These preliminary data reveal that our patients’ basal hormonal levels and responses to usual stimuli are partly similar to those of subjects with MAD and partly to those of patients with panic disorder. In fact, basal levels of GH and PRL were as high as in panic attacks, levels of b-EP and b-LPH were high and TSH, FSH, and LH levels were tendentially normal as has been ascertained in MAD. Administration of RH induced generally normal physiological responses, with the exception of the TSH response to TRH, which was blunted, as in both MAD and panic attacks. The unusual AP responses to RH administration were present in our patients and had the characteristics described for MAD, however, they occurred with a lower frequency. Since we examined only a small number of patients, it is possible that the investigation of a larger group cf subjects would reveal a higher frequency of these phenomena.
The analysis of the correlations between abnormal responses to RH admin­istration and clinical symptomatology did not show any correlation with in­somnia. Consequently, we can exclude a link between neuroendocrine alterations and impairments of the circadian secretion of the hormones owing to variations of sleep architecture, as suggested by Caroffet al. (11). Similarly, they cannot be the expression of an aspecific stress reaction, because they do not correlate with the degree of anxiety. The lack of an association between degree of depression and the unusual AP hormone responses to RH administration is not unexpected. In fact, we observed the same phenomena in depressed patients during phases of remission of the disease and in first-degree relatives, and with a total absence of depressive symp­tomatology (7). Our present and previous data suggest that the abnormal AP responses to RH administration are a trait marker of a spectrum of depressive disorders. They are probably the expression of neurotransmitter-neuromodulator alterations that are the common basis of various subtypes of affective disorders, possibly rep­resenting a continuum along the course of the mental disease, independent of its clinical manifestations and, in particular, of anxiety and sleep disorders.

This entry was posted on Monday, June 15th, 2009 at 4:57 pm and is filed under Neuroendocrine Aspects of Dysthymic Disorders. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.