Psychoimmunoendocrine Aspects of Panic Disorder

Abstract

Immunological, neuroendocrine and psychological parameters were examined in 14 psychophysically healthy subjects and in 17 panic disorder patients before and after a 30-day course of alprazolam therapy. T lymphocyte proliferation in response to the mitogen phytohemoagglutinin, lymphocyte beta-endorphin (β-EP) concentrations, plasma ACTH, cortisol and β-EP levels were examined in basal conditions and after corticotropin-releasing hormone (CRH) stimulation. Cortisol inhibition by dexamethasone (DST) and basal growth hormone (GH) and prolactin levels were also examined. Depression, state or trait anxiety, anticipatory anxiety, agoraphobia, simple and social phobias, severity and frequency of panic attacks were monitored by rating scales. The immune study did not reveal any significant difference between patients and controls, or any effect of alprazolam therapy. The hormonal data for the two groups were similar, except for higher than normal basal ACTH and GH plasma levels, lower than normal ratios between the ACTH and cortisol responses to CRH, and blunted DST in some patients. All the impairments improved after alprazolam therapy, in parallel with decreases in anxiety and in severity and frequency of panic attacks.

Psychoimmunoendocrine Investigation in Anorexia nervosa

“…It must be men tioned that a lack of correlation between immune func tion and a hyperactive HPA system has already been reported in MD and in panic disorder [72][73][74], and it is possible that a similar phenomenon could also occur in anorectics. This is reinforced by the observation that in our subjects CRH administration and the ensuing ACTH and cortisol hypersecretion failed to modify the T lym phocyte response to PHA, a phenomenon that we have previously observed in panic patients [74], We tested this response 30 min after CRH administration, and it is pos sible that a later observation would have disclosed some differences. However, in experimental animals it has been observed that in the 60 min following intracerebroventricular administration of CRH, T lymphocyte prolifera tion and natural killer cytotoxicity are already blunted [66].…”

HPA axis activity in patients with panic disorder: review and synthesis of four studies

“…No or inconsistent cortisol response with laboratoryinduced panic attacks Charney et al, 1985 (caffeine); Liebowitz et al, 1985;Levin et al, 1987;Seier et al, 1997;Peskind et al, 1998 (lactate); Sinha et al, 1999;van Duinen et al, 2004 Curtis et al, 1982;Lieberman et al, 1983;Sheehan et al, 1983;Goldstein et al, 1987 Elevated nonsuppression rate with repeat testing, linked to severity of depression Coryell et al, 1989 Basal studies Normal UFC (in uncomplicated panic) Uhde et al, 1988;Kathol et al, 1988 Elevated ACTH increased afternoon or nocturnal cortisol Brambilla et al, 1992Goldstein et al, 1987Bandelow et al, 1997;Bandelow et al, 2000b''Natural'' panic Increased cortisol Bandelow et al, 2000aInconsistent response Cameron et al, 1987Woods et al, 1987 …”

Psychoimmune Investigation in Obsessive-Compulsive Disorder: Assays of Plasma Transferrin, IL-2 and IL-6 Receptor, and IL-1β and IL-6 Concentrations

“…A neuroimmune investigation of OCD is, therefore, another way to determine how much overlap there is between these disorders. In addition, other anxiety disor ders, such as panic disorder, may be accompanied by alterations in CMI [ 18,19], Recently, complex relationships between in vivo and ex vivo immune and HPA axis function have been found in depression as well as in schizophrenia [20,21]. For example, in depression, positive relationships between increased IL-1(3 or IL-6 production and postdexamethasone HPA axis activity were found [5], whereas in schizo phrenia, a negative relationship between plasma IL-6 and baseline cortisol levels were found [Maes et al, unpubl.…”