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Catch-down of SGA and AGA Infants Born to Short-statured Parents« Back to Volume 22, Issue 4, December 2006 - Table of Contents Völkl and colleagues reported their findings of a cross-sectional analysis of linear growth during the first 4 years of life. The 96 subjects (38 females) were children, between 5 and 10 years of age, who were born to short parents and presented to the pediatric endocrine clinic for evaluation of short stature. Endocrine disorders were excluded in each case. All the children had familial short stature (FSS) defined as a height SDS ≤ –2.0 but within the normal range of parental height according to the calculated target height. At least one of the parents had short stature (height ≤ –2 SDS). Children were divided into 2 groups according to birth size; 41 (19 female) were in the small for gestational age (SGA) group for whom birth length or birth weight was ≤ –2.0 SDS, and 55 (19 female) were in the group of appropriate for gestational age (AGA) infants. All children were born at >36 weeks gestation and none were receiving any chronic medications. Cross-sectional data for length/height/weight/head circumference for the first 4 years of life were collected retrospectively from standardized German growth charts. The data analyses were performed at birth, 1, 2, and 4 years of age. The SDS of height and height velocity were calculated according to German and Swedish reference data. There was a significant (p <0.0001) decline of height SDS within the first 2 years of life, which was more prevalent in the AGA children. These children started with a mean height of 0.09 SDS ± 1.02 SDS at birth and ended up with a mean height of –2.36 ± 0.72 SDS at 4 years of age. The growth pattern of the SGA group was similar, but the height loss was less than for the AGA group (mean –2.04 SDS at birth, –3.05 SDS at 4 years). Even though the height of the SDS did not decrease as much as that of the AGA children, there was a significant difference between the mean height SDS data at all of the times studied. The absolute difference between height SDS values narrowed during the observation period. There was no significant difference in height and BMI SDS between those children having a father with short stature, compared with those with a mother with short stature. In addition, there was no relationship between the child’s gender and the gender of the short parent. The authors pointed out that there was selection bias inherent in their study since all children were initially identified in the pediatric endocrine clinic where they had been referred for evaluation of short stature. In addition, the short-stature children born SGA belonged to a subgroup of SGA children who did not experience postnatal catch-up growth. The authors stated that there is minimal information in the literature of spontaneous growth during the first years of life in children with idiopathic short stature born AGA. Of note, the SGA children increased their BMI to the same level as the AGA group after one year of age, but then these children tended to have a lower BMI SDS during the following years. This result was consistent with population-based data showing that SGA children weigh significantly less than AGA children at 3 to 6 years of age. The etiology of the growth failure in these children remains undefined. First Editor’s CommentVölkl and his colleagues have provided some very interesting data with regard to growth patterns in children identified as having familial short stature at 4 years of age. Both AGA and SGA children have losses in SDS over the first 4 years of life, but the loss appears to be greater in those children born SGA. The change in SDS is greater for those who were born AGA. As noted by the authors, the study was retrospective and it would be important to perform prospective studies on the children born SGA. Performance of these studies on the AGA children with short parents might prove more difficult, but the information to be gathered from such a study might be extremely important in understanding the auxilogical changes that occur in these children, and might lend support to therapies for improving final adult height. William L. Clarke, MD Second Editor’s CommentThe body weight and growth progression of patients with FSS with or without constitutional growth delay (CGD) was studied by Dr. Vaquero-Solans and me.1 The linear growth in infancy was similar in both groups of patients. Infants with FSS and CGD showed a sharp parallel fall from the 50 th percentile to –1 SD by 3 months of age and a more gradual, but steady, deterioration in length to –2 SD between 3 to 27 months of age. The z scores of height for age remained 2.0 – 2.5 SD below the mean until 12 years of age. In contrast, the body weight progression differed among the 2 types of patients. The CGD patients exhibited a marked impairment in body weight gain as compared with the FSS. Patients with CGD had body weight deficits for stature, whereas the FSS patients did not. The differences were more marked during infancy. The CGD patients attained an appropriate body weight for height by 9 to 10 years of age, whereas the FSS patients presented body weight excess after 4 years of age and remained progressively overweight until 12 years of age. The catch-down pattern of growth in CGD patients during infancy has been observed by others.2 The growth data of SGA and AGA infants in the paper by Völkl et al was similar to the growth exhibited by FSS patients, though they did not assess bone development or weight and height progression after 4 years of age. The pattern of growth and weight gain during infancy and childhood has become more important as it may set the stage for obesity and adult-onset disease.3,4 Fima Lifshitz, MD References - (linked to
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Volume 24 Number 1
May 2008
www.GGHjournal.com
ISSN 1932-9032
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