Prenatal diagnosis of fetal ovarian hyperstimulation

Berezowski, Aderson Tadeu; Machado, Jorge; Mendes, Maria Célia; Moura, Marcos Dias de; Duarte, Geraldo; Cunha, Sérgio Pereira da

doi:10.1046/j.1469-0705.2001.00349.x

Cited by 7 publications

(6 citation statements)

References 27 publications

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“…It is thought that lack of maturation of the hypothalamo-pituitary-gonadal axis and lack of complete development of negative feedback mechanisms with discontinuation of placental steroids are involved (42,46). It has been proposed that edema observed in the subjects is related with vascular endothelial growth factor released from the theca and granulosa cells (43,47). It has been reported that fetal ovarian hyperstimulation may occur rarely (47).…”

Section: Problems Related With Mini Pubertymentioning

confidence: 99%

“…It has been proposed that edema observed in the subjects is related with vascular endothelial growth factor released from the theca and granulosa cells (43,47). It has been reported that fetal ovarian hyperstimulation may occur rarely (47). In a fetus with a gestational age of 35 weeks, macrosomy, placental thickenning, polyhydramniosis, large ovaries (right 17.8, left 16.3 mL), 2 ovarian cysts with large septae and abdominal distention were observed and the clinical picture was associated with the increased level of beta-hCG found in the mother.…”

Section: Problems Related With Mini Pubertymentioning

confidence: 99%

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Mini puberty and its interpretation

Kurtoğlu

Baştuğ

2014

Turk Arch Ped

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Gonadotropins which are at high levels in the middle of the fetal life are considerably low in the cord blood and estrogen is measured to be high. The reason for this is the inhibitory effect of increased estrogen levels in the circulation arising from the placenta on gonadotropin releasing hormone (GnRH) pulse generator and pituitary gonadotropins (1, 2). In male fetuses, testosterone levels probably contribute additionally to inhibition (3). Gonadotropin inhibition discontinues with placental seperation, the hypothalamo-pituitary-gonadal axis is activated and the hormonal changes which occur are identified as mini puberty (2, 4). The activation of the hypothalamo-pituitary-gonadal axis reach a peak level approximately in the 6-8th week after delivery. In this period, the levels of sex steroids are similar to early-middle pubertal levels, but their peripheral effects are not realized (4).In boys, the level of luteinizing hormone (LH) increases approximately 10-fold in the minutes following delivery and the level of tesosterone increases. This state lasts approximately for 12 hours (5, 6). The increase in follicle stimulating hormone (FSH) and LH continues in the second week after delivery, reaches a peak in the 4-10 th week, decreases in the 6 th month to the prepubertal levels. The level of testosterone increased by release of luteinizing hormone reaches a peak at around the third month and decreases to the prepubertal levels in the 6-9 th months (1,7,8). Similarly, the levels of 17-hydroxyprogesteron and androstenodione which are increased with testosterone decrease with reduction of the level of LH (2). After delivery, an increase in the number of Leydig cells starts. This increase reaches a peak in the third month. Afterwards, reduction and apopytosis occur in fetal and infantile Leydig cells (9-11). Inhibin-B is a glycoprotein belonging to the family of transforming growth factor beta (TGF-β) and is released from Sertoli cells in the prepubertal period. It is considered an indicator of sertoli cell function in prepubertal male children, but it does not reflect the number and function of germ cells. Inhibin-B acts as a regulator of release of FSH (1). Inhibin-B can be measured in the cord blood, it increases after delivery, reaches a peak in the 4-12 th month (exceeds the male adult level). It is at a considerably low level at the age of 3-9 years and increases again with the initiation of the puberty (3, 7). Serum inhibin-B levels are low in cases of hypogonadotropic hypogonadism (1, 12).Anti-Mullerian hormone (AMH) is a glycoprotein released from the sertoli cells starting from the fetal period. It is found in the cord blood and its level increases in the first 30 months after delivery. It reaches a peak in the 6 th month, starts to decrease Mini puberty and its interpretation AbstractGonadotropins which are high in the middle of the fetal life are measured to be considerably low in the cord blood and estrogen is found to be high in the cord blood. Gonodotropins are supressed by estrogen. After delivery,...

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Section: Problems Related With Mini Pubertymentioning

confidence: 99%

Section: Problems Related With Mini Pubertymentioning

confidence: 99%

Mini puberty and its interpretation

Kurtoğlu

Baştuğ

2014

Turk Arch Ped

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“…This finding was first described by Sedin et al [ 27 ] in the context of ovarian hyperstimulation syndrome in preterm girls. It has also been proposed that edema observed in these subjects is related to vascular endothelial growth factor released from the theca and granulosa cells [ 28 , 29 ]. More recently, other authors reported clinical cases of MP characterized by swelling of the external genitalia observed in preterm girls [ 30 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

Different Faces of Minipuberty in Preterm Twin Girls: A Case Report and Review of the Literature

Pepe

Calafiore

Velletri

et al. 2023

JCM

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Minipuberty (MP) consists of a postnatal activation of the hypothalamic-pituitary-gonadal (HPG) axis, which occurs physiologically during the first months of life. In preterm infants, MP might lead to stronger hormonal stimulation, but specific literature is still scarce. We present the case of a pair of monochorionic diamniotic twin girls, born at 31 weeks of gestation and adequate for gestational age (AGA). At one month old, one of the twins presented with severe edema in the vulva and swelling of the major and minor labia. Laboratory evaluations highlighted increased LH, FSH and estradiol serum concentration. Pelvic ultrasonography and MRI showed a pubertal pattern. Brain imaging was unremarkable. During the one-year follow-up, a decreasing trend of hormonal levels was detected, together with the spontaneous regression of clinical and sonographic pubertal signs. The same hormonal workup was also performed on the other twin, who displayed mildly elevated gonadotropins and estradiol, without evidence of pubertal clinical signs. This case suggests that the amplitude of postnatal HPG activation might be exacerbated in preterm infants, with evidence of puberty changes in clinical, laboratory and sonography data. The spontaneous resolution, together with the exclusion of other causes of precocious puberty, is suggestive for MP of infancy.

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“…Breast growth (42,46) and solitary or monthly vaginal bleeding (47, 48) have been described. The ovarian hyperstimulation syndrome has been diagnosed even before birth (49) and its pathogenesis is still not fully understood. HPG axis immaturity with incomplete development of negative feedbacks after the removal of placental steroids could be involved (45,50).…”

Section: Figures 1 2 Summarize Prenatal and Early Postnatal Changes mentioning

confidence: 99%