Autologous Fat Transfer Procedure Complications in Four Emergency Departments in Miami, Florida.

Obesity is a multifactorial disease caused by the interaction of genetic susceptibility and environmental factors. Despite the prevalence of polygenic variation, its impact is minimal. Conversely, rare pathogenic variants in a single gene with a high magnitude of effect account for approximately 5% of cases of childhood obesity (El‐Sayed Moustafa and Froguel ). On a global scale, childhood obesity has emerged as the most prevalent form of malnutrition, surpassing hunger as the predominant health concern. According to the United Nations International Children's Emergency Fund (UNICEF) 2025 report, the number of obese children worldwide has reached 188 million, surpassing the number of underweight children for the first time in history. In certain Pacific Island countries, including Niue, the prevalence of childhood obesity has reached alarming levels, with rates as high as 38%. In China, the proportion of overweight and obese children and adolescents has also surpassed 30%. Childhood obesity is a grave public health concern, exerting a profound and multifaceted detrimental effect on physical and mental health. This phenomenon is not merely a concern during childhood; it also has ramifications for the quality of life throughout one's lifetime. It is noteworthy that up to 80% of obese adolescents will carry their obesity status into adulthood, thereby significantly increasing their risk of developing various chronic diseases. Clinically, patients with monogenic obesity develop excessive appetite and overeating symptoms in early childhood, primarily due to mutations in the genes encoding enzymes or receptors in the leptin‐melanocortin (Lep‐melanocortin) pathway, which plays a pivotal role in regulating satiety and maintaining energy balance in the body. The most prevalent of these mutations occurs in the gene encoding the melanocortin‐4 receptor (MC4R) (Farooqi et al. ; Farooqi and O'Rahilly ). Individuals who carry MC4R mutations are predisposed to develop obesity symptoms as a consequence of unselective overeating, a tendency that is particularly pronounced during early childhood (Farooqi et al. ). The MC4R gene contains seven transmembrane regions, three intracellular loops, and three extracellular loops (Farooqi et al. ). Reported mutation sites are distributed in the transmembrane regions and the intracellular and extracellular loops. The mutation, situated in the first transmembrane region of the patient, has been documented in China for the first time. This region has been deemed to be of minimal importance for ligand binding (Yang, Fong, Dickinson, Mao, et al. ). However, an analysis of foreign reports and the clinical phenotype of the patient revealed that the mutation located in the first transmembrane region can lead to early‐onset obesity, hyperinsulinemia, and excessive appetite. A comprehensive review of the clinical features associated with monogenic nonsyndromic obesity revealed new clinical phenotypes that were subsequently expanded and refined. These additional features include skin pallor (Neocleous et al. ), corneal small fiber degeneration (Gad et al. ), and gastrointestinal reflux (De Rosa et al. ), among others. The objective of this study was to provide evidence for the pathogenesis, diagnosis, treatment, and genetic counseling of monogenic nonsyndromic obesity variants.