Background: Gonadotropin-releasing hormone agonist (GnRHa) is the gold standard in the treatment of Central Precocious Puberty (CPP) with progressive puberty and accelerative growth. However, GnRHa treatment is reported to result in growth deceleration and prevents growth plate development which leads to a reduction in height velocity. Stanozolol (ST) has been used to stimulate growth in patients with delayed growth and puberty, nevertheless, the effects and mechanisms of ST on CPP with GnRHa treatment are currently unclear.Methods and Results: In the current study, we recorded the following vital observations that provided insights into ST induced chondrogenic differentiation and the maintenance of normal growth plate development: (1) ST efficiently prevented growth deceleration and maintained normal growth plate development in rats undergoing GnRHa treatment; (2) ST suppressed the inhibitory effect of GnRHa to promote chondrogenic differentiation; (3) ST induced chondrogenic differentiation through the activation of the JNK/c-Jun/Sox9 signaling pathway; (4) ST promoted chondrogenic differentiation and growth plate development through the JNK/Sox9 signaling pathway in vivo.Conclusions: ST mitigated the inhibitory effects of GnRHa and promoted growth plate development in rats. ST induced the differentiation of chondrocytes and maintained normal growth plate development through the activation of JNK/c-Jun/Sox9 signaling. These novel findings indicated that ST could be a potential agent for maintaining normal bone growth in cases of CPP undergoing GnRHa treatment.

Background: Overweight and obesity in children and adolescents have emerged as significant public health issues in China. This study aims to analyze the characteristics of serum uric acid (SUA) metabolism in overweight and obese children and adolescents in South China, exploring its associations with metabolic parameters. Methods: A single-center retrospective study was conducted, involving children and adolescents aged 3 to 18 years diagnosed with overweight and obesity. Spearman correlation coefficients were calculated to evaluate relationships between SUA and other metabolic parameters. Multivariate linear regression analyses were conducted to adjust for confounders. Comparisons were made between participants with hyperuricemia and those with normal SUA levels, and logistic regression analyses were conducted to adjust for confounders. Hierarchical clustering was performed to explore the relationships among the parameters. A dendrogram was generated to visualize the cluster structure. Results: Among 172 participants (96 males, 76 females), the mean age was 10.88± 2.70 years. The prevalence of hyperuricemia was 36.30%, with 38.46% in males and 33.82% in females. Every 1 kg/m² increase in body mass index was associated with a 7.156 μmol/L increase in SUA and an 8.9% increase in hyperuricemia risk. Significant correlations were observed between SUA levels and insulin resistance (HOMA-IR), fasting insulin, and high-density lipoprotein cholesterol. Hierarchical clustering analysis revealed two distinct clusters. One cluster includes SUA along with insulin resistance and lipid metabolism parameters, while the other comprises obesity metrics, urinary microalbumin, and blood glucose. Conclusion: The findings show a high prevalence of hyperuricemia in overweight and obese children and adolescents, linked to insulin resistance and dyslipidemia. These results highlight the need for early screening and targeted interventions to improve metabolic health outcomes in this vulnerable population.

Proteus syndrome (PS) is an exceptionally rare disorder characterized by asymmetric and disproportionate overgrowth of connective tissues. We report the case of an 8‐year‐old female presenting with irregular cranial protrusion, bilateral supraorbital ridge enlargement, overgrowth of the right hand and left foot, and a pelvic MRI revealing an ovarian tumor. Initially, the patient was suspected of having Maffucci syndrome (MS) upon admission. Genetic analysis of a lesion sample from the fifth toe of the left foot identified a heterozygous point mutation, 49G > A (p.Glu17Lys), in the AKT1 gene. The patient met the clinical‐molecular diagnostic criteria established by Leslie G. Biesecker, scoring 15 points, thereby confirming the diagnosis of AKT1‐related PS. This case report contributes to the enhanced understanding of PS diagnosis associated with AKT1 mutations.