ESPE Abstracts (2014) 82 P-D-1-1-178

University Hospital, Bonn, Germany

Background: Low birth weight, unfavourable intrauterine conditions, and post-natal catch-up growth are associated with a subsequent impact on growth, pubertal development, and metabolic disturbances later in life. Although the start of puberty is genetically determined it might be altered due to environmental influences.

Objectives: In a longitudinal study (birth to final height) we observed growth and pubertal development of genetically identical twins born with a significant intra-twin birth-weight (bw) difference.

Patients/method: 30 pairs of monozygotic twins with intra-twin bw-differences were seen at birth, at a mean of 2.8, 9.8, and 14.6 years. We defined concordant: bw-difference <1 SDS (n=14), discordant: bw-difference >1 SDS (n=16). Fasting blood sampling was performed at the mean age of 9.8 (prepubertal) and 14.6 years (during puberty).

Results: In the majority (67%) of the twin-pairs the former smaller twin started puberty earlier and progressed more rapidly through puberty than the co-twin. The difference was most pronounced in the discordant twins. At 9.8 years a significant intra-twin difference (P<0.01) was observed for DHEAS: mean DHEAS: 895 vs 1036 ng/ml in the former smaller co-twin. A similar – although not significant – difference was observed for androstendione (0.43 vs 0.72 ng/ml). At 14.6 years a significant difference was only found for those with discordant bw (1825 vs 2119 ng/ml, P<0.05).

A highly significant intra-twin correlation was found for sexual steroids during puberty (correlation-coefficient for testosterone: 0.9, P<0.001). However, neither prepubertal nor during puberty significant intra-twin differences were observed for gonadotropins, estradiol, and testosterone.

Conclusion: The high intra-twin correlation coefficient confirms that puberty and sexual steroids are genetically determined. However, the increased adrenal androgen secretion of the smaller twin during late childhood could have effects on rate of maturation and puberty. This could further impair final height and increase the risk for the polycystic ovary syndrome and insulin resistance.

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