Publications

Journal Article Corticotropin-Releasing Hormone Is not the Sole Factor Mediating Exercise-Induced Adrenocorticotropin Release in Humans Get access BONNIE SMOAK, BONNIE SMOAK 1Department of Military Medicine, Uniformed Services University of the Health Sciences Bethesda, Maryland 20814; The Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health Bethesda, Maryland 20892 Search for other works by this author on: Oxford Academic Google Scholar PATRICIA DEUSTER, PATRICIA DEUSTER 1Department of Military Medicine, Uniformed Services University of the Health Sciences Bethesda, Maryland 20814; The Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health Bethesda, Maryland 20892 Search for other works by this author on: Oxford Academic Google Scholar DOUGLAS RABIN, DOUGLAS RABIN 1Department of Military Medicine, Uniformed Services University of the Health Sciences Bethesda, Maryland 20814; The Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health Bethesda, Maryland 20892 Search for other works by this author on: Oxford Academic Google Scholar GEORGE CHROUSOS GEORGE CHROUSOS 1Department of Military Medicine, Uniformed Services University of the Health Sciences Bethesda, Maryland 20814; The Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health Bethesda, Maryland 20892 Search for other works by this author on: Oxford Academic Google Scholar The Journal of Clinical Endocrinology & Metabolism, Volume 73, Issue 2, 1 August 1991, Pages 302–306, https://doi.org/10.1210/jcem-73-2-302 Published: 01 August 1991 Article history Received: 22 October 1990 Published: 01 August 1991

The hypercortisolism of melancholic depression is thought to reflect hypothalamic hypersecretion of CRH and may be related to the hyperarousal associated with this syndrome. Although chronic administration of imipramine to experimental animals significantly decreases CRH messenger RNA levels in the paraventricular nucleus, it is generally thought that resolution of hypercortisolism following recovery from depression is related to the improvement in mood and decrease in anxiety that accompanies recovery rather than an intrinsic effect of imipramine. The present study was designed to explore whether chronic imipramine administration to healthy, nondepressed volunteers is associated with effects on hypothalamic-pituitary-adrenal (HPA) axis function. We studied basal and provocative measures of HPA axis function in 14 healthy volunteers before and after 6 weeks of imipramine treatment at therapeutic doses. Imipramine was associated with decreased responses in peak ACTH and cortisol to ovine CRH and in peak ACTH to arginine vasopressin (P = 0.02, P = 0.003, and P = 0.02, respectively) without changes in indices of basal HPA axis function. These data are consistent with preclinical findings and support the hypothesis that imipramine has an intrinsic effect on central components of HPA axis function, potentially related to its therapeutic effects.

Congenital adrenal hyperplasia describes a group of inherited autosomal recessive disorders characterized by an enzymatic defect in cortisol biosynthesis, compensatory increases in corticotropin secretion, and adrenocortical hyperplasia. 21-Hydroxylase deficiency is responsible for more than 95% of cases and is one of the most common known autosomal recessive disorders. The classic or severe type presents in the newborn period or early childhood with virilization and adrenal insufficiency, with or without salt loss; the mild or nonclassic form presents in late childhood or early adulthood with mild hyperandrogenism and is an important cause of masculinization and infertility in women. This wide range of phenotypic expression is mostly explained by genetic variation, although genotype-phenotype discrepancies have been described. Reproductive, metabolic, and other comorbid conditions, including risk for tumors, are currently under investigation in both forms of the disease. A high proportion of patients with adrenal incidentalomas may be homozygous or heterozygous for 21-hydroxylase deficiency. Women with congenital adrenal hyperplasia often develop the polycystic ovary syndrome. Ectopic adrenal rest tissue is often found in the testes of men with congenital adrenal hyperplasia; characteristic clinical and radiologic findings help differentiate this tissue from other tumors. Levels of corticotropin-releasing hormone are elevated in patients with depression and anxiety and are expected to be elevated in patients with congenital adrenal hyperplasia; it is unknown whether patients with 21-hydroxylase deficiency have an increased incidence of these psychiatric disorders. Abnormalities in both the structure and function of the adrenal medulla have been shown in patients with classic congenital adrenal hyperplasia, and the degree of adrenomedullary impairment may be a biomarker of disease severity. The 21-hydroxylase-deficient mouse has provided a useful model with which to examine disease mechanisms and test new therapeutic interventions in classic disease, including gene therapy. Treatment of this condition is intended to reduce excessive corticotropin secretion and replace both glucocorticoids and mineralocorticoids. However, clinical management is often complicated by inadequately treated hyperandrogenism, iatrogenic hypercortisolism, or both. New treatment approaches currently under investigation include combination therapy to block androgen action and inhibit estrogen production, and bilateral adrenalectomy in the most severely affected patients. Other approaches, which are in a preclinical stage of investigation, include treatment with a corticotropin-releasing hormone antagonist and gene therapy.

To explore the associations of vitamin D status and obesity with insulin resistance (IR) in children.A sample of 2282 schoolchildren (9-13 years old) in Greece was examined. Sociodemographic, anthropometric (weight, height), biochemical (fasting plasma glucose, serum insulin and 25(OH)D), pubertal status and physical activity data were collected, using standard methods. The "Vitamin D Standardization Program" protocol was applied to standardize serum 25(OH)D values.The prevalence of vitamin D insufficiency (serum 25(OH)D < 50 nmol/L) was higher in obese children compared to their over- and normal-weight counterparts (60.5% vs 51.6% and 51%, P = .017). Furthermore, children with IR (both obese and non-obese) had higher prevalence of vitamin D insufficiency compared to non-obese, non-insulin resistant children (66% and 59.2% vs 49.8%, P < .05), possibly indicating that IR is associated with vitamin D insufficiency, independently of obesity. In line with the above, the results from logistic regression analyses controlled for several potential confounders, showed a 1.48 (95% C.I: 1.2-1.84) higher likelihood for vitamin D insufficiency for insulin resistant children compared to the non-insulin resistant ones, while no significant association was observed with obesity.The present study revealed a high prevalence of vitamin D insufficiency among schoolchildren in Greece, particularly among obese and insulin resistant ones. In addition, it highlighted that the significant association of vitamin D insufficiency with IR is possibly independent of obesity. Further clinical trials are needed to confirm this possible independent association but also explore the potential beneficial effect of vitamin D supplementation on IR and possibly on weight management too.

Abstract Premature ovarian failure (POF) defines the occurrence of ovarian failure prior to the age of 40. It occurs in one out of 100 women but is very rare before age 20 (1:10,000). Maturity-onset diabetes of the young (MODY), caused by mutations in the HNF1A gene, is also a rare disorder; all types of MODY account for 1–2% of adult diabetic cases. These two rare nosologic entities coexisted in an adolescent girl evaluated for delayed puberty. Although this combination could represent a chance association, an interrelation might exist. We examined HNF1A expression in human fetal and adult ovaries by immunohistochemistry using a polyclonal HNF1A antibody. HNF1A protein was expressed in both the fetal and adult human ovaries. Based on these findings, we hypothesize that HNF1A participates in ovarian organogenesis and/or function and that mutations in the HNF1A gene might represent another molecular defect causing POF, possibly in combination with other genetic factors. The study underlines the importance of rare clinical paradigms in leading the way to elucidation of the pathogenetic mechanisms of rare diseases.

Aims and method To identify correlates between burnout and job stress of care staff at Leros PIKPA Asylum. Forty-nine asylum employees were assessed by Maslach's Burnout Inventory, a sociodemographic questionnaire, the Perceived Stress Scale and the Job Content Questionnaire. Results Emotional exhaustion is related negatively to social support (P = 0.010, r = -0.362). Lack of job achievements is related positively to overall job responsibility (P = 0.040) and negatively to lack of job satisfaction (r = -0.430). Depersonalisation was negatively associated with support from superiors (P = 0.036). Employees with high levels of perceived stress reported higher levels of fatigue (P = 0.050). Positive associations of perceived stress with depression (P = 0.011) and sleep problems (P<0.001) were also detected. Positive correlation was found between monthly salary and lack of sense of personal achievement (P = 0.020). Clinical implications It is necessary to address these issues through staff education and stress management.

BackgroundSeveral important socio-behavioral public health problems that either peak or start during the second decade of life contribute to young people's mortality. The aim of this study was to explore patterns, rates, trends and regional variations of external-cause (due to environmental events/circumstances) mortality among young people aged 10–24 years in Greece, over the decade 2000–09.