By H.A. Delemarre-van de Waal, P.-E. Mullis
This e-book on abnormalities in puberty provides an outline at the newest wisdom at the mechanisms of the developmental methods of puberty. even supposing 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. themes mentioned in person chapters comprise the endocrine and metabolic concerns on the topic of the 'developmental foundation of grownup ailment' 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 remedy of significant precocious puberty, and the psychosocial results of an early puberty. This quantity offers the paediatrician, endocrinologist, gynaecologist and surgeon with underlying info in addition to functional tokens on how you can deal with a number of the stipulations of a disturbed means of puberty.
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Additional resources for Abnormalities in puberty : scientific and clinical advances
11b-Hydroxysteroid Dehydrogenase A major source of interindividual variation in the effects of glucocorticoid exposure may arise from differences in activities of the 11␤-hydroxysteroid dehydrogenase (11␤-HSD) enzymes type 1 and 2, which shuttle active cortisol to inactive cortisone and vice versa . In the fetus, placental ␤-HSD2 activity largely prevents any maternal cortisol crossing the placenta. Dexamethasone, a synthetic fluorinated steroid, is a poor substrate for 11␤-HSD2, and the fetal effects of maternal dexamethasone therapy are therefore unlikely to vary with 11␤-HSD2 activity.
A study of premature (Ͻ32 weeks’ gestation), VLBW infants receiving ventilation support, showed that the majority had sub-optimal baseline cortisol levels (Ͻ414 nmol/l), and only 36–67% showed a response to increasing doses adrenocorticotrophic hormone (ACTH) . Lower cortisol levels in the newborn predict worse shortterm outcomes, including chronic lung disease and intraventricular hemorrhage Adrenal Function of Low-Birthweight Children 35 . In another large study of 125 VLBW infants, lower cortisol levels even within the first few days of life predicted airway inflammation, patent ductus arteriosus, duration of oxygen therapy and chronic lung disease .
Antenatal Dexamethasone Therapy in Congenital Adrenal Hyperplasia Maternal dexamethasone therapy effectively suppresses abnormal adrenal androgen production and virilization of the female fetus affected by congenital adrenal hyperplasia (CAH) . 02 mg/kg/day in three divided doses) should be started by 6–8 weeks’ gestation and, depending on the results of karyotyping and mutation analysis, treatment is discontinued around 10 weeks’ gestation in pregnancies with a male fetus, and around 14 weeks with an unaffected female fetus.
Abnormalities in puberty : scientific and clinical advances by H.A. Delemarre-van de Waal, P.-E. Mullis