Overweight and obesity in children and adolescents are overwhelming problems in western countries. Adipocytes, far from being only fat deposits, are capable of endocrine functions, and the endocrine activity of adipose tissue, resumable in adipokines production, seems to be a key modulator of central nervous system function, suggesting the existence of an “adipo-cerebral axis.” This connection exerts a key role in children growth and puberty development, and it is exemplified by the leptin–kisspeptin interaction. The aim of this review was to describe recent advances in the knowledge of adipose tissue endocrine functions and their relations with nutrition and growth. The peculiarities of major adipokines are briefly summarized in the first paragraph; leptin and its interaction with kisspeptin are focused on in the second paragraph; the third paragraph deals with the regulation of the GH-IGF axis, with a special focus on the model represented by growth hormone deficiency (GHD); finally, old and new nutritional aspects are described in the last paragraph.

Background: Individuals with hyperinsulinemia may initially not meet any diagnostic criteria for metabolic syndrome, though displaying a higher risk of cardiovascular complications combined with obesity, diabetes, and hypertension. Aim: The main objective of our study was to assess the diagnostic accuracy of various cardiovascular risk indices in hyperinsulinemic children and adolescents; a secondary objective was to estimate the optimal cut-offs of these indices. Patients and methods: This retrospective single-center study was conducted on 139 patients aged 12.1 ± 2.9 years, managed for hyperinsulinism. Results: We found statistically significant differences in homeostasis model assessment of insulin resistance index (HOMA-IR), triglyceride glucose index (TyG), TyG-body mass index, visceral adiposity index, lipid accumulation product index, fatty liver index, and hepatic steatosis index. At the linear logistic regression assessment, we found that insulin growth factor-1 (IGF-1), HOMA-IR, and ALT/AST ratio were independently associated with confirmed hyperinsulinism. At the multivariate analysis, IGF-1 levels over 203 ng/mL and HOMA-IR higher than 6.2 were respectively associated with a 9- and 18-times higher odds ratio for hyperinsulinism. The other investigated parameters were not significantly related to hyperinsulinism, and could not predict either the presence of hyperinsulinemia or a subsequent cardiovascular risk in our patients. Conclusion: Commonly used indices of cardiovascular risk in adults cannot be considered accurate in confirming hyperinsulinism in children, with the exception of HOMA-IR. Further studies are needed to verify the usefulness of specific cardiovascular risk indices in hyperinsulinemic children and adolescents.

Background/Objectives: Growth in childhood and adolescence is influenced by a complex interaction of genetic, environmental, and hormonal factors, with growth hormone (GH) and insulin-like growth factor 1 (IGF-1) playing crucial roles in linear growth and development. However, chronic inflammation, often detected in situations like inflammatory bowel disease and juvenile idiopathic arthritis, can significantly disrupt the GH/IGF-1 axis, causing a relevant growth impairment. Methods: We conducted a retrospective review focusing on the role of cytokines in the GH-IGF-1 axis and growth. Results: Inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 have been shown to contribute to GH resistance through an array of mechanisms that involve the downregulation of GH receptors and alterations in IGF-1 metabolism. This disruption negatively impacts the growth plate, particularly by impairing chondrocyte proliferation and differentiation, which are essential for proper bone elongation. This review delves into the intricate relationship among growth, chronic inflammation, and GH-IGF-1 axis, emphasizing the contribution of inflammatory cytokines in modulating GH signaling. It also highlights how cytokines can interfere with the molecular pathways that regulate skeletal growth, ultimately leading to growth disturbances in children suffering from chronic inflammatory diseases. Conclusions: The findings underscore the importance of controlling inflammation in affected individuals to mitigate its detrimental effects on growth and ensure that children may reach their growth full potential.

Introduction: Central nervous system (CNS) infections represent some of the most critical pediatric health challenges, characterized by high mortality rates and a notable risk of long-term complications. Despite their significance, standardized guidelines for endocrinological follow-up of CNS infection survivors are lacking, leading to reliance on the expertise of individual centers and clinicians. Materials and Methods: Prospective monocentric observational study conducted at the Fondazione Policlinico Universitario Agostino Gemelli in Rome, Italy. It included patients with a history of CNS infection, admitted to various pediatric departments of the hospital. The participants were selected based on a coded diagnosis of CNS infection and had completed their follow-up at the Pediatric Endocrinology Day Hospital after October 2019. Results: Eighty participants were included, comprising 53 patients with a prior CNS infection and 27 healthy controls, with a median age of 7.4 years (range 3.6–12.3 years). Endocrinologic alterations were detected in 13 patients, with 8 cases in those who had meningitis, 4 in encephalitis survivors, and 1 in a patient with a cerebral abscess. Patients with a history of CNS infections were shorter compared with healthy controls (P = 0.027). Moreover, those who had meningitis exhibited an increased risk of developing epilepsy (P = 0.01), neurosensory disabilities (P = 0.034) and the need for ventriculoperitoneal shunt insertion (P = 0.006). Patients with bacterial CNS infections were more prone to neurosensory and endocrine dysfunctions compared to those with viral or other infections. Significant differences were observed in hormone levels between previously infected patients and controls, specifically in TSH (P < 0.001), ACTH (P = <0.001), and cortisol (P = 0.019). IGF-1 levels were considerably lower in the infection group, both in absolute terms and when adjusted for sex and age (P < 0.001). The regression analysis suggested that the reduction in IGF-1 was more pronounced the earlier the CNS infection occurred, irrespective of infection type. Conclusions: Our study found several endocrinologic imbalances in children who survived CNS infections.

Background: Complete androgen insensitivity syndrome (CAIS) is a rare disorder of sex development characterized by 46,XY karyotype and testes, yet presenting with a complete female phenotype, which is related to mutations in the androgen receptor (AR) gene. Case presentation: We herein present the case of a 14-year-old adolescent with primary amenorrhea and suspected delayed puberty whose diagnostic journey led to the identification of CAIS through the demonstration of a novel AR variant (c.159_207del). Case-based review: Our report encompasses the complexity of CAIS management, focusing on the risk of malignancy, surveillance options, hormone replacement therapy, timing of an eventual gonadectomy, and the psychosocial impact of such a diagnosis. An algorithm has been formulated for the management of CAIS starting in adolescence, highlighting the conservative approach for those patients unwilling to undergo gonadectomy. Conclusions: Primary amenorrhea and delay in puberty development may provide clues, ultimately leading to a diagnosis of CAIS. This review emphasizes the cruciality of a multidisciplinary approach in managing patients with CAIS, needing for an individualized care to optimize the overall outcome.

Background/Objectives: Hypothyroidism can profoundly affect growth, particularly if it insidiously arises during early childhood. Congenital hypothyroidism is now detected through newborn screening, significantly improving the overall growth outcomes of these children. Conversely, acquired hypothyroidism often results in delayed somatic growth and shorter stature, with many affected children initially remaining non-symptomatic. The main objective of this review is to summarize the current knowledge about the impacts of acquired hypothyroidism on children’s growth outcomes. Methods: We performed a literature review to analyze growth and final height in children with acquired hypothyroidism, matching the following keywords: “hypothyroidism & growth”, “hypothyroidism & height”, “hypothyroidism & stature”, “hypothyroidism & development”, “hypothyroidism & auxological parameters”. We reviewed each article that met the eligibility criteria, and after a thorough selection, we included 16 studies. Results: Growth arrest is frequently noted as a symptom in hypothyroidic children, with substantial portions of affected children presenting below the third percentile for height. The timing of diagnosis significantly influences growth outcomes: those diagnosed during puberty tend to experience less catch-up growth due to accelerated skeletal maturation. Even if thyroxine replacement can induce rapid catch-up growth, it may be incomplete if treatment begins during puberty or if there is a markedly prolonged deficiency of thyroid hormones. While levothyroxine therapy typically results in some degree of catch-up growth, many children do not reach their expected genetic height. Conclusions: This review highlights the necessity of both early diagnosis and treatment of acquired hypothyroidism. Even if many children show improvements in height velocity post-treatment, the complete normalization of growth may remain elusive.