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BackgroundChildren born from mothers who underwent bariatric surgery were found to have an improved lipid profile and lower CRP levels compared to siblings born before surgery. We hypothesized that surgery before pregnancy might also influence endothelial function in the offspring.MethodsBlood sample analysis, blood pressure (BP) measurement, and peripheral arterial tonometry (PAT) were performed in 142 children (median age 10.5 years), either born from mothers who underwent bariatric surgery (BS) before pregnancy (n = 36) from mothers with overweight/obesity (OW/OB) (n = 71) or from normal weight (NW) mothers (n = 35), allowing the determination of the Reactive Hyperemia Index (RHI) in 111 children.ResultsChildren of the BS group had a higher diastolic blood pressure SDS and a lower RHI compared to the children of the OW/OB and NW group (1.32 versus 1.37 in OW/OB and 1.70 in NW; p = 0.004). After log transformation and correction for age, weight SDS, BMI SDS, body fat percentage, and diastolic BP SDS, RHI was comparable between the groups.ConclusionsChildren of mothers who underwent bariatric surgery before pregnancy do not have a disturbed endothelial function before puberty, when their increased diastolic BP and degree of adiposity is taken into account.ImpactChildren born after maternal bariatric surgery have a higher diastolic blood pressure without impaired endothelial function.To our knowledge, this is the first study that investigates the vascular function of children based on maternal characteristics during pregnancy.Adult offspring of mothers with obesity during pregnancy have an increased cardiovascular mortality. Since we cannot demonstrate a childhood-onset primary vascular dysfunction, this cardiovascular vulnerability might be more related to the hypertension and body adiposity. Thus, more emphasis should be made on the prevention of obesity and hypertension in the offspring at risk for development of obesity.

Background The alarming trend of paediatric obesity deserves our greatest awareness to hinder the early onset of metabolic complications impacting growth and functionality. Presently, insight into molecular mechanisms of childhood obesity and associated metabolic comorbidities is limited. Main body of the abstract This systematic review aimed at scrutinising what has been reported on putative metabolites distinctive for metabolic abnormalities manifesting at young age by searching three literature databases (Web of Science, Pubmed and EMBASE) during the last 6 years (January 2015–January 2021). Global metabolomic profiling of paediatric obesity was performed (multiple biological matrices: blood, urine, saliva and adipose tissue) to enable overarching pathway analysis and network mapping. Among 2792 screened Q1 articles, 40 met the eligibility criteria and were included to build a database on metabolite markers involved in the spectrum of childhood obesity. Differential alterations in multiple pathways linked to lipid, carbohydrate and amino acid metabolisms were observed. High levels of lactate, pyruvate, alanine and acetate marked a pronounced shift towards hypoxic conditions in children with obesity, and, together with distinct alterations in lipid metabolism, pointed towards dysbiosis and immunometabolism occurring early in life. Additionally, aberrant levels of several amino acids, most notably belonging to tryptophan metabolism including the kynurenine pathway and its relation to histidine, phenylalanine and purine metabolism were displayed. Moreover, branched-chain amino acids were linked to lipid, carbohydrate, amino acid and microbial metabolism, inferring a key role in obesity-associated insulin resistance. Conclusions This systematic review revealed that the main metabolites at the crossroad of dysregulated metabolic pathways underlying childhood obesity could be tracked down to one central disturbance, i.e. impending insulin resistance for which reference values and standardised measures still are lacking. In essence, glycolytic metabolism was evinced as driving energy source, coupled to impaired Krebs cycle flux and ß-oxidation. Applying metabolomics enabled to retrieve distinct metabolite alterations in childhood obesity(-related insulin resistance) and associated pathways at early age and thus could provide a timely indication of risk by elucidating early-stage biomarkers as hallmarks of future metabolically unhealthy phenotypes.

Up to 80% of children/adolescents with Graves’ disease (GD) may require second-line treatment with either surgery or radioactive iodine (RAI) therapy after treatment with antithyroid drugs. These interventions aim to induce permanent hypothyroidism, but are not always successful. We aimed to evaluate the initial success rate (within the first year) of RAI treatment and its determining factors as second-line treatment in teenagers with GD. We also assessed the tolerability of RAI therapy and the onset speed of RAI-induced hypothyroidism. We conducted a retrospective chart review of children < 18 years treated with RAI (scaled fixed dose) for GD between January 2007 and December 2022 at the UZ Brussels. Fourteen teenagers treated with RAI were identified. Their ages at time of treatment ranged from 9.8 to 17.3 years, with administered I131 doses between 5.8 and 15.0mCi (median 7.9mCi). All but two patients responded within six months. Thyroxine treatment was started between 4 and 14 weeks (median 9 weeks) after RAI therapy. The time to thyroxine substitution correlated positively with age (Rho = 0.498; p  = 0.099) and total I131-dose (Rho = 0.582; p  = 0.047). One patient experienced transient RAI induced sialadenitis. None of the patients relapsed during a follow-up period of 1.2 to 13 years. A cure rate of 86% was observed in GD teenagers receiving a second-line RAI treatment, with no major complications. Most patients became hypothyroid within three months, underscoring the importance of early thyroid function monitoring.

A fraction of children with obesity have increased serum cortisol levels. In this study, we describe the clinical characteristics of obese children and adolescents with elevated morning serum cortisol levels and the relationship between the cortisol levels and components of the metabolic syndrome. Retrospective medical record review study of children aged 4 to 18 years with overweight or obesity seen for obesity management in the Pediatric Obesity Clinic of the UZ Brussel between 2013 and 2015. A total of 234 children (99 boys and 135 girls) with overweight (BMI z-score > 1.3) without underlying endocrine or genetic conditions were included. Mean (SD) age was 10.1 (2.8) years, BMI SD-score 2.5 (0.6), and body fat percentage 37% (7.9). Serum fasting cortisol levels were elevated (>180 [mu]g/L) in 49 children, normal (62-180 [mu]g/L) in 168, and decreased (<62 [mu]g/L) in 12. Serum fasting cortisol was not significantly correlated with gender, age, or degree of adiposity. But correlated significantly with fasting glucose (R.sub.s = 0.193; p < 0.005), triglycerides (R.sub.s = 0. 143; p < 0.05), fibrinogen (R.sub.s = 0.144; p < 0.05) and leptin levels (R.sub.s = 0.145; p < 0.05). After adjustment for serum insulin and leptin, the correlation between serum cortisol and fasting glucose remained significant. Elevated morning serum cortisol levels were found in 20% of overweight or obese children and adolescents, irrespective of the degree of adiposity, and were associated with higher fasting glucose, irrespective of underlying insulin resistance. The long-term cardiometabolic consequences of hypercortisolemia in childhood obesity needs further study.

Klinefelter syndrome (KS; 47,XXY) affects 1–2 in 1000 males. Most men with KS suffer from an early germ cell loss and testicular fibrosis from puberty onwards. Mechanisms responsible for these processes remain unknown. Previous genomics studies on testis tissue from men with KS focused on germ cell loss, while a transcriptomic analysis focused on testicular fibrosis has not yet been performed. This study aimed to identify factors involved in the fibrotic remodelling of KS testes by analysing the transcriptome of fibrotic and non-fibrotic testicular tissue. RNA sequencing was performed to compare the genes expressed in testicular samples with (KS and testis atrophy) and without (Sertoli cell-only syndrome and fertile controls) fibrosis (n = 5, each). Additionally, differentially expressed genes (DEGs) between KS and testis atrophy samples were studied to reveal KS-specific fibrotic genes. DEGs were considered significant when p < 0.01 and log2FC > 2. Next, downstream analyses (GO and KEGG) were performed. Lastly, RNA in situ hybridization was performed to validate the results. The first analysis (fibrotic vs non-fibrotic) resulted in 734 significant DEGs (167 up- and 567 down-regulated). Genes involved in the extracellular structure organization (e.g. VCAM1 ) were found up-regulated. KEGG analysis showed an up-regulation of genes involved in the TGF-β pathway. The KS vs testis atrophy analysis resulted in 539 significant DEGs (59 up- and 480 down-regulated). Chronic inflammatory response genes were found up-regulated. The overlap of X-linked DEGs from the two analyses revealed three genes: matrix-remodelling associated 5 ( MXRA5 ), doublecortin ( DCX ) and variable charge X-Linked 3B ( VCX3B ). RNA in situ hybridization showed an overexpression of VCAM1 , MXRA5 and DCX within the fibrotic group compared with the non-fibrotic group. To summarize, this study revealed DEGs between fibrotic and non-fibrotic testis tissue, including VCAM1 . In addition, X-linked fibrotic genes were revealed, e.g.  MXRA5, DCX and VCX3B . Their potential role in KS-related testicular fibrosis needs further study.

ObjectiveThyroid hormones are essential for normal brain development. The aim of this study is to assess if high concentration of thyroid stimulating hormone (TSH) that is below the clinical threshold (5–15 mIU/L) at neonatal screening is linked to psychomotor development impairments in the offspring at preschool age.DesignA total of 284 Belgian preschool children 4–6 years old and their mothers were included in the study. The children were randomly selected from the total list of neonates screened in 2008, 2009 and 2010 by the Brussels newborn screening centre. The sampling was stratified by gender and TSH range (0.45–15 mIU/L). Infants with congenital hypothyroidism (>15 mIU/L), low birth weight and/or prematurity were excluded. Psychomotor development was assessed using the Charlop-Atwell scale of motor coordination. The iodine status of children was determined using median urinary iodine concentration. Socioeconomic, parental and child potential confounding factors were measured through a self-administered questionnaire.ResultsTSH level was not significantly associated with total motor score (average change in z-score per unit increase in TSH is 0.02 (−0.03, 0.07), p=0.351), objective motor score (p=0.794) and subjective motor score (p=0.124). No significant associations were found using multivariate regression model to control confounding factors.ConclusionsMild thyroid dysfunction in the newborn—reflected by an elevation of TSH that is below the clinical threshold (5–15 mIU/L)—was not associated with impaired psychomotor development at preschool age.

Childhood obesity, affecting 29% of 7–9-year-olds across 33 European countries, is a significant public health challenge. Its persistence into adulthood poses grave health risks influenced by genetic, environmental, and socio-economic factors. Belgium introduced a new care pathway in December 2023, based on the Edmonton Obesity Staging System for Pediatrics (EOSS-P), addressing four health domains and staging obesity severity. This pathway operates across three levels: primary care physicians, Paediatric Multidisciplinary Obesity Management Centres (PMOCs), and Centers of Expertise for Paediatric Obesity Management (CEPOs). Each stage of EOSS-P demands tailored interventions. Early stages involve dietary interventions, physical activity promotion, and behavior modifications. As obesity severity progresses, treatments intensify, encompassing psychological support, anti-obesity medications, and, in some cases, bariatric surgery. Throughout these stages, the involvement of multidisciplinary teams is crucial, emphasizing family-based approaches and continuous monitoring. This article provides detailed guidelines for healthcare professionals, delineating interventions and recommendations tailored to each EOSS-P stage. It emphasizes a holistic approach that extends beyond BMI-based diagnosis, promoting personalized care and prompt escalations between care levels, thereby ensuring optimal management of childhood obesity. This comprehensive framework aims to address the complexities of childhood obesity, emphasizing the importance of timely and targeted interventions for better health outcomes.

Background and aimA fraction of children with obesity have increased serum cortisol levels. In this study, we describe the clinical characteristics of obese children and adolescents with elevated morning serum cortisol levels and the relationship between the cortisol levels and components of the metabolic syndrome.MethodsRetrospective medical record review study of children aged 4 to 18 years with overweight or obesity seen for obesity management in the Pediatric Obesity Clinic of the UZ Brussel between 2013 and 2015.ResultsA total of 234 children (99 boys and 135 girls) with overweight (BMI z-score > 1.3) without underlying endocrine or genetic conditions were included. Mean (SD) age was 10.1 (2.8) years, BMI SD-score 2.5 (0.6), and body fat percentage 37% (7.9). Serum fasting cortisol levels were elevated (>180 μg/L) in 49 children, normal (62-180 μg/L) in 168, and decreased (<62 μg/L) in 12. Serum fasting cortisol was not significantly correlated with gender, age, or degree of adiposity. But correlated significantly with fasting glucose (Rs = 0.193; p < 0.005), triglycerides (Rs = 0. 143; p < 0.05), fibrinogen (Rs = 0.144; p < 0.05) and leptin levels (Rs = 0.145; p < 0.05). After adjustment for serum insulin and leptin, the correlation between serum cortisol and fasting glucose remained significant.ConclusionElevated morning serum cortisol levels were found in 20% of overweight or obese children and adolescents, irrespective of the degree of adiposity, and were associated with higher fasting glucose, irrespective of underlying insulin resistance. The long-term cardiometabolic consequences of hypercortisolemia in childhood obesity needs further study.

The main objective of the study was to investigate the effect of MID during late pregnancy, assessed by the thyroid-stimulating hormone (TSH) concentration at neonatal screening, on cognitive development of preschool children. A retrospective cohort study including 311 Belgian preschool children of 4–6 years old was conducted. Children were selected at random from the total list of neonates screened in 2008, 2009, and 2010 by the Brussels new-born screening center. Infants with congenital hypothyroidism, low birth weight, and/or prematurity were excluded from the selection. The selected children were stratified by gender and TSH-range (0.45–15 mIU/L). Cognitive abilities were assessed using Wechsler Preschool and Primary Scale of Intelligence—third edition. In addition, several socioeconomic, parental, and child confounding factors were assessed. Neonatal TSH concentration—a surrogate marker for MID—was not associated with Full Scale and Performance IQ scores in children. Lower Verbal IQ scores were found in children with neonatal TSH values comprised between 10–15 mIU/L compared to lower TSH levels in univariate analysis but these results did not hold when adjusting for confounding factors. Current levels of iodine deficiency among pregnant Belgian women may not be severe enough to affect the neurodevelopment of preschool children.

The STRONGkids is a nutritional screening tool for hospitalized children, which was found to predict a negative weight for height (WFH) standard deviation score (SDS) and a prolonged hospital length of stay (LOS) in a Dutch population of hospitalized children. This study aimed to test the ease of use and reproducibility of the STRONGkids, and to confirm its concurrent and prospective validity in a Belgian population of hospitalized children. Reproducibility was tested in a cohort of 29 hospitalized children in a tertiary center and validity was tested in 368 children (105 hospitalized in a tertiary and 263 in three secondary hospitals) ages between 0.08 and 16.95 y (median 2.2 y). Substantial intrarater (κ = 0.66) and interrater (κ = 0.61) reliabilities were found between observations. STRONGkids scores correlated negatively with WFH SDS of the patients (ρ = –0.23; P < 0.01; odds ratio [OR], 2.47; 95% confidence interval [CI], 1.11–5.49; P < 0.05). It had a sensitivity and negative predictive value (NPV) of respectively 71.9% and 94.8% to identify acutely undernourished children. STRONGkids did not correlate with weight loss during hospitalization, but correlated with LOS (ρ = 0.25; OR 1.96; 95% CI, 1.25–3.07; both P < 0.01) and the set-up of a nutritional intervention during hospitalization (OR, 18.93; 95% CI, 4.48–80.00; P < 0.01). The sensitivity and NPV to predict a LOS ≥ 4 d were respectively 62.6% and 72%, and respectively 94.6% and 98.9% to predict a nutritional intervention. STRONGkids is an easy-to-use screening tool. Children classified as “low risk” have a 5% probability of being acutely malnourished, with only a 1% probability of a nutritional intervention during hospitalization.