Abnormalities in Puberty: Scientific and Clinical Advances by H.A. Delemarre-van de Waal, P.-E. Mullis

By H.A. Delemarre-van de Waal, P.-E. Mullis

This publication on abnormalities in puberty provides an summary at the most modern wisdom at the mechanisms of the developmental strategies of puberty. even though the precise mechanisms of reawakening of the GnRH pulse generator on the onset of puberty nonetheless need to be elucidated, many genetic and environmental elements were pointed out to play an important function. issues mentioned in person chapters comprise the endocrine and metabolic matters concerning the 'developmental starting place of grownup affliction' 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 program of GnRH analogues within the remedy of crucial precocious puberty, and the psychosocial results of an early puberty. This quantity presents the paediatrician, endocrinologist, gynaecologist and doctor with underlying details in addition to useful tokens on the best way to deal with a few of the stipulations of a disturbed technique of puberty.

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Additional resources for Abnormalities in Puberty: Scientific and Clinical Advances (Endocrine Development, Vol. 8)

Example text

Such rapid adaptation of the hypothalamicpituitary-adrenal axis to enhance cortisol secretion may be beneficial in the shortterm, for example, by reducing chronic lung disease [13]. However, as seen following postnatal dexamethasone therapy [6], the continuation of higher glucocorticoid production could impair growth during early childhood. Even longerterm persistence of elevated cortisol levels might contribute to the fetal origins of adult disease links between low birthweight and metabolic disease risks.

In the IUGR male rat, the low circulating testosterone levels at that time can be the result of either central dysregulation or dysfunction of the Leydig cells. Both have its origin during the intra-uterine period [55, 61–69]. Modification of GnRH neurons at the hypothalamic level may cause an impaired gonadotropin secretion leading to delayed puberty. On the other hand, we cannot exclude gonadal impairment since a disturbance in LH receptor production of the Leydig cell may cause in impaired sexual development as well [70].

Human studies with respect to the LH secretory pattern in relation to Leydig cell number and function have not been done yet. On the other hand, also in the human male one cannot exclude a gonadal impairment since a disturbance in LH receptor production of the Leydig cell itself may induce changes in sexual development. In the male FR rat delayed onset of puberty was accompanied by low testosterone levels secreted by a lower number of Leydig cells. Postnatal undernutrition may influence the central regulation of the gonadal axis, since hypothalamic GnRH neurons and GnRH secretion continue to develop during that period [73].

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