Ultrasonic characteristics of the uterus and ovaries in relation to pubertal development and serum LH, FSH, and estradiol concentrations

Cacciatore, Bruno; Apter, Dan; Alfthan, Henrik; Stenman, Ulf‐Hǎkan

doi:10.1016/s0932-8610(12)80084-3

Cited by 15 publications

(23 citation statements)

References 17 publications

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“…Ultrasound examination showed an uterine volume of 12.38 ml, which was smaller than normal for age-matched normal girls (Cacciatore et al 1991); the right ovary, at 4.5 cm from the uterus, was 1.56 x 0.82 x 1.55 cm; the left ovary was 1.96 x 1.03 x 1.63 cm. Antiovary autoantibodies were absent.…”

Section: Case Reportsmentioning

confidence: 83%

Balanced autosomal translocations and ovarian dysgenesis

et al. 1994

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We report two unrelated women with gonadal dysgenesis, and a (6;15)(p21.3;q15) and a (8;9)(p11.2;q12) balanced translocation, respectively. The patients were of normal stature and showed no phenotypic abnormality or malformation other than ovarian failure. We are not aware of other reports of balanced autosomal translocations associated with gonadal dysgenesis in women. The occurrence of chromosome anomaly and sterility in the two females may be coincidental. However, studies on mouse gametic progression indicate that balanced autosomal translocations can cause oocyte degeneration and reduction of reproductive lifespan. On the basis of these observations, we cannot exclude that the ovarian failure in our patients is the result of oocyte degeneration because of as yet unidentified consequences of the balanced translocations.

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Section: Case Reportsmentioning

confidence: 83%

Balanced autosomal translocations and ovarian dysgenesis

et al. 1994

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“…During childhood, continous follicular growth and atresia occur in the ovaries. The first observations were based on autopsy materials, 15,16 and recently ultrasonography has confirmed the findings 17–20 . The very early follicular development to the stage of antrum formation (approximately 0.25‐mm diameter) is regarded to be independent of gonadotrophic stimulation 21 .…”

Section: Childhoodmentioning

confidence: 93%

“…Before the onset of puberty, blood concentrations of FSH do not rise sufficiently to sustain development beyond this stage; therefore, all antral follicles become atresic. However, even in the 7‐ to 9‐year‐old prepubertal girls, ovarian volume correlates significantly with FSH concentrations 20 . It remains to be examined with the new sensitive estradiol assay, whether the follicular growth seen at this age is indeed reflected in changes in serum estradiol levels.…”

Section: Childhoodmentioning

confidence: 99%

“…In midchildhood, follicles up to 5 mm in diameter are seen. From 7 to 10 years of age, the number of follicles exceeding 5 mm in diameter increases significantly 20 . The size of the largest visible follicle expressed in millimeters corresponds to the age in years; for example, 9‐year‐old girls may display 9‐mm follicles.…”

Section: Childhoodmentioning

confidence: 99%

“…The ovaries have a typical multifollicular appearance by ultrasonography in early puberty 18–20,34. They are full of 5‐ to 12‐mm follicles, but have scanty stroma, which distinguish this pattern from polycystic ovaries.…”

Section: Pubertymentioning

confidence: 99%

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Development of the Hypothalamic‐Pituitary‐Ovarian Axis

Apter

1997

Annals of the New York Academy of Sciences

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The onset of puberty is a centrally driven process, the detailed mechanisms of which are not known. It is translated into an increased activity of the hypothalamic GnRH pulse generator. This in turn is seen as increased pituitary pulsatile secretion of LH and FSH. LH pulses are observed even in midchildhood, particularly after the onset of sleep. Onset of puberty is associated with a greater increase in LH pulse amplitude than frequency and a much greater increase in LH and FSH. A progressive increase in daytime pulsatility occurs, with a gradual reduction of sleep-entrained amplification. Prepubertal FSH concentrations are relatively high in girls, and continous ovarian follicular growth and atresia take place, with estradiol concentrations being higher than in boys. Only after the steep early pubertal increase in LH, ovarian steroidogenesis is activated, with increases in androgen and estrogen secretion. Under further FSH stimulation, follicular growth and maturation proceed. The first menstrual cycles are mostly anovulatory for 1 to 2 years. Luteal phase insufficiency is common the first five years after menarche.

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Expanding the evolutionary explanations for sex differences in the human skeleton

Dunsworth

2020

Evolutionary Anthropology

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While the anatomy and physiology of human reproduction differ between the sexes, the effects of hormones on skeletal growth do not. Human bone growth depends on estrogen. Greater estrogen produced by ovaries causes bones in female bodies to fuse before males' resulting in sex differences in adult height and mass. Female pelves expand more than males' due to estrogen and relaxin produced and employed by the tissues of the pelvic region and potentially also due to greater internal space occupied by female gonads and genitals. Evolutionary explanations for skeletal sex differences (aka sexual dimorphism) that focus too narrowly on big competitive men and broad birthing women must account for the adaptive biology of skeletal growth and its dependence on the developmental physiology of reproduction. In this case, dichotomizing evolution into proximate‐ultimate categories may be impeding the progress of human evolutionary science, as well as enabling the popular misunderstanding and abuse of it.

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Ultrasonic characteristics of the uterus and ovaries in relation to pubertal development and serum LH, FSH, and estradiol concentrations

Cited by 15 publications

References 17 publications

Balanced autosomal translocations and ovarian dysgenesis

Balanced autosomal translocations and ovarian dysgenesis

Development of the Hypothalamic‐Pituitary‐Ovarian Axis

Expanding the evolutionary explanations for sex differences in the human skeleton

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