*Paolo Pini Psychiatric Hospital, 20161 Milan, Italy; ** Department of Psychiatry, University of Milan Medical School, 20161 Milan, Italy; t Institute of Obstetrics and Gynecology, University of Modena, 41100 Modena, Italy
In previous studies we observed that patients with Primary Affective Disorders (PAD), according to RDC (26), or Major Affective Disorders (MAD), according to DSM-III (1), responded to thyrotropin-releasing hormone (TRH) adminis­tration with abnormal rises of growth hormone (GH), follicle-stimulating hor­mone (FSH), luteinizing hormone (LH), and /3-endorphin ((3-EP) and jS-lipo-thropin (/3-LPH) plasma levels, and to luteinizing hormone-releasing hormone (LHRH) with rises of GH, prolactin (PRL), /3-EP, and 0-LPH (5-8). The ab­normal GH, FSH, and LH responses to TRH administration occurred not only in depression, but also in anorexia nervosa, schizophrenia and drug addiction (3,4,10,15,16,19,20,22-24,27,29-31). This would suggest that the phenomenon is not specifically related to the basic brain impairments of depression, but to still undefined alterations of neurotransmitter-neuromodulator secretory patterns in the central nervous system that may occur in various mental disorders. It has been suggested that abnormal GH response to stimulation with releasing hormones (RH) may be owing to impairments of the rest/activity cycle and of sleep architecture, which frequently occur in mental disorders (21) since they are also present in normal humans after prolonged periods of wakefulness (11,28). Severe anxiety may be another factor that can elicit hormonal alterations and may be present in several mental disorders. Patients suffering from generalized anxiety, panic disorders, or phobias have been observed to have multiple neu­roendocrine abnormalities. Higher than normal basal plasma levels of GH, PRL, adrenocorticotropic hormone (ACTH), and Cortisol, blunted thyroid-stimulating hormone (TSH) and PRL responses to TRH stimulation, blunted ACTH-cortisol responses to corticotropin-releasing hormone (CRH) stimulation, and positive Dexametha-sone Suppression Test (DST) have been reported to occur in the aforementioned psychopathologies (9,13,14,17,18,25). Lactate infusion, which induces the appearance of panic attacks exclusively in patients with panic disorder, stimulates in these subjects GH and PRL secre­tion, whereas Cortisol, /?-EP, LH, and vasopressin levels do not change or are increased slightly. GH and PRL rises never occur in control subjects under the same experimental conditions (2,12,18). We have investigated the influence of severe anxiety and sleep disorders on the responses of anterior pituitary (AP) hormones to RH stimulation in a group of subjects with anxious depression, defined, according to DSM-III, as Dysthymic Disorder. The aim of this study was to see whether the neuroendocrine alterations ob­served in PAD were present also in this subgroup of depressive disorders and to determine if their presence could be attributed to anxiety and/or reduced sleep efficiency. (more…)

If the DSM-III diagnostic criteria (2) are applied to patients classified as neu­rotic-reactive depressives according to our research diagnostic criteria, it is obvious that there is no diagnostic category in DSM-III that is directly comparable to our subgroup of patients (Table 1). This finding must be kept in mind when our results are compared with results obtained by means of other diagnostic criteria. As many as 50% of our patients with neurotic-reactive depression fulfill the DSM-III criteria for major depression, a finding that has direct relevance when family studies are discussed.
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edited by G. Racagni and E. Smeraldi. Raven Press, New York © 1987.

Thus, in the family studies, twin studies, and adoption studies presented so far, there is no strong support for a specific genetic factor in neurotic-reactive depression. However, there are some results from studies concerning biological markers under genetic control, indicating that genetic factors may still be of some importance, at least in subgroups of patients with neurotic-reactive depres­sion. It should also be kept in mind that as long as there is no generally accepted subclassification of patients with nonpsychotic depressive disorders, a genetic contribution in one of the subgroups may well be recognized in family studies, twin studies, and adoption studies. One biological marker that has been of certain interest in relation to affective disorders is the main degrative enzyme in the monoamine turnover —monoamine oxidase (MAO). MAO exists in two forms, A and B. Form A is only present in the brain, whereas form В is present in the brain and in platelets. Because of the easier access to MAO in platelets and based on the assumption of a relationship between brain and platelet MAO activities, a series of studies have been performed on platelet MAO activity in patients with affective disorders. In general, the results have been disappointing, but there are some results indicating a genetic component in a subgroup of patients with neurotic-reactive depression.