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Prof. Panagiota Pervanidou
Unit of Developmental and Behavioral Pediatrics, First Department of Pediatrics, School of Medicine, National and Kapodistrian University of Athens, 115 27 Athens, Greece

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0 Childhood Obesity
0 Language Disorders
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Stress
PTSD
Childhood Obesity
autism spectrum disorder

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Journal article
Published: 05 June 2021 in Children
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High mobility group box 1 protein (HMGB1) has been suggested to be involved in the immune dysfunction and inflammation reported in autism spectrum disorder (ASD). We aimed to assess HMGB1 serum concentrations (SCs) in high-functioning ASD children compared to typically developing (TD) controls and to explore their associations with the autism spectrum quotient (AQ), the empathy quotient (EQ), and the systemizing quotient (SQ). The study involved 42 ASD children and 38 TD children, all-male, aged between 6.1 and 13.3 years old. HMGB1 SCs were measured by enzyme-linked immunosorbent assay (ELISA). Groups were comparable regarding age, general IQ, birth weight, and maternal age at birth. ASD children showed significantly higher HMGB1 SCs compared to TD children (1.25 ± 0.84 ng/mL versus 1.13 ± 0.79 ng/mL, respectively, p = 0.039). The Spearman’s rho revealed that HMGB1 SCs were positively correlated with the AQ attention to detail subscale (rs = 0.46, p = 0.045) and with the SQ total score (rs = 0.42, p = 0.04) in the ASD group. These results show that HMGB1 serum concentrations are altered in ASD children, and suggest that inflammatory processes mediated by HMGB1 may be associated with specific cognitive features observed in ASD.

ACS Style

Gerasimos Makris; Giorgos Chouliaras; Filia Apostolakou; Charalabos Papageorgiou; George Chrousos; Ioannis Papassotiriou; Panagiota Pervanidou. Increased Serum Concentrations of High Mobility Group Box 1 (HMGB1) Protein in Children with Autism Spectrum Disorder. Children 2021, 8, 478 .

AMA Style

Gerasimos Makris, Giorgos Chouliaras, Filia Apostolakou, Charalabos Papageorgiou, George Chrousos, Ioannis Papassotiriou, Panagiota Pervanidou. Increased Serum Concentrations of High Mobility Group Box 1 (HMGB1) Protein in Children with Autism Spectrum Disorder. Children. 2021; 8 (6):478.

Chicago/Turabian Style

Gerasimos Makris; Giorgos Chouliaras; Filia Apostolakou; Charalabos Papageorgiou; George Chrousos; Ioannis Papassotiriou; Panagiota Pervanidou. 2021. "Increased Serum Concentrations of High Mobility Group Box 1 (HMGB1) Protein in Children with Autism Spectrum Disorder." Children 8, no. 6: 478.

Review
Published: 14 March 2020 in Brain Sciences
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Traumatic stress exposure during critical periods of development may have essential and long-lasting effects on the physical and mental health of individuals. Two thirds of youth are exposed to potentially traumatic experiences by the age of 17, and approximately 5% of adolescents meet lifetime criteria for posttraumatic stress disorder (PTSD). The role of the stress system is the maintenance of homeostasis in the presence of real/perceived and acute/chronic stressors. Early-life stress (ELS) has an impact on neuronal brain networks involved in stress reactions, and could exert a programming effect on glucocorticoid signaling. Studies on pediatric PTSD reveal diverse neuroendocrine responses to adverse events and related long-term neuroendocrine and epigenetic alterations. Neuroendocrine, neuroimaging, and genetic studies in children with PTSD and ELS experiences are crucial in understanding risk and resilience factors, and also the natural history of PTSD.

ACS Style

Panagiota Pervanidou; Gerasimos Makris; George Chrousos; Agorastos Agorastos. Early Life Stress and Pediatric Posttraumatic Stress Disorder. Brain Sciences 2020, 10, 169 .

AMA Style

Panagiota Pervanidou, Gerasimos Makris, George Chrousos, Agorastos Agorastos. Early Life Stress and Pediatric Posttraumatic Stress Disorder. Brain Sciences. 2020; 10 (3):169.

Chicago/Turabian Style

Panagiota Pervanidou; Gerasimos Makris; George Chrousos; Agorastos Agorastos. 2020. "Early Life Stress and Pediatric Posttraumatic Stress Disorder." Brain Sciences 10, no. 3: 169.

Abstract
Published: 27 July 2017 in European Journal of Psychotraumatology
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The term ‘early life stress’ has been used to describe a broad spectrum of adverse exposures during foetal life, childhood and adolescence. Early life stress and trauma are associated with a higher risk for later mental and physical health disorders, such as anxiety, depression, and post-traumatic stress disorder (P.T.S.D.) as well as cardiometabolic and inflammatory diseases and chronic pain syndromes. The objective of this brief review is to investigate the neuroendocrine responses to early life stress and their role as biological predisposing factors for later disease. Stress-related neuroendocrine alterations in response to early adversity include hyper- or hypo-activation of the stress system and may persist or worsen in later life, acting as biological vulnerability factors for the development of later disease. A key effect of stress during foetal life, childhood, and adolescence is that it programmes the developing brain, especially brain structures involved in stress reactions, such as the prefrontal cortex, the hippocampus, and the amygdala, to hyper- or hypo-react to ensuing stressors. Animal studies have shown that chronically elevated stress mediators may lead to alterations in brain development through mechanisms of accelerated loss of neurons, delays in myelination, or abnormalities in developmentally appropriate neural synaptic pruning. Critical periods of brain development represent time-windows of elevated synaptic plasticity, mediating vulnerability, or establishing resilience to stress. Stress is generally associated with acute activation of the hypothalamic-pituitary-adrenal (H.P.A.) axis and the arousal/sympathetic nervous system, as evidenced, in most studies, by elevated cortisol and catecholamine concentrations in the periphery. However, the chronic and/or intense experience of stress may be associated with chronic hyper- or hypo-activation of mediators of the stress system. This chronic condition represents dyshomeostasis, also called allostasis or cacostasis, which is related to further morbidity, such as obesity and the metabolic syndrome, diabetes mellitus type 2, atherosclerosis, osteoporosis, and immune dysfunction (Pervanidou & Chrousos, 2012 Pervanidou, P., & Chrousos, G. P. (2012). Metabolic consequences of stress during childhood and adolescence. Metabolism, 61(5), 611–619. [Google Scholar]). P.T.S.D., the most common stress-related disorder, is typically associated with increased secretion of corticotropin-releasing hormone centrally, with paradoxically decreased cortisol secretion peripherally, and elevated circulating catecholamine concentrations. Stress-related neuroendocrine alterations during early life might result in conditions characterized by chronic hypo-activation of the H.P.A. axis, as typically observed in P.T.S.D. and atypical depression. Scarce data exist on the longitudinal course of P.T.S.D. development and maintenance, beginning from the exposure to the traumatic event. We investigated the natural history of neuroendocrine changes in relation to P.T.S.D. development in children and adolescents experiencing a motor vehicle accident. This longitudinal study provided evidence for an initial elevation of evening salivary cortisol and an alteration in cortisol circadian secretion in response to the experience of an intense stressor. This initial alteration was followed by a gradual normalization of cortisol with time, leading potentially to decreased cortisol concentrations in the periphery, months or years after the traumatic exposure. At the same time, a progressive elevation of circulating norepinephrine (N.E.) was noted in children that continued to exhibit P.T.S.D. This longitudinal interaction of peripheral cortisol and NE concentrations seems to characterize those that develop and maintain P.T.S.D. (Pervanidou et al., 2007 Pervanidou, P., Kolaitis, G., Charitaki, S., Lazaropoulou, C., Papassotiriou, I., Hindmarsh, P., … Chrousos, G. P. (2007). The natural history of neuroendocrine changes in pediatric posttraumatic stress disorder (PTSD) after motor vehicle accidents: Progressive divergence of noradrenaline and cortisol concentrations over time. Biological Psychiatry, 62(10), 1095–1102. [Google Scholar]). Thus, low cortisol, together with high N.E. concentrations, that characterize adult P.T.S.D., may be the end stage of the disorder. These data are also in accordance with findings in adults, showing hypocortisolism in the aftermath of a stressful experience to predict P.T.S.D. development. Several parameters affect the direction of the H.P.A. axis (increased or decreased cortisol production) in P.T.S.D., and among them, previous trauma and time since the trauma occurred seem to be crucial determinants of hyper- or hypo- activation of the H.P.A. axis. Other parameters include: genetic and epigenetic vulnerability; transgenerational actions; environmental influences in the management of early life stress; the nature, severity, and duration of the traumatic event; the developmental stage, age at the time of trauma; and comorbidities (Pervanidou, 2008 Pervanidou, P. (2008). Biology of post traumatic stress disorder in childhood and adolescence. Journal of Neuroendocrinology, 20(5), 1–2. [Google Scholar]). In conclusion, early life stress exposures result in neuroendocrine alterations and programming of the neuronal networks of the brain, acting as predisposing factors for further mental and physical health problems.

ACS Style

Panagiota Pervanidou; Agorastos Agorastos; Gerasimos Kolaitis; George P Chrousos. Neuroendocrine responses to early life stress and trauma and susceptibility to disease. European Journal of Psychotraumatology 2017, 8, 1 .

AMA Style

Panagiota Pervanidou, Agorastos Agorastos, Gerasimos Kolaitis, George P Chrousos. Neuroendocrine responses to early life stress and trauma and susceptibility to disease. European Journal of Psychotraumatology. 2017; 8 (sup4):1.

Chicago/Turabian Style

Panagiota Pervanidou; Agorastos Agorastos; Gerasimos Kolaitis; George P Chrousos. 2017. "Neuroendocrine responses to early life stress and trauma and susceptibility to disease." European Journal of Psychotraumatology 8, no. sup4: 1.

Journal article
Published: 02 February 2013 in Current Pediatrics Reports
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Childhood obesity and its related comorbidities, such as dyslipidemia, arterial hypertension and impaired glucose metabolism, which constitute the Metabolic Syndrome, are associated with an increased risk for early onset endothelial dysfunction, atherosclerosis, and cardiovascular disease later in life. Genetic, epigenetic and developmental influences, such as maternal weight status during pregnancy, birth weight, nutrition and early stress, interact with modern lifestyle factors producing the obese phenotype. Increased insulin secretion, together with disturbed concentrations of adipokines and inflammation-related molecules secreted by adipose tissue contribute, through complex pathophysiologic pathways, to the development of endocrine and metabolic complications of childhood obesity.

ACS Style

Panagiota Pervanidou; Evangelia Charmandari; George P. Chrousos. Endocrine Aspects of Childhood Obesity. Current Pediatrics Reports 2013, 1, 109 -117.

AMA Style

Panagiota Pervanidou, Evangelia Charmandari, George P. Chrousos. Endocrine Aspects of Childhood Obesity. Current Pediatrics Reports. 2013; 1 (2):109-117.

Chicago/Turabian Style

Panagiota Pervanidou; Evangelia Charmandari; George P. Chrousos. 2013. "Endocrine Aspects of Childhood Obesity." Current Pediatrics Reports 1, no. 2: 109-117.

Other
Published: 02 October 2012 in Science Signaling
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Posttraumatic stress disorder (PTSD) is a syndrome of distress that develops after exposure to traumatic life experiences. Dysregulation of both the hypothalamic-pituitary-adrenal (HPA) axis and the locus caeruleus/norepinephrine–sympathetic nervous system (LC/NE-SNS) is associated with the pathophysiology of the disorder. Studies have demonstrated a neuroendocrine profile unique to adults with PTSD, with centrally elevated corticotropin-releasing hormone (CRH), low cortisol in the periphery, and elevated catecholamines. Traumatic stress experiences in early life are strong predisposing factors for later PTSD development. In addition, early life stress programs the developing brain to overreact to future stressors. In children and adolescents involved in motor vehicle accidents, we found that high evening salivary cortisol and morning serum interleukin 6 concentrations were predictive of PTSD development 6 months later. We demonstrated a progressive divergence of the HPA and LC/NE-SNS axes of the stress system, which may be part of the pathophysiologic mechanism responsible for PTSD maintenance. An initial elevation of cortisol in the aftermath of the trauma, followed by a gradual normalization and finally low cortisol secretion, together with a gradual elevation of catecholamines over time, may represent the natural history of neuroendocrine changes in pediatric PTSD. Thus, the low cortisol concentrations found in adults with PTSD may reflect prior trauma and might represent a biologic vulnerability factor for later PTSD development.

ACS Style

Panagiota Pervanidou; George P. Chrousos. Posttraumatic Stress Disorder in Children and Adolescents: Neuroendocrine Perspectives. Science Signaling 2012, 5, pt6 -pt6.

AMA Style

Panagiota Pervanidou, George P. Chrousos. Posttraumatic Stress Disorder in Children and Adolescents: Neuroendocrine Perspectives. Science Signaling. 2012; 5 (245):pt6-pt6.

Chicago/Turabian Style

Panagiota Pervanidou; George P. Chrousos. 2012. "Posttraumatic Stress Disorder in Children and Adolescents: Neuroendocrine Perspectives." Science Signaling 5, no. 245: pt6-pt6.

Research article
Published: 04 June 2012 in Stress
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Obesity is highly co-morbid with anxiety and/or depression in children, conditions that may further worsen the metabolic and cardiovascular risks for obese individuals. Dysregulation of the hypothalamic–pituitary–adrenal axis is involved in the pathophysiology of anxiety disorders, depression, and obesity, and diverse cortisol concentrations may be found in obese children, depending on their degree of psychological distress. The aim of this study was to examine cortisol profiles among obese children with or without symptoms of anxiety and depression. A group of 128 children (53% females; mean age ± SD: 11.2 ± 2.2 years) derived from a pediatric obesity clinic were studied. Anxiety and depressive symptomatology were assessed with appropriate instruments. Morning serum and five diurnal salivary cortisol concentrations were measured. Obese children were 3.1/2.3 times more likely to report state and trait anxiety, respectively, and 3.6 times more likely to report depressive symptoms than children of the same age group, from a contemporary Greek sample. Trait anxiety and noon salivary cortisol concentrations were significantly positively correlated (p = 0.002). Overall, salivary cortisol concentrations were increased in children with anxiety or depression symptomatology compared to obese children without any affective morbidity (p = 0.02) and to those with anxiety and depression co-morbidity (p = 0.02). In conclusion, in obese children, emotional distress expressed by symptoms of anxiety and/or depression is associated with circadian cortisol profiles reflecting a potential pathway for further morbidity. Longitudinal studies may reveal a role of cortisol in linking obesity, anxiety, and depression to the development of further psychological and physical morbidity.

ACS Style

Panagiota Pervanidou; Despoina Bastaki; Giorgos Chouliaras; Katerina Papanikolaou; Eleftheria Laios; Christina Kanaka-Gantenbein; George P. Chrousos. Circadian cortisol profiles, anxiety and depressive symptomatology, and body mass index in a clinical population of obese children. Stress 2012, 16, 34 -43.

AMA Style

Panagiota Pervanidou, Despoina Bastaki, Giorgos Chouliaras, Katerina Papanikolaou, Eleftheria Laios, Christina Kanaka-Gantenbein, George P. Chrousos. Circadian cortisol profiles, anxiety and depressive symptomatology, and body mass index in a clinical population of obese children. Stress. 2012; 16 (1):34-43.

Chicago/Turabian Style

Panagiota Pervanidou; Despoina Bastaki; Giorgos Chouliaras; Katerina Papanikolaou; Eleftheria Laios; Christina Kanaka-Gantenbein; George P. Chrousos. 2012. "Circadian cortisol profiles, anxiety and depressive symptomatology, and body mass index in a clinical population of obese children." Stress 16, no. 1: 34-43.

Review
Published: 01 May 2012 in Metabolism
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Stress, that is, the state of threatened or perceived as threatened homeostasis, is associated with activation of the stress system, mainly comprised by the hypothalamic-pituitary-adrenal axis and the arousal/sympathetic nervous systems. The stress system normally functions in a circadian manner and interacts with other systems to regulate a variety of behavioral, endocrine, metabolic, immune, and cardiovascular functions. However, the experience of acute intense physical or emotional stress, as well as of chronic stress, may lead to the development of or may exacerbate several psychologic and somatic conditions, including anxiety disorders, depression, obesity, and the metabolic syndrome. In chronically stressed individuals, both behavioral and neuroendocrine mechanisms promote obesity and metabolic abnormalities: unhealthy lifestyles in conjunction with dysregulation of the stress system and increased secretion of cortisol, catecholamines, and interleukin-6, with concurrently elevated insulin concentrations, lead to development of central obesity, insulin resistance, and the metabolic syndrome. Fetal life, childhood, and adolescence are particularly vulnerable periods of life to the effects of intense acute or chronic stress. Similarly, these life stages are crucial for the later development of behavioral, metabolic, and immune abnormalities. Developing brain structures and functions related to stress regulation, such as the amygdala, the hippocampus, and the mesocorticolimbic system, are more vulnerable to the effects of stress compared with mature structures in adults. Moreover, chronic alterations in cortisol secretion in children may affect the timing of puberty, final stature, and body composition, as well as cause early-onset obesity, metabolic syndrome, and type 2 diabetes mellitus. The understanding of stress mechanisms leading to metabolic abnormalities in early life may lead to more effective prevention and intervention strategies of obesity-related health problems.

ACS Style

Panagiota Pervanidou; George P. Chrousos. Metabolic consequences of stress during childhood and adolescence. Metabolism 2012, 61, 611 -619.

AMA Style

Panagiota Pervanidou, George P. Chrousos. Metabolic consequences of stress during childhood and adolescence. Metabolism. 2012; 61 (5):611-619.

Chicago/Turabian Style

Panagiota Pervanidou; George P. Chrousos. 2012. "Metabolic consequences of stress during childhood and adolescence." Metabolism 61, no. 5: 611-619.

Review article
Published: 01 September 2011 in Pediatric Obesity
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Chronic distress contributes to the development of obesity and comorbid states. Stress is the disturbance of the complex dynamic equilibrium that all organisms must maintain, and is associated with activation of the Stress system comprising of the hypothalamic-pituitary-adrenal axis and the arousal/sympathetic nervous systems. The stress system functions in a baseline circadian fashion and interacts with other systems of the organism to regulate a variety of behavioral, endocrine, metabolic, immune and cardiovascular functions. The experience of perceived or real uncontrollable intense and/or chronic stress (distress) may lead to several psychopathologic conditions, including anxiety, depressive and psychosomatic disorders, substance abuse, obesity and the metabolic syndrome, and osteoporosis, as well as impaired reproductive and immune functions. Developing children and adolescents are particularly vulnerable to the effects of chronic stress. Both behavioral and biological pathways are involved in the connection between chronic stress and obesity in adults and children. Emotional "comfort" eating, lack of sleep, impulsive behaviours and selection of specific foods often characterize stressed individuals. In addition to specific behaviours, dysregulation of the stress system through increased secretion of cortisol and catecholamines, especially in the evening hours, and in concert with concurrently elevated insulin concentrations, leads to development of central obesity, insulin resistance and the metabolic syndrome. In children, chronic alterations in cortisol secretion may have additional effects on cognitive and emotional development, timing of puberty and final stature. Obese children and adolescents are frequently entangled in a vicious cycle between distress, impairing self-image and distorted self-image, maintaining and worsening distress.

ACS Style

Panagiota Pervanidou; George P. Chrousos. Stress and obesity/metabolic syndrome in childhood and adolescence. Pediatric Obesity 2011, 6, 21 -28.

AMA Style

Panagiota Pervanidou, George P. Chrousos. Stress and obesity/metabolic syndrome in childhood and adolescence. Pediatric Obesity. 2011; 6 (S1):21-28.

Chicago/Turabian Style

Panagiota Pervanidou; George P. Chrousos. 2011. "Stress and obesity/metabolic syndrome in childhood and adolescence." Pediatric Obesity 6, no. S1: 21-28.

Review
Published: 05 May 2011 in BMC Medicine
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Metabolic syndrome (MetS) is a complex disorder defined by a cluster of interconnected factors that increase the risk of cardiovascular atherosclerotic diseases and diabetes mellitus type 2. Currently, several different definitions of MetS exist, causing substantial confusion as to whether they identify the same individuals or represent a surrogate of risk factors. Recently, a number of other factors besides those traditionally used to define MetS that are also linked to the syndrome have been identified. In this review, we critically consider existing definitions and evolving information, and conclude that there is still a need to develop uniform criteria to define MetS, so as to enable comparisons between different studies and to better identify patients at risk. As the application of the MetS model has not been fully validated in children and adolescents as yet, and because of its alarmingly increasing prevalence in this population, we suggest that diagnosis, prevention and treatment in this age group should better focus on established risk factors rather than the diagnosis of MetS.

ACS Style

Eva Kassi; Panagiota Pervanidou; Gregory Kaltsas; George Chrousos. Metabolic syndrome: definitions and controversies. BMC Medicine 2011, 9, 48 -48.

AMA Style

Eva Kassi, Panagiota Pervanidou, Gregory Kaltsas, George Chrousos. Metabolic syndrome: definitions and controversies. BMC Medicine. 2011; 9 (1):48-48.

Chicago/Turabian Style

Eva Kassi; Panagiota Pervanidou; Gregory Kaltsas; George Chrousos. 2011. "Metabolic syndrome: definitions and controversies." BMC Medicine 9, no. 1: 48-48.

Book chapter
Published: 01 January 2010 in Neuroendocrinology - Pathological Situations and Diseases
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Dysregulation of the stress system, including the hypothalamic-pituitary-adrenal (HPA) axis and the locus caeruleus/norepinephrine-sympathetic nervous system (SNS), is involved in the pathophysiology of post-traumatic stress disorder (PTSD), an anxiety disorder that develops after exposure to traumatic life events. Neuroendocrine studies in individuals with PTSD have demonstrated elevated basal cerebrospinal fluid corticotropin-releasing hormone concentrations and contradictory results from peripheral measurements, exhibiting low 24 hours excretion of urinary free cortisol, low or normal circulating cortisol levels or even high plasma cortisol levels. The direction of HPA axis activity (hyper-/or hypo-activation), as evidenced by peripheral cortisol measures, may depend on variables such as genetic vulnerability and epigenetic changes, age and developmental stage of the individual, type and chronicity of trauma, co-morbid depression or other psychopathology, alcohol or other drug abuse and time since the traumatic experience. On the other hand, peripheral biomarkers of the SNS activity are more consistent, showing increased 24h urinary or plasma catecholamines in PTSD patients compared to control individuals. Chronically disturbed hormones in PTSD may contribute to brain changes and further emotional and behavior symptoms and disorders, as well as to an increased cardiometabolic risk.

ACS Style

Panagiota Pervanidou; George P. Chrousos. Neuroendocrinology of Post-Traumatic Stress Disorder. Neuroendocrinology - Pathological Situations and Diseases 2010, 182, 149 -160.

AMA Style

Panagiota Pervanidou, George P. Chrousos. Neuroendocrinology of Post-Traumatic Stress Disorder. Neuroendocrinology - Pathological Situations and Diseases. 2010; 182 ():149-160.

Chicago/Turabian Style

Panagiota Pervanidou; George P. Chrousos. 2010. "Neuroendocrinology of Post-Traumatic Stress Disorder." Neuroendocrinology - Pathological Situations and Diseases 182, no. : 149-160.

Journal article
Published: 10 August 2009 in Hormone and Metabolic Research
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N-terminal pro-Brain Natriuretic Peptide (NT-proBNP) is an established biomarker for heart failure in adults, while its plasma concentrations are altered in adult obesity. Plasma adiponectin concentrations are decreased in obesity and low levels are associated with disorders with an increased cardiometabolic risk. A few studies support an association between these two markers in adults with coronary heart disease. Such relations have not been investigated in children with obesity, which is the most prevalent risk factor for cardiovascular disease. Ninety-six children, 24 obese/25 normal BMI boys, and 23 obese/24 normal BMI girls, aged 10–16, were studied. Plasma NT-proBNP was measured using electrochemiluminescence, and adiponectin and other metabolic risk factors, such as glucose, insulin, cholesterol, triglycerides (TG), HDL, and LDL using standard methodology. The findings were gender dimorphic. In overweight and obese females (mean BMI z-score: 2.65±1.69), plasma NT-proBNP concentrations correlated significantly with adiponectin levels (r=0.4, r2=0.05, p=0.013), while in those with obesity defined as BMI z-score >2.5 (mean BMI z-score: 3.67±1.08, n=20) this association was stronger (r=0.6, r2=0.22, p=0.005). Adiponectin also correlated significantly with BMI z-scores, TG, HDL, and insulin levels. In boys, there was no correlation between NT-proBNP and adiponectin. NT-proBNP correlated significantly with HDL, while adiponectin correlated with TG, fasting insulin, and the Homeostasis Assessment Model (HOMA) Index. The positive association between NT-proBNP and adiponectin depends on the severity of obesity and is gender dimorphic. This positive correlation in females might be a potential protective mechanism against atherosclerosis in later life.

ACS Style

P. Pervanidou; A. Margeli; A. Akalestos; S. Sakka; C. Kanaka-Gantenbein; I. Papassotiriou; G. P. Chrousos. Associations Between Circulating N-terminal pro-Brain Natriuretic Peptide (NT-proBNP) and Adiponectin Concentrations Depend on Obesity Level in Female Adolescents: Gender Dimorphic Findings. Hormone and Metabolic Research 2009, 41, 829 -833.

AMA Style

P. Pervanidou, A. Margeli, A. Akalestos, S. Sakka, C. Kanaka-Gantenbein, I. Papassotiriou, G. P. Chrousos. Associations Between Circulating N-terminal pro-Brain Natriuretic Peptide (NT-proBNP) and Adiponectin Concentrations Depend on Obesity Level in Female Adolescents: Gender Dimorphic Findings. Hormone and Metabolic Research. 2009; 41 (11):829-833.

Chicago/Turabian Style

P. Pervanidou; A. Margeli; A. Akalestos; S. Sakka; C. Kanaka-Gantenbein; I. Papassotiriou; G. P. Chrousos. 2009. "Associations Between Circulating N-terminal pro-Brain Natriuretic Peptide (NT-proBNP) and Adiponectin Concentrations Depend on Obesity Level in Female Adolescents: Gender Dimorphic Findings." Hormone and Metabolic Research 41, no. 11: 829-833.

Comparative study
Published: 01 May 2008 in Journal of Neuroendocrinology
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Diverse patterns of cortisol secretion with consistently high circulating catecholamines have been reported in post-traumatic stress disorder (PTSD), an anxiety state that develops after exposure to traumatic life events. Indeed, peripheral cortisol levels have been reported to be low or normal in the majority of adult chronic PTSD studies, whereas, in most paediatric studies, high cortisol values have been documented. Longitudinal studies on PTSD biology, including the transition from childhood to adulthood, may shed light on these discrepancies. In children, elevated evening salivary cortisol in the aftermath of the trauma was predictive of PTSD development 6 months later, whereas plasma interleukin-6 correlated positively with evening cortisol and was equally predictive of later PTSD. Longitudinal assessment of PTSD children 1 and 6 months later revealed progressive normalisation of cortisol levels, whereas noradrenaline concentrations became gradually higher. We hypothesise that, in adults with chronic PTSD, low cortisol levels, together with high catecholamines, may reflect a late event in the natural history of the disorder, months or years after the trauma. The progressive divergence of cortisol and noradrenaline concentrations over time may be responsible for PTSD maintenance in children and explain the differences between the child and adult PTSD endophenotypes. In adults studied immediately after the trauma, and by contrast to children, low cortisol levels are predictive of later PTSD development. Our hypothesis that low cortisol levels may reflect a previous trauma, earlier in development, is supported by the well established observation that prior trauma is a risk factor for a new PTSD diagnosis. The developmental stage of an individual in relation to previous exposure to trauma and PTSD vulnerability are crucial variables that may determine clinical and biological PTSD phenotypes and explain the discrepancies between adults and children in reported cortisol levels.

ACS Style

P. Pervanidou. Biology of Post-Traumatic Stress Disorder in Childhood and Adolescence. Journal of Neuroendocrinology 2008, 20, 632 -638.

AMA Style

P. Pervanidou. Biology of Post-Traumatic Stress Disorder in Childhood and Adolescence. Journal of Neuroendocrinology. 2008; 20 (5):632-638.

Chicago/Turabian Style

P. Pervanidou. 2008. "Biology of Post-Traumatic Stress Disorder in Childhood and Adolescence." Journal of Neuroendocrinology 20, no. 5: 632-638.

Original
Published: 01 January 2008 in Stress
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Motor vehicle accidents (MVA) represent a complex physical and emotional stressor. Consequent short- and/or long-term alterations on the circulating concentrations of stress hormones and adipo-cytokines may have potential health implications. Fifty-nine children and adolescents, aged 7–18 years, were evaluated within 24 h after hospitalization for a MVA, and 1 and 6 months later; 40 children served as controls. We examined longitudinally the effects of physical injury-associated (PI) group vs. emotional-only stress (ES) group on circulating cortisol, catecholamine, interleukin (IL)-6, leptin and adiponectin concentrations. Within 24 h after the accident, serum cortisol concentration was greater than the controls in the PI but not the ES group (p = 0.02), while serum IL-6 concentration was greater in both trauma groups than in the controls (p = 0.004 for PI, p = 0.04 for ES). Adiponectin concentration was lower in the PI than the ES (p = 0.031) and the control (p = 0.019) groups and this was mainly attributed to females. The catecholamine and leptin concentrations were similar in the three groups. At the 1 and 6 month evaluations, cortisol and IL-6 concentrations in both trauma groups became normal. Adiponectin concentration in females, however, remained low 1 and 6 months after the accident (p = 0.03 for month six). In conclusion, circulating IL-6 concentration was influenced equally by the physical and emotional stress shortly after the trauma. Physical but not emotional-only stress lowered the circulating adiponectin concentrations in females and this effect persisted for at least 6 months.

ACS Style

P. Pervanidou; A. Margeli; Ch. Lazaropoulou; I. Papassotiriou; G. P. Chrousos. The immediate and long-term impact of physical and/or emotional stress from motor vehicle accidents on circulating stress hormones and adipo-cytokines in children and adolescents. Stress 2008, 11, 438 -447.

AMA Style

P. Pervanidou, A. Margeli, Ch. Lazaropoulou, I. Papassotiriou, G. P. Chrousos. The immediate and long-term impact of physical and/or emotional stress from motor vehicle accidents on circulating stress hormones and adipo-cytokines in children and adolescents. Stress. 2008; 11 (6):438-447.

Chicago/Turabian Style

P. Pervanidou; A. Margeli; Ch. Lazaropoulou; I. Papassotiriou; G. P. Chrousos. 2008. "The immediate and long-term impact of physical and/or emotional stress from motor vehicle accidents on circulating stress hormones and adipo-cytokines in children and adolescents." Stress 11, no. 6: 438-447.

Evaluation study
Published: 30 November 2007 in Psychoneuroendocrinology
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This study examined prospectively the activity of the hypothalamic–pituitary–adrenal axis, the sympathetic nervous system and inflammatory factors in children shortly after a motor vehicle accident (MVA) in relation to later posttraumatic stress disorder (PTSD) development. Fifty six children, aged 7–18, were studied after an MVA and 1 and 6 months later; 40 subjects served as controls. Morning serum cortisol and interleukin (IL)-6 and plasma catecholamine concentrations were measured within 24 h after the event. Salivary cortisol was measured 5 times at defined time points during the same day. PTSD diagnoses 1 and 6 months later were based on K-SADS interview. Morning serum IL-6 concentrations, measured within the first 24 h after the accident, were higher in children that developed PTSD 6 months later than those who did not and those of the control group. Longitudinal IL-6 measurements revealed normalization of IL-6 in the PTSD group, while no differences between the three groups were detected 1 and 6 months later. Evening salivary cortisol and morning serum IL-6 after the accident were positively inter-related (r=0.54, p<0.001) and in separate regression analyses both predicted PTSD development 6 months later. In contrast, morning serum IL-6 did nor correlate with morning serum or salivary cortisol concentrations. Immediate posttraumatic alterations in neuroendocrine or inflammatory factors—increased evening salivary cortisol and/or increased morning serum IL-6 concentrations—are involved in subsequent PTSD development in children and adolescents.

ACS Style

Panagiota Pervanidou; Gerasimos Kolaitis; Stella Charitaki; Alexandra Margeli; Spyros Ferentinos; Chrysa Bakoula; Christina Lazaropoulou; Ioannis Papassotiriou; John Tsiantis; George P. Chrousos. Elevated morning serum interleukin (IL)-6 or evening salivary cortisol concentrations predict posttraumatic stress disorder in children and adolescents six months after a motor vehicle accident. Psychoneuroendocrinology 2007, 32, 991 -999.

AMA Style

Panagiota Pervanidou, Gerasimos Kolaitis, Stella Charitaki, Alexandra Margeli, Spyros Ferentinos, Chrysa Bakoula, Christina Lazaropoulou, Ioannis Papassotiriou, John Tsiantis, George P. Chrousos. Elevated morning serum interleukin (IL)-6 or evening salivary cortisol concentrations predict posttraumatic stress disorder in children and adolescents six months after a motor vehicle accident. Psychoneuroendocrinology. 2007; 32 (8-10):991-999.

Chicago/Turabian Style

Panagiota Pervanidou; Gerasimos Kolaitis; Stella Charitaki; Alexandra Margeli; Spyros Ferentinos; Chrysa Bakoula; Christina Lazaropoulou; Ioannis Papassotiriou; John Tsiantis; George P. Chrousos. 2007. "Elevated morning serum interleukin (IL)-6 or evening salivary cortisol concentrations predict posttraumatic stress disorder in children and adolescents six months after a motor vehicle accident." Psychoneuroendocrinology 32, no. 8-10: 991-999.

Journal article
Published: 15 November 2007 in Biological Psychiatry
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The hypothalamic-pituitary-adrenal axis and the catecholaminergic system are involved in the pathophysiology of post-traumatic stress disorder (PTSD). This was a prospective and longitudinal study of neuroendocrine physiology in children with PTSD following a motor vehicle accident (MVA). Sixty children aged 7-18 were studied immediately after an MVA and 1 and 6 months later. Fasting morning plasma catecholamine and serum cortisol concentrations were measured. Salivary cortisol concentrations were measured serially five times daily to examine circadian variation in all three assessments. Values were compared between those who did (PTSD) or did not develop PTSD (non-PTSD) after the trauma and a control group at months 1 and 6. Twenty-three of the children had PTSD at the 1-month and 9 children at the 6-month evaluations. 1) Plasma noradrenaline concentrations were higher in the PTSD group than in the other two groups at both months 1 and 6 (p = .001 and p = .001, respectively). Additionally, the PTSD patients presented with significantly higher salivary cortisol concentrations at 18.00 (p = .03) and 21.00 (p = .04) at month 1.2) Eight children suffering from PTSD at both months 1 and 6 had significantly elevated plasma noradrenaline concentrations at month 6 compared with those at month 1 and at baseline and to the other two groups (within subjects: p < .001; between subjects: p = .005). The initially elevated evening salivary cortisol concentrations in this group normalized at month 6. This progressive divergence of noradrenaline and cortisol concentrations over time might underlie the natural history and pathophysiology of PTSD.

ACS Style

Panagiota Pervanidou; Gerasimos Kolaitis; Stella Charitaki; Christina Lazaropoulou; Ioannis Papassotiriou; Peter Hindmarsh; Chrysa Bakoula; John Tsiantis; George P. Chrousos. The Natural History of Neuroendocrine Changes in Pediatric Posttraumatic Stress Disorder (PTSD) After Motor Vehicle Accidents: Progressive Divergence of Noradrenaline and Cortisol Concentrations Over Time. Biological Psychiatry 2007, 62, 1095 -1102.

AMA Style

Panagiota Pervanidou, Gerasimos Kolaitis, Stella Charitaki, Christina Lazaropoulou, Ioannis Papassotiriou, Peter Hindmarsh, Chrysa Bakoula, John Tsiantis, George P. Chrousos. The Natural History of Neuroendocrine Changes in Pediatric Posttraumatic Stress Disorder (PTSD) After Motor Vehicle Accidents: Progressive Divergence of Noradrenaline and Cortisol Concentrations Over Time. Biological Psychiatry. 2007; 62 (10):1095-1102.

Chicago/Turabian Style

Panagiota Pervanidou; Gerasimos Kolaitis; Stella Charitaki; Christina Lazaropoulou; Ioannis Papassotiriou; Peter Hindmarsh; Chrysa Bakoula; John Tsiantis; George P. Chrousos. 2007. "The Natural History of Neuroendocrine Changes in Pediatric Posttraumatic Stress Disorder (PTSD) After Motor Vehicle Accidents: Progressive Divergence of Noradrenaline and Cortisol Concentrations Over Time." Biological Psychiatry 62, no. 10: 1095-1102.

Review
Published: 18 June 2007 in Hormone and Metabolic Research
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Post-traumatic Stress Disorder (PTSD) is an anxiety syndrome that develops after exposure to traumatic life events. Symptoms include re-experience of the initial trauma, avoidance of stimuli associated with the trauma and symptoms of excessive arousal. Neuroendocrine studies in adults with PTSD have demonstrated that basal cerebrospinal fluid (CSF) CRH levels are elevated and urinary cortisol levels are variable - low in the majority of cases - whereas other studies demonstrate no differences in urinary and plasma cortisol concentrations. Urinary catecholamine excretion is higher in PTSD patients than those of control subjects and other psychiatric disorders. Children may differ from adults in their psychologic and physiologic responses to severe stressors. Also, exposure to stress during critical periods of development may have irreversible effects on behavioral maturation and may affect specific vulnerable brain areas, altering CNS development. Similar to findings in adult studies, PTSD in children is characterized by increased sympathetic nervous system (SNS) activity, as indicated by elevated norepinephrine levels in the periphery. High cortisol levels in urine or saliva have been reported in most studies of childhood PTSD, while prospective longitudinal studies concerning the natural history of neuroendocrine changes in pediatric PTSD after an acute stressor are limited. The identification of neurobiologic changes in response to early adverse experiences is of major importance for the prognosis, prevention, management, and treatment of children and adolescents at risk for or suffering from PTSD.

ACS Style

P. Pervanidou; G. P. Chrousos. Post-traumatic Stress Disorder in Children and Adolescents: From Sigmund Freud's “Trauma” to Psychopathology and the (Dys)metabolic Syndrome. Hormone and Metabolic Research 2007, 39, 413 -419.

AMA Style

P. Pervanidou, G. P. Chrousos. Post-traumatic Stress Disorder in Children and Adolescents: From Sigmund Freud's “Trauma” to Psychopathology and the (Dys)metabolic Syndrome. Hormone and Metabolic Research. 2007; 39 (6):413-419.

Chicago/Turabian Style

P. Pervanidou; G. P. Chrousos. 2007. "Post-traumatic Stress Disorder in Children and Adolescents: From Sigmund Freud's “Trauma” to Psychopathology and the (Dys)metabolic Syndrome." Hormone and Metabolic Research 39, no. 6: 413-419.

Review
Published: 01 September 2006 in Current Opinion in Clinical Nutrition & Metabolic Care
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The metabolic syndrome, a clustering of abnormalities such as hyperglycemia, insulin resistance, hypertension, dyslipidemia, and central obesity, is a principal risk factor for cardiovascular disease, the leading cause of morbidity and mortality in the Western world. There are several definitions of the metabolic syndrome, all aiming at including as many persons at risk as possible. The assessment and, hence, the identification of such persons in a clinical setting is of utmost importance. Clinicians should document the presence of central obesity, assessed by waist circumference measurement or determination of body composition using dual X-ray absorptiometry or measurement of visceral fat using computed tomography or magnetic resonance imaging. The presence of dyslipidemia, insulin resistance, and arterial hypertension constitutes the full profile of the metabolic syndrome. Nevertheless, elevated uric acid levels or presence of nonalcoholic fatty liver, or the diagnosis of the polycystic ovary syndrome in women of reproductive age, all are reflected in high risk of later occurrence of the full metabolic syndrome and atherosclerotic cardiovascular disease. Although no unified definition for the metabolic syndrome exists, it is important to identify persons at risk, in order to reduce the resultant high morbidity and mortality rates.

ACS Style

Panagiota Pervanidou; Christina Kanaka-Gantenbein; George P Chrousos. Assessment of metabolic profile in a clinical setting. Current Opinion in Clinical Nutrition & Metabolic Care 2006, 9, 589 -595.

AMA Style

Panagiota Pervanidou, Christina Kanaka-Gantenbein, George P Chrousos. Assessment of metabolic profile in a clinical setting. Current Opinion in Clinical Nutrition & Metabolic Care. 2006; 9 (5):589-595.

Chicago/Turabian Style

Panagiota Pervanidou; Christina Kanaka-Gantenbein; George P Chrousos. 2006. "Assessment of metabolic profile in a clinical setting." Current Opinion in Clinical Nutrition & Metabolic Care 9, no. 5: 589-595.