Bibian van der Voorn

14 CHAPTER 1 a sustained increase in the response to CRH. It has not been tested whether such phenomena, which are probably adaptive in nature, persist beyond the early postnatal period and, subsequently, become maladaptive. DEVELOPMENTAL TRAJECTORIES INVERY PRETERM SURVIVORS BEYOND THE NEONATAL PHASE: FOOTPRINTS OF INCREASED HPA AXIS ACTIVITY? After an initial weight loss, birth weight is usually regained between the end of the 1 st week and the 3 rd week of life. Once birth weight is regained, the growth velocity increases to a level that approaches the intrauterine growth rate 51 . However, the rate of weight gain during hospital stay was shown to be slower in sick infants 51 , which could be explained by suboptimal protein and calorie supplies for the level of illness. After clinical improvement, CUG in weight and length is initiated. At term age, while still being smaller and lighter, absolute fat mass and abdominal fat content were greater than in full-term newborns 52 . Although the major part of CUG is completed by the age of 4 yrs, continuing CUG in height, weight and BMI was observed in late childhood and adolescence, albeit at a slower pace 51 . On average, in subjects born very preterm or with VLBW, final height was reduced by 0.5 SD compared to population- specific reference data 51 . Young adults born preterm or with VLBW, despite having a relatively normal BMI, exhibited a lower lean mass, increased fat content and centralization of fat distribution 11,14,53,54 . It is unlikely that the reduction in final height could be explained by an earlier onset or a more rapid progression of puberty. In cross-sectional studies of children aged 11–15 yrs, no differences in Tanner pubertal stages were demonstrated between boys and girls with VLBW and term-born children of the same age 55,56 . Moreover, girls with VLBW reported a similar age at menarche as their term counterparts 55-57 . However, very preterm birth and/or VLBW were associated with an earlier pubertal growth spurt 57 , a more advanced bone age at adolescence 55,56 and adrenal hyperandrogenism in young adulthood 58,59 . In very preterm survivors, antecedents of the metabolic syndrome were already present in childhood. Very preterm birth was associated with a relatively high blood pressure at 7.5 yrs of age, irrespective of the presence of nephrocalcinosis 60 . Furthermore, insulin sensitivity during an intravenous glucose tolerance test was reduced 4–10 yrs after very preterm birth. This was accompanied by a compensatory increase in acute insulin release 61 .