Читать книгу Nutrition and Growth - Группа авторов - Страница 20

Hak SF¹, Arets HGM², van der Ent CK², van der Kamp HJ¹

¹Department of Pediatric Endocrinology, University Medical Center Utrecht, Utrecht, The Netherlands; ²Department of Pediatric Pulmonology, Cystic Fibrosis Center Utrecht, University Medical Centre Utrecht, Utrecht, The Netherlands

Pediatric Pulmonology 2019;54:1209–1215

Background: Growth failure and short stature is a common consequence of children and adolescents with cystic fibrosis (CF). Previous studies have documented associations between short stature and clinical outcomes, including reduced life expectancy. It was previously thought that the underlying aetiology of growth failure in CF is due to reduced food intake/absorption and concurrent increased energy losses. More recent studies demonstrate that growth failure and poor pubertal growth spurt is still observed in contemporary cohorts of children and adolescents with CF. Recent reports also document that obesity is also seen in the CF clinic, which may be a reflection of the obesitogenic environment we live in or the over-aggressive management of nutrition. There are very few longitudinal studies of linear growth and body mass index (BMI) in CF. The aim of this study was to evaluate stature in a cohort of Dutch children with CF diagnosed clinically (born between 1997 and 2001) from 0.5 until 18 years. The secondary aim was to evaluate the associations of increase in BMI between 1 and 6 years, lung function and CF-related diabetes.

Methods: A retrospective study from one single centre. All subjects were diagnosed clinically and not via newborn screening. Subjects were excluded if there was another significant co-morbidity, missing height data during follow-up. All subjects had reached adult height-defined as increase in height of <0.2 cm over at least 6 months.

Results: Height deficits were observed at presentation in both boys and girls even after accounting for parental height (target height), which increased following diagnosis. In boys, height for age minus target height Z-scores declined during puberty, leading to reduction in adult height corresponding to 4 cm lower (p = 0.001) than the healthy population. In girls, height for age minus target height Z-scores declined briefly after age 8 years but increased subsequently, with adult height of only 2 cm lower (p = 0.22) than the healthy population. Low BMI Z-scores were observed for both boys and girls only in the first year of life. The presence of CF-related diabetes and pulmonary function were not associated with adult height. Increase in BMI Z-scores between 1 and 6 years were associated with adult height in boys (Model R² = 0.176, r = –0.420, p = 0.0230 and girls (Model R² = 0.217, r = –0.466, p = 0.0019).

Conclusion: Adult height deficits were still observed in boys with CF despite improvement in clinical care. Associations between increase in BMI in infancy/early childhood and adult height in CF should be addressed in future studies.

Reprinted with permission from John Wiley & Sons, Inc.

Comments

In this longitudinal retrospective study, the authors document that height deficits may still be observed in males with cystic fibrosis (CF). The gender difference for growth failure has also been shown in another group of childhood chronic disease, inflammatory bowel disease (Gupta et al. Inflamm Bowel Dis 2011;17:2318–2325; Mason et al. Horm Res Pediatr 2015;83:45–54), and this should be addressed in future studies in CF that include disease severity. Whilst statistical significant adult height deficits were documented in males with CF in this current study, it is encouraging to note that the magnitude of height deficit is only 4 cm (although the authors did not report 95% CI for the height deficit). Long-term adult height data in children with CF identified from newborn screening are now needed. The authors speculate that increase in body mass index (BMI) in infancy/early childhood may lead to increased production of adrenal androgens with associated earlier onset of puberty and therefore reduction in adult height. The associations reported in this study were obtained from univariate analysis which only explained approximately 18 and 22% of variation in adult height of males and females. Such a hypothesis needs to be proven in future studies, which take into account disease severity and nutritional status/management strategies. An alternative explanation could be that those children with more severe disease and/or nutritional issues were managed with aggressive nutritional management leading to greater increase in BMI. Optimal nutritional management in CF and impact on all health outcomes including linear growth and pulmonary function require further studies.

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