Bibliometric and LDA analysis of the correlation between childhood obesity and precocious puberty (2005-2025).

KBG syndrome (KBGS) is a rare autosomal dominant neurodevelopmental disorder caused by heterozygous pathogenic variants in the gene (OMIM 611192), located on chromosome 16q24, caused by haploinsufficiency of , a gene that plays a critical role in transcriptional regulation and chromatin remodeling (, ). Herrmann proposed that the name KBG represents the initials of the surnames of the first three unrelated families diagnosed with this disorder. The three letters correspond to the last names of the affected index families, commonly denoted in the literature as K, B, and G, and, as reported in 1975 the actual surnames behind the letters remain undisclosed in the public literature (). KBGS is characterized by a recognizable constellation of clinical features, including intellectual disability, developmental delay, short stature, macrodontia, and distinctive craniofacial dysmorphism such as a round face and brachycephaly. Skeletal anomalies involving the spine, ribs, and limbs are also reported (, ). In addition to structural abnormalities, a distinct neurobehavioral profile has been increasingly recognized, including features of autism spectrum disorder, attention deficits, and behavioral disturbances (). Neuroimaging findings may include cerebellar vermis hypoplasia, corpus callosum abnormalities, brain calcifications, and optic nerve hypoplasia, reflecting the broad neurological involvement associated with dysfunction (). Phenotypic expression in KBG syndrome appears to evolve with age, with some features becoming more recognizable over time while others may diminish or normalize, potentially contributing to delayed diagnosis ().