The Most Pressing Challenges in the Management of Pediatric Growth Disorders and Childhood Obesity

A special issue of Children (ISSN 2227-9067). This special issue belongs to the section "Global Pediatric Health".

Deadline for manuscript submissions: closed (10 January 2026) | Viewed by 575

Special Issue Editors


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Guest Editor
Department of Human Pathology in Adulthood and Childhood, University of Messina, Messina, Italy
Interests: pathology

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Guest Editor
UniME, Department of Adult and Childhood Human Pathology “Gaetano Barresi”, University of Messina, Messina, Italy
Interests: pediatric endocrinology; thyroid diseases; autoimmune diseases
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Special Issue Information

Dear Colleagues,

Pediatric growth disorders and childhood obesity represent critical and escalating public health concerns globally. Over the past few decades, significant advances have been made in understanding the biological, environmental, and socio-economic determinants of these conditions. However, the rising prevalence of early-onset non-syndromic obesity and the increasing identification of genetic variants associated with abnormal growth trajectories highlight the urgent need for integrative and multidisciplinary approaches.

This Special Issue aims to explore the multifaceted challenges in diagnosing, monitoring, and treating pediatric growth disorders and obesity. It seeks to bridge the gap between cutting-edge genomic research and clinical practice, emphasizing the importance of early identification, personalized interventions, and long-term prevention strategies.

We welcome original research, reviews, case reports, case series, and clinical studies that address novel mechanisms of growth regulation, the role of rare and common genetic variants in pediatric obesity, and innovative prevention and treatment strategies. Submissions focusing on translational research, public health approaches, ethical implications, methods of prevention, and early genetic screening in children are particularly welcome.

By gathering high-quality contributions, this Special Issue aspires to foster dialogue and collaboration across disciplines to advance knowledge and improve outcomes in pediatric health.

Dr. Giovanni Luppino
Dr. Domenico Corica
Guest Editors

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Published Papers (1 paper)

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8 pages, 739 KB  
Case Report
Severe Short Stature and rhGH Resistance in a Child Born SGA: The Role of a Novel IGF1R Mutation, Case Report and Narrative Review
by Giovanni Luppino, Eleonora Ini’, Letteria Anna Morabito, Tiziana Abbate, Cecilia Lugarà, Tommaso Aversa, Malgorzata Wasniewska and Domenico Corica
Children 2026, 13(4), 458; https://doi.org/10.3390/children13040458 - 27 Mar 2026
Viewed by 313
Abstract
Background: Genetic causes of growth failure should be suspected in patients born small for gestational age (SGA) who fail to show postnatal catch-up growth, present with severe short stature (SS), and exhibit a poor or absent response to growth hormone (rhGH) therapy. [...] Read more.
Background: Genetic causes of growth failure should be suspected in patients born small for gestational age (SGA) who fail to show postnatal catch-up growth, present with severe short stature (SS), and exhibit a poor or absent response to growth hormone (rhGH) therapy. Mutations in the insulin-like growth factor 1 receptor (IGF1R) gene are associated with impaired growth, intrauterine growth restriction (IUGR), low birth weight and/or length, and postnatal SS. Case Description: A 9-year-old boy, born SGA for birth length, was evaluated for severe SS. Common causes of SS were excluded. At 9 years and 7 months of age, his height was 112.6 cm (−3.99 SDS), weight 18 kg (−3.79 SDS), and BMI 14.2 kg/m2 (−1.8 SDS); pubertal development was Tanner stage 1. The target height was 158 cm (−2.62 SDS). Bone age was delayed by approximately one year compared with chronological age. Serum IGF-1 levels were within the upper-normal range for age. GH therapy (0.035 mg/kg/day) was initiated due to the lack of catch-up growth in an SGA subject. After three years of treatment, the height gain was only 0.5 SDS. IGF-1 levels showed a transient treatment-related increase, followed by persistent normalization during ongoing therapy. Next-generation sequencing (NGS) analysis identified novel heterozygous paternal nonsense variant in the IGF1R gene: c.3498C>G (p.Tyr1166Ter). At 12 years of age, impaired fasting glucose and reduced glucose tolerance were detected; consequently, it was decided to discontinue rhGH therapy, also in light of the IGF1R mutation and the lack of height recovery. Conclusions: This case underlines the critical role of genetic testing in the evaluation of patients born SGA. The coexistence of SGA status and an IGF1R gene mutation may provide a clear explanation for both the poor response to rhGH therapy and the increased risk of alterations in glucose metabolism. An extensive narrative review of the literature on growth outcomes and glucose metabolism abnormalities during GH treatment in SGA patients carrying IGF1R variants was also performed. Full article
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