The objective is to assess the circulating lipidome of children with obesity before and after lifestyle intervention and to compare the data to the circulating lipidome of adults with obesity before and after bariatric surgery. Ten pediatric (PE) and thirty adult (AD) patients with obesity were prospectively recruited at a referral single center. The PE cohort received lifestyle recommendations. The AD cohort underwent bariatric surgery. Clinical parameters and lipidome were analyzed in serum before and after six months of metabolic intervention. The abundance of phosphatidylinositols in the PE cohort and phosphatidylcholines in the AD significantly increased, while O-phosphatidylserines in the PE cohort and diacyl/triacylglycerols in the AD decreased. Fifteen lipid species were coincident in both groups after lifestyle intervention and bariatric surgery. Five species of phosphatidylinositols, sphingomyelins, and cholesteryl esters were upregulated. Eight species of diacylglycerols, glycerophosphoglycerols, glycerophosphoethanolamines, and phosphatidylcholines were downregulated. Most matching species were regulated in the same direction except for two phosphatidylinositols: PI(O-36:2) and PI(O-34:0). A specific set of lipid species regulated after bariatric surgery in adult individuals was also modulated in children undergoing lifestyle intervention, suggesting they may constitute a core circulating lipid profile signature indicative of early development of obesity and improvement after clinical interventions regardless of individual age.

Since the first case of dextranomer/hyaluronic acid (Dx/HA) implant calcification in 2008, concern about the long-term sequelae of Dx/HA injection has been growing. According to previous reports, the incidence of Dx/HA calcification 4 years after injection would be around 2%. The primary aim was to estimate the incidence of Dx/HA implant calcification after endoscopic treatment of vesicoureteral reflux in pediatric patients. Secondary objectives were to establish risk factors and to perform a survival analysis after Dx/HA injection. Patients undergoing Dx/HA endoscopic injection from 2007 to 2014 were prospectively registered. The database included clinical, surgical and radiological outcomes. Patients that showed Dx/HA implant calcification during follow-up were compared to those who did not. Univariable and survival statistical analyses were performed. 30 implants calcified over 355 ureters endoscopically treated. Age at first treatment was lower in patients with implant calcification (2.4 ± 1.3 years vs 3.6 ± 2.5 years; p < 0.005). The risk of implant calcification was 8.45% (95% CI: 5.96-11.85%). Median follow-up was 7.6 years (IQR: 5.2-9.5). The incidence rate was 12.06 cases per 1000 ureters-year. The period of highest hazard of implant calcification was between 3 and 5 years after injection. The only risk factor related to implant calcification was the age at first injection: relative risk of implant calcification was 4.4 (95% CI: 1.6 to 12.4; p = 0.002) for patients first treated before the age of 3.5 years. The risk and the incidence rate of Dx/HA implant calcification were higher than previous data. The period of highest hazard and detection of implant calcification were consistent with previous reports. Patients first treated before the age of 3.5 had shorter survival time without implant calcification. These are the first data about risk factors and survival function of Dx/HA implant calcification. However, our conclusions about the clinical significance of Dx/HA implant calcification were limited because the patients with implant calcification were asymptomatic. Further studies with larger sample and longer follow-up should confirm the clinical significance and life-long tendency of Dx/HA implant calcification. The risk and the incidence rate of Dx/HA implant calcification were higher than expected. The hazard of calcification was higher between 3 and 5 years after injection. The risk was especially higher in patients treated before the age of 3.5. Caution should be taken not to confuse implant calcifications with ureteric stones. A 5-year follow-up would set a better understanding of the actual incidence and clinical significance of implant calcification.

Childhood obesity is associated with lifelong metabolic risk, yet depot-specific alterations in adipose tissue metabolism during early life remain poorly understood. This study aimed to characterize the metabolic differences between subcutaneous (sWAT) and visceral (vWAT) white adipose tissue in pediatric obesity using untargeted metabolomics. Adipose tissue samples were collected from 12 children with overweight/obesity (OW/OB) and 18 who were of normal weight (NW). Untargeted metabolomics was performed using capillary electrophoresis-mass spectrometry to profile polar metabolites in sWAT and vWAT, and free fatty acids (FFAs) were analyzed using liquid chromatography-mass spectrometry. Comparison of children with OW/OB vs NW revealed pronounced depot-specific heterogeneity. vWAT in children with OW/OB exhibited 24 significantly altered metabolites compared with NW controls. This visceral profile was characterized by elevated ketone bodies (3-hydroxybutyrate and acetoacetic acid), tricarboxylic acid cycle intermediates (citric and pyruvic acids), and long-chain FFAs (palmitic and oleic acids). Concurrently, amino acid imbalances, specifically elevated leucine and arginine but reduced histidine and carnosine, suggested heightened mitochondrial stress and inflammation. In contrast, sWAT from children with OW/OB showed fewer variations (12 metabolites), defined primarily by elevated glutamate, leucine, and short-chain FFAs, reflecting a milder metabolic disruption. Direct comparison between depots revealed that vWAT was enriched in amino acids and carnitine, while sWAT showed relatively higher levels of glycolytic and ketone body intermediates in NW conditions. Depot-specific metabolic differences are evident in pediatric obesity. vWAT in children with OW/OB displays a metabolic profile consistent with heightened lipotoxicity and mitochondrial stress, whereas sWAT exhibits fewer, less pronounced metabolic differences.