Neuroendocrine and circadian aspects (melatonin and β-endorphin) of atopic dermatitis in the child

Atopic dermatitis (AD) is a disease of increasing incidence among paediatric patients. Among the factors involved in its pathogenesis is the alteration of the immune response, and so the objective of this study was to evaluate the involvement of certain neuroendocrine factors with immune properties in the development of the disease. Fifty-five subjects were selected and divided into the following three groups: healthy subjects, those diagnosed with symptomatic AD and those with asymptomatic AD. Plasma levels of melatonin and beta-endorphins were measured by radioimmunoassay, in serum samples obtained at 9 am and 9 pm, with two samples being obtained from each of the patients and controls. In the phases of AD outbreaks, there is a reduction in the serum levels of both melatonin and beta-endorphin. In the case of melatonin, the difference is statistically significant only during the day, although nocturnal levels are greater for both hormones. In AD, a central neuroendocrine dysfunction may be a primary pathogenic event. Our hypothesis is that the physiological nocturnal peak of melatonin due to pineal gland production may mask the decline of melatonin of possibly extrapineal (immunological) origin during episodes of dermatitis outbreaks. Further studies are required, particularly of neurovegetative and hormonal aspects, to better define this process. Such a definition would also be of therapeutic interest.     

Neuroendocrine regulation of food intake

Maintenance of appropriate stores of metabolic fuels depends on carefully matching caloric intake to caloric expenditure. Achieving such 'energy balance' is a product of complex interactions of peripheral hormones with effector systems in the central nervous system (CNS) that regulate food intake and energy expenditure. Leptin is a hormone that is made in the adipocytes, circulates in the blood and interacts with receptors in the CNS. These receptors can be found in two different types of systems. One effector system is termed 'anabolic' and is activated by low levels of leptin during negative energy balance. This system (exemplified by the hypothalamic neuropeptide Y system) increases food intake and decreases energy expenditure to facilitate the regaining of lost energy stores. The other effector system is termed 'catabolic' and is activated by high levels of leptin during positive energy balance. This system (exemplified by the hypothalamic melanocortin and corticotrophin-releasing hormone systems) decreases food intake and increases energy expenditure to facilitate the loss of excess energy stores. Further understanding of these systems is necessary to develop adequate treatments for disorders of energy balance, such as obesity and wasting.     

Esophageal pH monitoring in children. Methodological aspects and a review of the literature related to indications]

Because it offers high sensitivity and specificity, esophageal pH monitoring has become the reference method for the diagnosis of gastroesophageal reflux. This review was undertaken to evaluate methodologic problems raised by this method, involving selection of the electrode, selection of equipment, and criteria of normality according to the patient's symptoms. In some instances, multiple recordings are needed to detect correlations between clinical symptoms and esophageal pH, cardiac and respiratory tracings and esophageal pH, or oxygen saturation and esophageal pH. These studies allow improved qualitative interpretation of results. Emphasis is put on the value of esophageal pH recordings for the evaluation of medical or surgical therapies.     

Neuroendocrine regulation of food intake

Despite a global obesity epidemic suggesting that human physiology is unable to prevent unhealthy gains in body weight, ample evidence indicates that weight can be tightly regulated. Food intake regulation is complex and in this article we will present a basic endocrine feedback loop model of energy homeostasis. Next, integration of long-term regulation with short-term, meal specific regulation and satiety will be discussed. Finally, the role of adiposity signals in modulation of food reward will be highlighted. A basic understanding of the structure-function of these systems will inform the challenges of clinical care for those with disorders of energy balance.     

Neuroendocrine regulation of food intake

Seeley RJ, Schwartz MW. Neuroendocrine regulation of food intake. Acta Pædiatr 1999; Suppl 428: 58–61. Stockholm. ISSN 0803–5326
Maintenance of appropriate stores of metabolic fuels depends on carefully matching caloric intake to caloric expenditure. Achieving such'energy balance'is a product of complex interactions of peripheral hormones with effector systems in the central nervous system (CNS) that regulate food intake and energy expenditure. Leptin is a hormone that is made in the adipocytes, circulates in the blood and interacts with receptors in the CNS. These receptors can be found in two different types of systems. One effector system is termed'anabolic'and is activated by low levels of leptin during negative energy balance. This system (exemplified by the hypothalamic neuropeptide Y system) increases food intake and decreases energy expenditure to facilitate the regaining of lost energy stores. The other effector system is termed'catabolic'and is activated by high levels of leptin during positive energy balance. This system (exemplified by the hypothalamic melanocortin and corticotrophin-releasing hormone systems) decreases food intake and increases energy expenditure to facilitate the loss of excess energy stores. Further understanding of these systems is necessary to develop adequate treatments for disorders of energy balance, such as obesity and wasting. □ Corticotrophin-releasing hormone, energy balance, food intake, leptin, melanocortin, neuropeptide Y     

Neuroendocrine consequences of traumatic brain injury

Severe to moderate traumatic brain injury (TBI) is associated with a high frequency of morbidity in survivors. The pituitary gland is vulnerable to damage following TBI and long-term neuroendocrine dysfunction is a potential complication. Until recently little has been known about the natural history, presentation and characteristics of hypothalamic-pituitary dysfunction following TBI. This article reviews the emerging body of contemporary data from adult survivors of TBI, which suggests that the prevalence of pituitary hormone problems following head injury may be much more common than previously thought. We also review the epidemiology of childhood TBI and historical case reports that show that pituitary dysfunction has been observed to occur after both mild and severe TBI and may not present clinically until many years after the event. A recent analysis of a large paediatric growth hormone (GH) deficiency patient database highlights fewer than expected registered cases of TBI-related GH deficiency, suggesting that this may be an overlooked phenomenon. This hypothesis is supported by recently published data from the first systematic studies to be carried out in the childhood TBI setting. Given the critical role of anterior pituitary hormones in the regulation of growth and pubertal and neurocognitive development in childhood, early detection of hormone abnormalities is important. We propose that a multidisciplinary approach to follow-up and endocrine assessment is required for the long-term management and rehabilitation of children and adolescents who survive moderate to severe head injury.     

Decreased monocyte class II MHC expression following major abdominal surgery in children is related to operative stress

Monocyte class II major histocompatibility complex (MHC) expression is necessary for antigen presentation and stimulation of T-cells. The aim of this study was to correlate monocyte class II MHC response to operative stress in children and the possible influence of cytokines in the postoperative period. We studied 21 children undergoing elective abdominal surgery. Operative stress score (OSS) was calculated. Monocyte class II MHC expression was measured preoperatively, immediately after surgery, 24 and 48 h postoperatively, using flow cytometry. Class II MHC is expressed as mean fluorescence intensity (MFI) of monocytes expressing MHC (mean±SD). Cytokine levels (interleukins 1ra, 6, and 10, and tumor necrosis factor-α) were also measured. Data between time points were compared using repeated measures ANOVA. There was an immediate postoperative decrease in class II MHC expression, with lowest levels 24 h postoperatively (preoperative 50±23.6, 24 h 18.2±9.4, P<0.0001 vs. preoperative). At 48 h there was partial recovery in class II MHC, but levels were still significantly lower than preoperative (23.9±11.1, P<0.001). The degree of monocyte depression was related to the magnitude of operative stress. Patients who had OSS <10 displayed some recovery in expression at 48 h 25.5±11.1), whereas in patients with OSS ≥10 (severe surgical stress), expression further decreased at 48 h (MFI 14.0±0.1). There was an elevation of interleukin-1ra in the immediate postoperative period in both groups. There was no elevation in the other cytokines. Abdominal surgery in children decreases monocyte MHC expression. Class II MHC depression was related to magnitude of surgical trauma, implying that more severe immuneparesis follows surgery of greater magnitude. This may predispose to postoperative infection.     

Neuroendocrine and immune responses to acute endotoxemia in suckling and weaned piglets

The objective of this study was to characterize effects of weaning stress on behavioural, endocrine and immune responses to acute peripheral lipopolysaccharide (LPS) challenge in neonatal pigs. Weaning in 28-day-old piglets was accompanied by a significant increase in ACTH concentrations (p = 0.0378) and an increase in basal cortisol level (p = 0.0135). There was also a significant suppressive effect on lymphocyte proliferation in response to concanavalin A (p = 0.0048) in newly weaned piglets. Peripheral administration of LPS induced vomiting, diarrhoea and somnolence in both suckling and weaned piglets. The frequency of these signs of sickness was significantly higher in weaned piglets compared with suckling piglets (p = 0.0049). Additionally, LPS significantly increased plasma concentrations of TNF-alpha, cortisol and ACTH. While weaned piglets reacted to LPS with a higher release of ACTH (p = 0.0239) and cortisol (p = 0.0015) than suckling piglets there was no significant effect of weaning on the magnitude of TNF-alpha. The present data indicate that weaning suppresses the lymphocyte function, causes changes in endocrine regulation and has a substantial effect on the behavioural and endocrine response to an acute peripheral LPS challenge; consequently it could increase disease susceptibility.     

婴儿母亲育儿压力及相关影响因素分析

目的调查南京市主城区6个月婴儿母亲的育儿压力,并分析相关的影响因素。方法采用简式育儿压力问卷(中文版)(parenting stress index-short form,PSI-SF)和自编基本情况调查表对随机抽取的420组南京市的6个月婴儿及其母亲进行调查并比较分析。结果母亲的文化程度与育儿压力呈负相关;婴儿的性别、家庭收入及母亲年龄与母亲的育儿压力差异无统计学意义。结论在婴幼儿期,母亲的受教育程度是影响其育儿压力的重要因素之一。