Context Since the COVID-19 outbreak, the number of girls with suspected precocious puberty has increased. Objective To compare the incidence of idiopathic central precocious puberty (ICPP) during COVID-19 with that of the previous 4 years. Methods Anthropometric, biochemical, and radiological parameters were collected between January 2016 and June 2021 from 133 girls who met the Rapidly Progressive ICPP criteria (RP-ICPP). Results We found a higher incidence of RP-ICPP between March 2020 and June 2021 (group 2) compared with January 2016 through March 2020 (group 1) (53.5% vs 41.1%); 2021 showed the highest annual incidence (P < .05). Group 1 and group 2 differed in age at diagnosis (7.96 ± 0.71 vs 7.61 ± 0.94; P < .05), mean Tanner stage (2.86 ± 0.51 vs 2.64 ± 0; P < .05), and in the time between the appearance of thelarche and diagnosis (0.93 ± 0.75 vs 0.71 ± 0.62 years, P < .05). There was an increase in the number of girls aged 8 years was found in group 1 (42 in group 1 vs 20 in group 2, P < 0.05). Overall body mass index SD score showed higher values ​​in group 2 (1.01 ± 1.23 vs 0.69 ± 1.15; P = .18), which spent an average of 1.94 ± 1.81 hours per day using electronic devices; 88.5% of this group stopped any physical activity. Conclusions A spike in new diagnoses of idiopathic (1.79-fold higher) and RP-CPP coincided with the COVID-19 pandemic. The incidence of RP-ICPP was 1.3-fold higher during COVID-19 with a trend toward an increase in body mass index SD score. The expanding use of digital devices and the reduction of daily physical activity represent possible risk factors.

Context Rapid-onset obesity with central hypoventilation, hypothalamic dysfunction, and autonomic dysregulation with neural crest tumors (ROHHAD-NET) syndrome pathophysiology remains elusive. Acquired neuroimmunological dysfunction has been proposed as a possible pathogenetic pathway. Objective The aim of our study was to characterize lymphocyte subpopulations subsets in peripheral blood (PB) and to evaluate a panel of proinflammatory cytokines/chemokines in ROHHAD(NET) patients vs controls. Methods We included 11 ROHHAD(NET) patients, 7 ROHHAD and 4 ROHHAD-NET, selected by clinical criteria. Controls were 11 simple obese children, matched for age and sex. Flow cytometric analysis and enzyme-linked immunosorbent assay were performed on PB and serum samples of the 2 groups. Results Analysis revealed that T lymphocytes are significantly increased in ROHHAD(NET) patients (P = .04) with a prevalence of CD4-T cells (P = .03) and a lower number of activated CD8-T cells (P = .02). With regard to regulatory subset, patients displayed increased regulatory B cells (P = .05) and type-1 regulatory T cells (P = .03). With regard to CD8-T cells, a lower number of T effector memory was observed (P = .02). In contrast, among CD4-T cells, we found a higher number of T naive (P = .04) and T effector (P = .0008). Interleukin-8 (IL-8) levels and monocyte chemotactic protein-1 were increased in patients vs controls (P = .008 and P = .01, respectively). Furthermore, IL-8 levels were higher in the subgroup with neural tumor (P = .0058) (ROHHAD-NET) than in patients without neural tumor (ROHHAD). Soluble HLA-G was significantly lower in patients vs controls (P = .03). Conclusion Our findings contribute to support the hypothesis of immune dysregulation, which may underlie this complex, often fatal disease. Because ROHHAD(NET) syndrome is an ultra-rare disease, multicentric studies are needed to improve the effect of our data in the management of this condition.

Background: Foramen magnum stenosis (FMS) is a serious complication in children with achondroplasia that may necessitate cervicomedullary decompression (CMD). It is unclear how FMS and CMD influence growth in these children. This study aimed to assess the effects of FMS and CMD on the growth of children with achondroplasia. Methods: Eighty-seven children (45 males, 42 females) with achondroplasia, aged 4 to 6 years, were evaluated. Height, weight, head circumference, and body mass index were expressed as standard deviation scores (SDS) according to Merker et al., while sitting height SDS was derived using Tanner’s methods. FMS was graded on magnetic resonance imaging using Fornarino’s score. Results: Fifty-two patients (26 males, 26 females) underwent CMD at a median age of 0.95 years (IQR 0.52;1.50). Of these, 28 (53.8%) were under one year old at the time of CMD, with a median age of 0.6 years (0.4;0.7). The remaining 24 children had CMD after their first year of life, with a median age of 1.6 years (1.3;2.8). The median age at anthropometric assessment was 5.16 years (4.74;5.50). Children who underwent CMD showed significantly lower median height SDS, particularly among males compared to females (p=0.026). Conclusions: Impaired growth in children with foramen magnum stenosis requiring cervicomedullary decompression may primarily reflect greater disease severity, while the potential contribution of surgery remains uncertain.

Background/Objectives. Pediatric brain tumor survivors (PBTS) are at increased risk of cardiometabolic complications due to tumor- and treatment-related hypothalamic–pituitary (HP) damage and adverse body composition. We evaluated associations of the Single-Point Insulin Sensitivity Estimator (SPISE) with central adiposity, DXA-derived body composition, metabolic abnormalities, and HP involvement. Methods. In this retrospective study, 119 PBTSs (median age, 12.7 years; median time since therapy, 2.4 years) were evaluated. SPISE, BMI, waist-to-height ratio (WHtR), DXA-derived fat-to-lean ratio (FLR), and metabolic syndrome (MetS) were assessed. Multivariable logistic regression evaluated the association between SPISE and central adiposity. Exploratory receiver operating characteristic analyses compared the discriminatory performance of SPISE, BMI-SDS, HOMA-IR, and FLR. Results. Central adiposity was present in 58.8% of participants, whereas BMI-defined obesity occurred in 21.8%. Lower SPISE values were associated with central adiposity, obesity, MetS, HP damage, and multiple pituitary hormone deficiencies (all p < 0.05). SPISE declined across pubertal stages and remained associated with central adiposity after adjustment for age and selected HP variables (OR = 0.58, 95% CI 0.46–0.73). SPISE showed good discrimination of central adiposity (AUC = 0.81), with an exploratory, cohort-derived threshold of 7.82; FLR provided complementary information on body composition. Conclusions. Central adiposity was common and not fully captured by BMI-defined obesity. Lower SPISE values were associated with concurrent anthropometric and metabolic abnormalities, while DXA-derived FLR added descriptive information on body composition. Whether these indices improve cardiometabolic risk stratification beyond conventional measures requires prospective investigation.