Small For Gestational Age Girls Research Articles

Pubertal course of persistently short children born small for gestational age (SGA) compared with idiopathic short children born appropriate for gestational age (AGA)

Few data are available on the pubertal development of children born small for gestational age (SGA) who fail to show catch-up growth. A longitudinal analysis compared the pubertal course of persistently short children born SGA compared to children with idiopathic short stature who were appropriate for gestational age (AGA). One hundred and twenty-eight short children (height SDS<-1.7), including 76 (31 boys) born SGA and 52 (22 boys) born AGA, were regularly followed from early childhood to completion of puberty. Puberty was attained at normal age (10.5-14 Years in boys, 9.5-13 Years in girls) for most children in both the SGA and AGA groups (boys, 80% and 77%; girls, 76% and 78% respectively). The duration of puberty was similar in the SGA and AGA groups. Menarche occurred at normal age range but was significantly earlier in the SGA girls (P<0.01 by ANOVA). Despite the similar total pubertal growth, the patterns of growth differed significantly: SGA group - accelerated growth and bone maturation rates from onset of puberty with peak height velocity at Tanner stages 2-3, followed by a decelerated growth rate and earlier fusion of the epiphyses; AGA group - steady progression of bone elongation and maturation throughout puberty (pubertal growth, P<0.05 in both sexes; bone maturation, P<0.001 in both sexes). Final height in the SGA group was compromised compared with their target height (P<0.001). Children born SGA have a normal pubertal course with a distinct pubertal growth pattern. This pattern may represent an altered regulation of their growth modalities.

Hypergonadotrophinaemia with reduced uterine and ovarian size in women born small-for-gestational-age.

Fetal growth restraint has been associated with FSH hypersecretion in early infancy and in early post-menarche, and with reduced uterine and ovarian size in adolescence. It is unknown whether these reproductive anomalies persist, respectively, into late infancy and into the reproductive age range. We report follow-up findings in two age groups of girls. A cohort of infants [n=26; n=10 born appropriate-for-gestational-age (AGA) and n=16 born small-for-gestational-age (SGA)], who had been studied at the age of approximately 4 months, was assessed again at the age of 12 months. A cohort of teenagers (n=28), who had been studied at the age of approximately 14 years, was assessed again at the age of approximately 18 years; this group was complemented by a transversal cohort of similar age (n=19) for a total of 47 young women (n=27 AGA; n=20 SGA). In infants, only serum FSH was measured; adolescents underwent endocrine-metabolic screening, ultrasound assessment of uterine-ovarian size, and evaluation of body composition by dual X-ray absorptiometry. Serum FSH levels were higher in SGA than AGA infant girls at 4 and 12 months, and higher in SGA than AGA adolescents at 14 and 18 years (all P<0.01). Longitudinal ultrasound assessments disclosed a late-adolescent increment of uterine size that was less obvious in SGA than AGA girls. In contrast, ovarian volume remained stable in both subgroups. Compilation of longitudinal and transversal results at 18 years of age corroborated the persistent reduction in the uterine size of SGA girls (by approximately 20%; P<0.005) and in their ovarian volume (by approximately 40%; P<0.0001); moreover, SGA girls displayed not only a persistent elevation of FSH (by approximately 50%; P<0.001), but also a rise of LH and fasting insulin, as well as an excess of abdominal fat (all P<0.01). The gynaecology of young women born SGA was found to be characterized by hypergonadotrophinaemia and by a reduced uterine and ovarian size.

Reduced ovulation rate in adolescent girls born small for gestational age.

FSH and insulin are key hormones involved in spontaneous ovulation. Adolescent girls born small for gestational age (SGA) are at risk for FSH and insulin resistance. We have assessed whether ovulation rate is reduced in SGA girls. Ovulatory function was assessed by weekly filter paper progesterone measurements, obtained by finger-stick auto-sampling for 3 consecutive months in matched populations of asymptomatic, nonobese girls (mean age, 15.5 yr; > or =3 yr postmenarche) who were either born with an appropriate weight for gestational age (AGA; n = 24; mean birthweight, 3.3 kg) or born small for gestational age (SGA; n = 25; mean birthweight, 2.3 kg). The prevalence of anovulation was higher among SGA than AGA girls (40% vs. 4%; P = 0.002). Moreover, in the relatively small fraction of ovulating SGA girls, the ovulation rate was lower than in AGA adolescents (average number of ovulations during the study, 1.4 vs. 1.9; P < 0.01). In conclusion, the endocrine correlates of prenatal growth restraint are herewith extended to include oligo-ovulation and anovulation in adolescence. It remains to be verified whether this SGA-related phenomenon persists into the reproductive age range. If it does, then fetal growth restraint may prove to be one of the enigmatic components underpinning hitherto unexplained female subfertility.

Hypersecretion of FSH in infant boys and girls born small for gestational age.

Prenatal growth restraint, as reflected in a low birthweight for gestational age, is a risk factor for postpubertal FSH hypersecretion and for reduced gonadal size. The ontogeny of the low-birthweight effect on the FSH-inhibin B feedback loop is unknown. Infancy is an episode of choice to study the possibility of an early low-birthweight effect on the FSH-inhibin B loop because this phase is characterized by high activity within the gonadal axis. We assessed serum concentrations of FSH and inhibin B in 46 infants [26 girls and 20 boys; mean age, 4 months; range, 3-6 months; 17 appropriate for gestational age (AGA), 29 small for gestational age (SGA); mean birthweight, 3.2 kg for AGA vs. 2.3 kg for SGA], together with circulating levels of LH, E2, and free androgen index. In SGA girls and boys, serum FSH levels were 2- and 4-fold higher (P < 0.001), respectively, than in AGA controls of the same gender (7.3 +/- 0.9 vs. 3.8 +/- 0.4 IU/ml and 2.9 +/- 0.5 vs. 0.7 +/- 0.2 IU/ml). Serum LH, inhibin B, and free androgen index/E2 concentrations were similar in AGA and SGA infants. In conclusion, prenatal growth restraint was found to be followed by elevated serum FSH concentrations in infant girls and boys. SGA infants seem to need an augmented FSH drive to fulfill inhibin B requirements on the afferent side of the feedback loop. The late-endocrine correlates of early growth restraint are herewith extended to include the main axis of reproduction in both genders. It remains to be studied whether FSH hypersecretion in infancy is a marker of subsequent subfertility.

Birthweight and stature, body mass index and fat distribution of 14-year-old Polish adolescents.

The relationships between intra-uterine growth retardation and stature, relative weight and fat distribution at adolescence have not been comprehensively established. The aim of this report is to assess the effect of low birthweight on stature, relative weight and fat distribution in 14-year-old boys and girls from Wroclaw, Poland. Cross-sectional measurements of 1197 boys and 819 post-menarcheal girls aged 13.50-14.49 years were performed during medical examinations in 1997. Stature, body mass index (BMI; kg/m2), waist-to-hip ratio (WHR) and waist-to-thigh ratio (WTR) were used in the present study. A cut-off value of the 10th percentile of birthweight for particular gestational weeks was used in order to define subjects born small for gestational age (SGA) or appropriate for gestational age (AGA). Two-way ANOVA was used to evaluate the effect of birthweight on anthropometric variables of 14-year-old adolescents, allowing for socioeconomic status (determined by the level of the mother's education). Birthweight affected stature in boys and girls (P < 0.001), BMI in boys (P < 0.05) and WHR and WTR in girls (P < 0.001 and P < 0.05, respectively). At the age of 14 years, both SGA boys and girls were shorter than their AGA peers. The SGA boys had lower BMI, whereas SGA girls accumulated more centralized fat compared with their AGA counterparts. Fetal growth retardation has a long-lasting adverse effect on later physical growth. Polish SGA children do not catch up with their peers in terms of stature by adolescence. Moreover, central fat distribution, as observed among SGA girls, constitutes a significant risk for several adult degenerative diseases.

Adrenarche ,pubertal development ,age at menarche and final height of full-term ,born small for gestational age (SGA) girls

Children born small for gestational age (SGA) may present advanced bone maturation in childhood and reduced final height. The objectives of the study were to evaluate adrenarche ,pubertal development ,ageat menarche and final height in full-term born-SGA girls. Twenty-four girls (12 born-SGA and 12 matched controls) were evaluated at 6-7.5 years of age for clinical signs of puberty and dehydroepiandrosteronesulfate (DHEAS) levels ,as a marker of adrenarche. Thirty-eight girls (19 born-SGA and 19 matched controls) were evaluated at 17.5-18.5 years of age to assess final height ,sexual maturation and age atmenarche. SGA girls had a mean final height (160.1 cm vs 165.8 cm ,p < 0.01) and mean weight (52.1 kg vs 56.5 kg ,p < 0.05) significantly lower than controls. Controls had a mean finalheight significantly higher than their mean target height. Sexual maturation was at stage 5 of Tanner's staging in SGA girls and control subjects. SGA girls had a slightly anticipated puberty (9.9 vs 10.4years for initial breast development) and a lower age at menarche (11.9 vs 12.3 years). At 6-7.5 years of age ,SGA females and controls did not show any difference for clinical signs of puberty; however,DHEAS levels (0.75 + 0.18μg/ml vs 0.57 + 0.22μg/ml ,p < 0.05) were significantly higher in SGA girls than in control subjects.We concluded that full-term born-SGA females have impairedfinal height and weight in adolescence but substantially normal sexual maturation and age at menarche. Increased DHEAS levels before puberty in born-SGA girls may predispose to increased bone maturationin childhood with a reduced final height. In our population a progressive increment in final stature is evident.

Exaggerated Adrenarche and Hyperinsulinism in Adolescent Girls Born Small for Gestational Age

Serum dehydroepiandrosterone-sulfate (DHEAS) is a classic marker for adrenarche and, subsequently, for the individual hormonal milieu. We have tested the hypothesis that prenatal growth reduction is followed by exaggerated adrenarche. Serum DHEAS, androstenedione and insulin concentrations were determined together with fasting glycemia in matched populations of asymptomatic, non-obese, post-menarcheal girls (mean age 14 yr) who were born either with a strictly appropriate weight for gestational age (AGA) or small for gestational age (SGA). When compared to AGA girls, the SGA girls had identical glucose levels, higher values for insulin and androstenedione (p<0.01), and a two-fold rise of DHEAS concentrations (p<0.0001). In conclusion, girls with prenatal growth reduction were found to be prone to develop, besides hyperinsulinism, a variant of exaggerated adrenarche. It remains to be verified whether the exaggerated adrenarche in adolescence is followed by adrenal hyperandrogenism throughout adulthood and senescence.