This International Consensus Guideline was developed by experts in the field of small for gestational age (SGA) of 10 pediatric endocrine societies worldwide. A consensus meeting was held and 1300 articles formed the basis for discussions. All experts voted about the strengths of the recommendations. The guideline gives new and clinically relevant insights into the etiology of short stature after SGA birth, including novel knowledge about (epi)genetic causes. Further, it presents long-term consequences of SGA birth and also reviews new treatment options, including treatment with gonadotropin-releasing hormone agonist (GnRHa) in addition to growth hormone (GH) treatment, as well as the metabolic and cardiovascular health of young adults born SGA after cessation of childhood GH treatment in comparison with appropriate control groups.To diagnose SGA, accurate anthropometry and use of national growth charts are recommended. Follow-up in early life is warranted and neurodevelopment evaluation in those at risk. Excessive postnatal weight gain should be avoided, as this is associated with an unfavorable cardiometabolic health profile in adulthood. Children born SGA with persistent short stature < −2.5 SDS at age 2 years or < −2 SDS at 3 to 4 years of age, should be referred for diagnostic workup. In case of dysmorphic features, major malformations, microcephaly, developmental delay, intellectual disability, and/or signs of skeletal dysplasia, genetic testing should be considered. Treatment with 0.033 to 0.067 mg GH/kg/day is recommended in case of persistent short stature at age of 3 to 4 years. Adding GnRHa treatment could be considered when short adult height is expected at pubertal onset. All young adults born SGA require counseling to adopt a healthy lifestyle.

Prenatal events appear to program hormonal homeostasis, contributing to the development of somatic disorders at an adult age. The aim of this study was to examine whether maternal exposure to cytokines or to dexamethasone (Dxm) would be followed by hormonal consequences in the offspring at adult age. Pregnant rats were injected on days 8, 10, and 12 of gestation with either human interleukin-6 (IL-6) or tumor necrosis factor-α (TNF-α) or with Dxm. Control dams were injected with vehicle. All exposed offspring developed increased body weight (P < 0.05–0.001), apparently due to an increase of 30–40% in adipose tissue weight (P < 0.05–0.01). Corticosterone response to stress was increased in the IL-6 group (P < 0.05–0.01). Dxm-treated male rats exhibited blunted Dexamethasone suppression test results. In male rats, insulin sensitivity was decreased after IL-6 exposure (P < 0.01), whereas basal insulin was elevated in the TNF-α group (P < 0.01). In female rats, plasma testosterone levels were higher in all exposed groups compared with controls (P < 0.01–0.001), with the exception of Dxm-exposed offspring. Males in the TNF-α group showed decreased locomotor activity (P < 0.05), and females in the IL-6 group showed increased locomotor activity (P < 0.05). These results indicate that prenatal exposure to cytokines or Dxm leads to increased fat depots in both genders. In females, cytokine exposure was followed by a state of hyperandrogenicity. The results suggest that prenatal exposure to cytokines or Dxm can induce gender-specific programming of neuroendocrine regulation with consequences in adult life.

Introduction: Children and adolescents with autism spectrum disorder (ASD) appear to be at greater risk of excess weight gain. The aim of this systematic review and meta-analysis was to examine whether children with ASD have a greater prevalence of obesity and whether the prevalence of ASD is higher in children with obesity. Methods: We conducted a systematic search on PubMed, Scopus, and PsychINFO until May 21, 2021. We used the meta package in the R in order to calculate the pooled prevalence and relative risk of obesity in children with ASD. Results: We found 20 eligible studies investigating the prevalence of obesity in children with ASD, with the prevalence ranging from 7.9 to 31.8% and from 1.4 to 23.6% among controls. All but three studies originated from the USA. The proportion of children with obesity in ASD populations was 17% (95% confidence interval [CI]: 13–22). The relative risk of obesity in children with ASD compared with control children was 1.58 (95% CI: 1.34–1.86). There were no controlled studies reporting on the prevalence of ASD in children with obesity. Conclusion: Children and adolescents with ASD have a higher prevalence of obesity than healthy controls. There is a need for further prevalence studies of obesity in children with ASD, especially outside the USA, since the few European studies carried out have failed to show a significant difference between obesity prevalence in children with and without ASD. There is no knowledge at all regarding the prevalence of ASD among children with obesity.