. This phenomenon coupled to a preserved or even increased suprarenal function enables one to differentiate cachexia resulting from anorexia nervosa and hypopituitarism leading eventually to cachexia.