Purpose of review We aim to describe current concepts on childhood and adolescent obesity with a strong focus on its sequela. Childhood obesity is a national epidemic with increasing prevalence over the past three decades placing children at increased risk for many serious comorbidities, previously felt to be only adult-specific diseases, making this topic both timely and relevant for general pediatricians as well as for subspecialists. Recent findings Childhood obesity develops through an interplay of genetics, environment, and behavior. Treatment includes lifestyle modification, and now metabolic and bariatric surgery is more commonly considered in carefully selected adolescents. The off-label use of adjunct medications for weight loss in childhood and adolescent obesity is still in its infancy, but will likely become the next logical step in those with lifestyle modification refractory obesity. Obesity can lead to several comorbidities, which can persist into adulthood potentially shortening the child's lifespan. Summary Efforts should be focused primarily on reducing childhood and adolescent obesity, and when indicated treating its sequela in effort to reduce future morbidity and mortality in this precious population. Video abstract http://links.lww.com/MOP/A36.
Alagille syndrome (ALGS) is an autosomal dominant disorder caused by pathogenic variants in JAG1 or NOTCH2, which encode fundamental components of the Notch signaling pathway. Clinical features span multiple organ systems including hepatic, cardiac, vascular, renal, skeletal, craniofacial, and ocular, and occur with variable phenotypic penetrance. Genotype–phenotype correlation studies have not yet shown associations between mutation type and clinical manifestations or severity, and it has been hypothesized that modifier genes may modulate the effects of JAG1 and NOTCH2 pathogenic variants. Medical management is supportive, focusing on clinical manifestations of disease, with liver transplant indicated for severe pruritus, liver synthetic dysfunction, portal hypertension, bone fractures, and/or growth failure. New therapeutic approaches are under investigation, including ileal bile acid transporter (IBAT) inhibitors and other approaches that may involve targeted interventions to augment the Notch signaling pathway in involved tissues.
Acute cellular rejection (ACR) is a common complication in liver transplantation recipients (LTRs), especially within the first 12 months, and it is associated with increased morbidity and mortality. Although abnormalities in standard liver biochemistries may raise the clinical suspicion for ACR, it lacks specificity, and invasive liver biopsies, which are associated with numerous risks, are required for definitive diagnoses. Biomarker discovery for minimally invasive tools for diagnosis and prognostication of ACR after liver transplantation (LT) has become a rapidly evolving field of research with a recent shift in focus to omics‐based biomarker discovery. Although none are yet ready to replace the standard of care, there are several promising minimally invasive, blood‐derived biomarkers that are under intensive research for the diagnosis of ACR in LTRs. These omics‐based biomarkers, encompassing DNA, RNA, proteins, and metabolites, hold tremendous potential. Some are likely to become integrated into ACR diagnostic algorithms to assist clinical decision making with a high degree of accuracy that is cost‐effective and reduces or even obviates the need for an invasive liver biopsy.
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