Hypothalamic–pituitary–adrenal activity among Armenian adolescents with PTSD symptoms
Armen GoenjianRobert S. PynoosAlan M. SteinbergDavid B. EndresKhachik AbrahamMitchell E. GeffnerLynn A. Fairbanks
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This study evaluated basal levels and responsiveness to exercise of plasma adrenocorticotropic hormone (ACTH), and serum thyroid stimulating hormone (TSH), growth hormone (GH) and cortisol among adolescents from two differentially exposed groups 6 1/2 years after the 1988 earthquake in Armenia. Severity of total PTSD and Category C and D symptoms were negatively correlated with baseline cortisol. Preexercise ACTH was significantly lower, and preexercise TSH higher, among adolescents with more exposure. Depressive symptoms were negatively correlated with baseline cortisol and positively with TSH. Mean GH, TSH, and cortisol levels in both groups fell within normal limits. The pre- to postexercise increase in GH, TSH, and cortisol suggests that exercise challenge may be useful in the field investigation of neurohormonal activity among traumatized individuals.Keywords:
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Certain studies suggest that percutaneous absorption of topical steroids may cause suppression of hypothalamic-pituitary-adrenal axis (HPAA) in atopic dermatitis (AD) patients. This study aimed to investigate the basal serum cortisol, adrenocorticotropic hormone (ACTH), and IgE levels in patients with AD and their correlation with the disease severity.Levels of basal serum cortisol, ACTH, and IgE were assessed by ELISA in 31 patients with AD and 31 controls. Clinical severity of AD was evaluated by the scoring of atopic dermatitis (SCORAD) index.No statistical difference was observed between the two groups for basal serum cortisol and ACTH levels. The serum IgE level was significantly higher in the AD group. The SCORAD index was correlated with serum IgE level.Basal serum cortisol and ACTH levels are normal in AD patients. Serum IgE level is significantly higher in AD patients and is correlated with the disease severity.
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Corticosterone (CORT) and other glucocorticoids cause peripheral insulin resistance and compensatory increases in β-cell mass. A prolonged high-fat diet (HFD) induces insulin resistance and impairs β-cell insulin secretion. This study examined islet adaptive capacity in rats treated with CORT and a HFD. Male Sprague-Dawley rats (age ∼6 weeks) were given exogenous CORT (400 mg/rat) or wax (placebo) implants and placed on a HFD (60% calories from fat) or standard diet (SD) for 2 weeks (N = 10 per group). CORT-HFD rats developed fasting hyperglycemia (>11 mM) and hyperinsulinemia (∼5-fold higher than controls) and were 15-fold more insulin resistant than placebo-SD rats by the end of ∼2 weeks (Homeostatic Model Assessment for Insulin Resistance [HOMA-IR] levels, 15.08 ± 1.64 vs 1.0 ± 0.12, P < .05). Pancreatic β-cell function, as measured by HOMA-β, was lower in the CORT-HFD group as compared to the CORT-SD group (1.64 ± 0.22 vs 3.72 ± 0.64, P < .001) as well as acute insulin response (0.25 ± 0.22 vs 1.68 ± 0.41, P < .05). Moreover, β- and α-cell mass were 2.6- and 1.6-fold higher, respectively, in CORT-HFD animals compared to controls (both P < .05). CORT treatment increased p-protein kinase C-α content in SD but not HFD-fed rats, suggesting that a HFD may lower insulin secretory capacity via impaired glucose sensing. Isolated islets from CORT-HFD animals secreted more insulin in both low and high glucose conditions; however, total insulin content was relatively depleted after glucose challenge. Thus, CORT and HFD, synergistically not independently, act to promote severe insulin resistance, which overwhelms islet adaptive capacity, thereby resulting in overt hyperglycemia.
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Background: Atopic dermatitis (AD) is an inflammatory skin disease with eczematous pruritic lesions.Topical corticosteroids are the most widely used and the mainstay of treatment for AD.There are some studies that percutaneous systemic absorption of topical steroids may occur and lead to suppression of hypothalamic-pituitaryadrenal axis (HPAA).However, almost in all of these studies, "basic" HPAA function (before application of topical steroids) was not evaluated. Aim:The aim of this study was to investigate basal serum cortisol, adrenocorticotropic hormone (ACTH), and IgE levels in patients with AD and their correlation with disease severity.Methods: Levels of basal serum cortisol, ACTH, and IgE were assessed by ELISA in 31 patients with AD and 31 control subjects.Clinical severity of AD was evaluated by the SCORAD (SCORing Atopic Dermatitis) index.Results: Data analysis showed no statistical difference for basal serum cortisol and ACTH levels between two groups.The serum IgE level was significantly higher in AD group (P=0.02).The SCORAD index was correlated with serum IgE level, but not with the basal serum cortisol level and ACTH level. Conclusions:Basal serum cortisol and ACTH levels are normal in AD patients.Serum IgE level is significantly higher in AD patients and correlated with disease severity.
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