Food IgG4 antibodies are elevated not only in children with wheat allergy but also in children with gastrointestinal diseases.

BACKGROUND: Food sIgG and sIgG4 are highly individually versatile. We put a hypothesis that one of the responsible factors is the presence of gastrointestinal inflammatory diseases. The objectives were: 1. An analysis of wheat and rice sIgG and sIgG4 in healthy children, children with IgE-mediated wheat allergy (WA), coeliac disease (CD) and Helicobacter pylori infection (HP). 2. Usability of wheat sIgG and sIgG4 in the WA diagnostics. METHODS: We compared 388 each wheat and rice sIgG and sIgG4 in a group of 200 children: 50 WA (diagnosis, diet treatment, tolerance), 50 CD (diagnosis and remission), 50 HP and 50 healthy. SIgE, sIgG, sIgG4 were determined with the FEIA method (Pharmacia CAP System). RESULTS: In healthy children food sIgG were the lowest; no sIgG4 were found. In the CD diagnosis group wheat and rice sIgG and rice sIgG4 were the most common and their concentrations were the highest (p < .001, p < .05). Wheat sIgG4 were the highest in WA children (diagnosis and tolerance) to fall during the elimination diet (p < .05). Wheat and rice sIgG remained the same in all allergy phases. Rice sIgG also did not differ in the class G4. CONCLUSIONS: 1. Serum concentrations of wheat and rice sIgG and sIgG4 are elevated in children with CD, HP and WA. 2. Sub-clinical incidence of some gastrointestinal inflammatory diseases may be responsible for high individual versatility of food sIgG and sIgG4 concentrations in serum. 3. Wheat sIgG and sIgG4 in children do not correlate with WA clinical picture.

Serum leptin concentrations in children with mild and moderate malnutrition.

INTRODUCTION: Numerous studies have reported a strong relationship between plasma leptin concentration and percentage of body fat, fat mass, and body mass index (BMI) in obese and non-obese children. The objective of the present study was to assess the usefulness of serum leptin concentration in disclosing prepubertal malnutrition. MATERIAL AND METHOD: Leptin concentrations in serum were determined and anthropometric parameters were measured in 149 children (3-6 and 7-10 years old). The Cole index of nutritional status was calculated. 44 children (I) presented with long-standing malnutrition due to celiac disease or food allergy and 105 children (II) were healthy. RESULTS: Leptin concentrations in both age groups of undernourished boys (median 2.7 and 2.7 microg/L) and in younger undernourished girls (median 4.2 microg/L) did not differ from concentrations in healthy children (median 2.9, 2.9, and 3.4 microg/L, respectively). Leptin concentrations in older undernourished girls were significantly lower than in healthy girls (median 4.2 vs. 8.8 microg/L, respectively; p < 0.05) of comparable age. In healthy children, leptin levels correlated with gender, body mass, BMI, Cole ratio (r = 0.39-0.41, r = 0.33, r = 0.28, r = 0.22, respectively; p < 0.005), and height (r = 0.19; p < 0.05). Serum leptin concentrations in undernourished children correlated with gender, arm circumference, and BMI (r = 0.27-0.35, r = 0.27, r = 0.25, respectively; p < 0.05). CONCLUSIONS: Our results show that serum leptin concentration is not a useful indicator of mild and moderate malnutrition in prepubertal children.

Relation of low-grade inflammation and endothelial activation to blood pressure in obese children and adolescents.

OBJECTIVE: To determine the role of low-grade, systemic inflammation and endothelial activation in the modulation of blood pressure (BP) independently of other traditional risk factors in obese children and adolescents. DESIGN: We surveyed 281 obese subjects, aged 6-18 years to investigate the relationship of serum inflammation and endothelial activation markers and blood pressure. MEASUREMENTS: Clinical variables, indices of obesity, ambulatory 24-h blood pressure and serum concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-1 beta (IL-1 beta), intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), glucose and insulin. HOMA IR was used as a marker of insulin resistance (IR). RESULTS: CRP, IL-6, IL-1 beta, and ICAM-1 correlated significantly with mean 24-h systolic BP, whereas CRP and IL-6 was positively correlated with mean 24-h diastolic BP. Multiple regression analysis showed that serum IL-6 (P < .001) concentration, HOMA IR (P < .01), and waist to hip ratio (P < .05) were the significant determinants of systolic BP, whereas CRP (P < .05) level was the only predictor of diastolic BP. There were no significant associations of cell adhesion molecules with BP. CONCLUSIONS: These results indicate that low-grade inflammation may play a role in the modulation of arterial BP relatively early in life.

Low-grade systemic inflammation and the risk of type 2 diabetes in obese children and adolescents.

BACKGROUND: There is growing evidence that low-grade systemic inflammation is closely involved in the pathogenesis of type 2 diabetes. OBJECTIVE: The aim of this study was to investigate the relationship between serum inflammatory markers and selected parameters known as risk factors of type 2 diabetes in obese children and adolescents. SUBJECTS AND METHODS: Fasting levels of C-reactive protein (CRP), fibrinogen (FB) interleukin-6 (IL-6), interleukin 1-beta (IL-1beta), glucose, insulin, total, HDL and LDL cholesterol, triglycerides, white blood cell count (WBC) and fasting glucose to insulin ratio (FGIR) were measured in 281 obese children and adolescents. Pearson's correlation was used for assessing the relationship between inflammatory markers and selected clinical parameters. RESULTS: Inflammatory markers correlated significantly with insulin resistance indices, HbA1c, lipid profile, hypertension, positive family history of type 2 diabetes, low physical fitness, and mixed high-fat and high-carbohydrate diet. CONCLUSIONS: Serum inflammatory markers were significantly correlated with most factors implicated in the development of type 2 diabetes. These data provide additional support for previously reported in adults relationship between subclinical inflammation and the risk of type 2 diabetes.

[Correlation between serum homocysteine levels and selected atherosclerosis risk factors in children and adolescents with simple obesity]. / Zaleznosc pomiedzy stezeniem homocysteiny a wybranymi czynnikami ryzyka miazdzycy u dzieci i mlodziezy z otyloscia prosta.

Homocysteine is known as an independent risk factor of atherosclerosis. The aim of this study was assessment of serum homocysteine concentrations in obese children and evaluation of possible relationship between homocysteine and risk factors of atherosclerosis. 498 children with simple obesity were included into our study. There was a significant correlation between serum homocysteine levels and both traditional and new risk factors of atherosclerosis. The issues confirm a necessity of evaluation serum homocysteine levels of obese children in estimation of cardiovascular disease risk.

Relation of acute-phase reaction and endothelial activation to insulin resistance and adiposity in obese children and adolescents.

OBJECTIVES: There is increasing evidence that an ongoing cytokine-induced acute-phase response is closely involved in the pathogenesis of type 2 diabetes and associated complications such as dyslipidemia and atherosclerosis. The aim of this study was to investigate the relationship of inflammation and endothelial activation with insulin resistance in childhood obesity. METHODS: Two hundred and eleven (122 boys) obese children and adolescents were examined. Fasting levels of ultra-sensitive C-reactive protein (CRP), fibrinogen (FB), interleukin-6 (IL-6), interleukin-1beta (IL-1beta), intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), von Willebrand factor (vWF), glucose, insulin, and HbA1c were determined. Insulin resistance was assessed by the homeostasis method. RESULTS: HOMA IR correlated significantly with all measures of adiposity as well as with majority of inflammation and endothelial dysfunction markers. After adjustment for age, gender, BMI and fat mass, the correlation with insulin resistance remained significant for CRP, ICAM-1 and von Willebrand factor. There was a trend for association between HOMA IR and IL-6 as well as HOMA IR and fibrinogen. CONCLUSION: Acute-phase reaction and endothelial activation correlate with insulin resistance in obese youth. It is possible that the cluster of these pro-atherogenic factors may contribute to the accelerated atherosclerosis in obese children.

Serum markers of inflammation and endothelial activation in children with obesity-related hypertension.

OBJECTIVES: It has been suggested that a rise in blood pressure (BP) causes low-grade inflammation of the endothelium which, in turn, may be responsible for further damage of endothelium and worsening of BP control. The aim of the study was to evaluate serum levels of inflammation and endothelial activation markers in children with obesity-related hypertension and normotensive controls in relation to other traditional risk factors of arterial hypertension. METHODS: Plasma insulin, glucose, C-reactive protein (CRP), fibrinogen (FB) interleukin-6 (IL-6), interleukin-1 beta (IL-1 beta), intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and lipids levels were determined in 50 children with obesity-related hypertension and 143 obese children with normal BP. Insulin resistance was assessed by the homeostasis model. RESULTS: Children with hypertension had significantly higher levels of all inflammatory markers as well as endothelial activation indices compared with normotensive subjects. In the stepwise regression model significant independent correlates for systolic BP were CRP, FB, VCAM-1, HOMA IR, LDL cholesterol and fat mass, whereas CRP, IL-6, ICAM-1, FB, LDL and HDL cholesterol were the determinants of diastolic BP in children with obesity-related hypertension. CONCLUSION: These results indicate that low-grade inflammation and endothelial dysfunction are closely involved in the pathogenesis of obesity-related hypertension relatively early in life.

Reversal of the sex difference in plasma leptin levels in obese children with impaired glucose tolerance.

INTRODUCTION: Basal leptin level has been demonstrated to correlate positively with many indices of obesity, as well as insulin resistance. However, to date, little is known about regulation of leptin in obese children with incipient glucose metabolic disorders. OBJECTIVE: The aim of this study was to define the precise influence of the glucose tolerance status on plasma leptin in obese boys and girls separately. MATERIAL AND METHODS: 70 obese children with impaired glucose tolerance (IGT) and well-matched 70 normal glucose-tolerant (NGT) subjects were examined. Fasting and 2-h post glucose load plasma glucose and insulin levels as well as fasting leptin levels were determined, apart from anthropometric measurements. RESULTS: Leptin levels were significantly lower in girls with IGT compared to NGT girl (17.7+/-6.5 microg/L vs. 23.1+/-7.7 microg/L; p<.001). No such difference was observed in boys. In a multiple regression analysis adjusting for age and adiposity, in the female group plasma glucose and insulin levels 2-h after glucose load were the best predictors of fasting plasma leptin (r=-0.49, p<.005 and r=0.34, p<.05; respectively). In boys, plasma insulin level 2-h after glucose load was the independent determinant of leptin (r=0.36, p<.05). CONCLUSION: The differences between regulation of leptin synthesis in girls and boys with simple obesity were found. The stimulatory effect of insulin on leptin synthesis was greater in girls with normoglycemia than in girls with impaired glucose tolerance.

Reversal of the sex difference in plasma leptin levels in obese children with impaired glucose tolerance.

INTRODUCTION: Basal leptin level has been demonstrated to correlate positively with many indices of obesity, as well as insulin resistance. However, to date, little is known about regulation of leptin in obese children with incipient glucose metabolic disorders. OBJECTIVE: The aim of this study was to define the precise influence of the glucose tolerance status on plasma leptin in obese boys and girls separately. MATERIAL AND METHODS: 70 obese children with impaired glucose tolerance (IGT) and well-matched 70 normal glucose-tolerant (NGT) subjects were examined. Fasting and 2-h post glucose load plasma glucose and insulin levels as well as fasting leptin levels were determined, apart from anthropometric measurements. RESULTS: Leptin levels were significantly lower in girls with IGT compared to NGT girl (17.7+/-6.5 microg/L vs. 23.1+/-7.7 microg/L; p<.001). No such difference was observed in boys. In a multiple regression analysis adjusting for age and adiposity, in the female group plasma glucose and insulin levels 2-h after glucose load were the best predictors of fasting plasma leptin (r=-0.49, p<.005 and r=0.34, p<.05; respectively). In boys, plasma insulin level 2-h after glucose load was the independent determinant of leptin (r=0.36, p<.05). CONCLUSION: The differences between regulation of leptin synthesis in girls and boys with simple obesity were found. The stimulatory effect of insulin on leptin synthesis was greater in girls with normoglycemia than in girls with impaired glucose tolerance.

[Immaturity or hypotrophy? The cord blood leptin levels in preterm and small-for-gestational age neonates]. / Niedojrzalosc czy niedozywienie? Poziom leptyny we krwi pepowinowej noworodków urodzonych przedwczesnie i z hipotrofia wewnatrzmaciczna.

OBJECTIVES: To assess cord blood leptin levels in preterm and small-for-gestational age neonates and determine whether fetal leptin levels correlate with selected clinical parameters associated with prematurity and undernutrition at birth. DESIGN: Study of preterm newborns (p-AGA; n = 31) and small-for-gestational age (t-SGA; n = 23) cases in a population of neonates born in Szczecin between September 2001 and June 2002. METHODS: Fetal cord blood was sampled after delivery. Leptin levels were measured by RIA. Anthropometric data (birth weight, birth length, head and chest circumferences, body mass index, Ponderal index) were also recorded. RESULTS: Cord blood leptin levels did not differ significantly between p-AGA and t-SGA neonates with similar birthweight. Among the two groups of newborns the correlations between fetal leptin and anthropometric data were only observed in p-AGAs, but not in t-SGA group. CONCLUSIONS: We suggest that cord blood leptin level depends on body mass rather than maturity of newborn. It is also hypothesized that leptin level in SGA neonates is determined by other than anthropometric parameters used in this study.