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In human women, oogenesis produces one mature egg cell or ovum for every precursor cell that enters meiosis. This process differs in two unique ways from the equivalent procedure of spermatogenesis in males. First, meiotic divisions during oogenesis are asymmetric, meaning that a large oocyte (containing most of the cytoplasm) and minor polar body are produced as a result of meiosis I, and again following meiosis II. Since only oocytes will go on to form embryos if fertilized, this unequal...
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Related Experiment Video

Updated: May 8, 2026

Fertility Preservation Through Oocyte Vitrification: Clinical and Laboratory Perspectives
08:46

Fertility Preservation Through Oocyte Vitrification: Clinical and Laboratory Perspectives

Published on: September 16, 2021

Spontaneous ovarian hyperstimulation syndrome.

Miro Kasum1, Slavko Oresković, Davor Jezek

  • 1University of Zagreb, School of Medicine, Zagreb University Hospital Center, Department of Obstetrics and Gynaecology, Zagreb, Croatia. mkasum@gmail.com

Collegium Antropologicum
|August 15, 2013
PubMed
Summary

Spontaneous ovarian hyperstimulation syndrome (sOHSS) can occur due to pregnancy hormones or pituitary adenomas. Genetic mutations in the follicle-stimulating hormone receptor (FSHr) can also cause sOHSS, often triggered by specific hormone levels.

Related Experiment Videos

Last Updated: May 8, 2026

Fertility Preservation Through Oocyte Vitrification: Clinical and Laboratory Perspectives
08:46

Fertility Preservation Through Oocyte Vitrification: Clinical and Laboratory Perspectives

Published on: September 16, 2021

Area of Science:

  • Reproductive Endocrinology
  • Medical Genetics
  • Gynecology

Background:

  • Spontaneous ovarian hyperstimulation syndrome (sOHSS) typically manifests during early pregnancy (8-14 weeks) or with pituitary adenomas producing follicle-stimulating hormone (FSH).
  • Previous cases linked sOHSS to elevated human chorionic gonadotrophin (hCG) from multiple pregnancies or hydatidiform mole, polycystic ovary disease, and high thyroid-stimulating hormone (TSH) in hypothyroidism.
  • These hormonal surges can promiscuously activate the wild-type FSH receptor (FSHr), leading to sporadic sOHSS presentations.

Purpose of the Study:

  • To investigate the genetic basis of familial or habitual spontaneous ovarian hyperstimulation syndrome (sOHSS).
  • To characterize the functional consequences of identified follicle-stimulating hormone receptor (FSHr) gene mutations on receptor activation by different hormones.
  • To differentiate the activation patterns of novel FSHr mutants compared to previously reported mutations.

Main Methods:

  • Analysis of familial and habitual sOHSS cases to identify activating mutations in the follicle-stimulating hormone receptor (FSHr) gene.
  • Characterization of five previously reported mutations in the transmembrane helices and one novel germline mutation (c.383C > A, p. Ser 128 Tyr) in the extracellular domain.
  • Assessing the activation of wild-type and mutated FSHrs by thyroid-stimulating hormone (TSH) and human chorionic gonadotrophin (hCG).

Main Results:

  • Six activating FSHr gene mutations have been reported since 2003 for familial/habitual sOHSS.
  • Five previously identified mutations in transmembrane helices showed abnormal activation by TSH with normal hCG levels, exhibiting constitutive activity.
  • The novel p.Ser128Tyr mutant in the extracellular domain demonstrated increased sensitivity specifically to hCG, unlike the other mutants.

Conclusions:

  • Mutated FSH receptors can be hyperstimulated by pregnancy-derived hCG or TSH, precipitating sOHSS.
  • Differential diagnosis must exclude malignancy, pregnancy luteoma, and hyperreactio luteinalis.
  • Most cases of sOHSS resolve spontaneously, managed conservatively, though pregnancy termination or surgery may be needed for complications.