By H.A. Delemarre-van de Waal, P.-E. Mullis
This publication on abnormalities in puberty offers an outline at the most modern wisdom at the mechanisms of the developmental techniques of puberty. even supposing the precise mechanisms of reawakening of the GnRH pulse generator on the onset of puberty nonetheless must be elucidated, many genetic and environmental components were pointed out to play a tremendous position. issues mentioned in person chapters contain the endocrine and metabolic concerns with regards to the 'developmental starting place of grownup sickness' speculation and polycystic ovary syndrome in addition to abnormalities in GnRH controlling genes, GnRH-secreting hamartoma as a version for the onset of puberty, event at the software of GnRH analogues within the therapy of vital precocious puberty, and the psychosocial results of an early puberty. This quantity offers the paediatrician, endocrinologist, gynaecologist and medical professional with underlying details in addition to functional tokens on how you can deal with some of the stipulations of a disturbed means of puberty.
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Additional resources for Abnormalities in Puberty: Scientific and Clinical Advances (Endocrine Development, Vol. 8)
Weissenbruch/Engelbregt/Veening/Delemarre-van de Waal 30 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 Gluckman PD, Harding JE: Fetal growth retardation: Underlying endocrine mechanisms and postnatal consequences. Acta Paediatr Suppl 1997;422:69–72. Gluckman PD, Harding JE: The physiology and pathophysiology of intrauterine growth retardation. Horm Res 1997;48(suppl 1):11–16. Godfrey KM, Barker DJP: Fetal nutrition and adult disease. Am J Clin Nutr 2000;71(suppl): 1344S–52S.
Adrenal androgen secretion rises again from around the age of 6 years onwards at ‘adrenarche’ . Low-birthweight infants have relative hypoplasia of the fetal zone , and lower DHEAS levels in both plasma and urine during the first 24 h of life compared with normal birthweight infants [64, 65]. Norman et al.  studied 22 twin pregnancies, each with one IUGR twin and one normal birthweight twin. In each pair, the IUGR twin had lower DHEAS levels in umbilical arterial blood at birth than their larger twin, but cortisol levels were no different.
The fetal zone does not express 3␤-HSD (required for cortisol production), but does express P450scc and P450c17 (required to produce DHEAS). This fetal zone rapidly disappears during the first few weeks after birth and DHEA and DHEAS levels are usually undetectable [61, 62]. Adrenal androgen secretion rises again from around the age of 6 years onwards at ‘adrenarche’ . Low-birthweight infants have relative hypoplasia of the fetal zone , and lower DHEAS levels in both plasma and urine during the first 24 h of life compared with normal birthweight infants [64, 65].