CASE REPORT: Ovarian Hyperstimulation Syndrome Complicating a Spontaneous Singleton Pregnancy: A Case Report

University of Ulsan, Asan Medical Center
Journal of Assisted Reproduction and Genetics (Impact Factor: 1.77). 01/2001; 18(2):120-123. DOI: 10.1023/A:1026543027300

ABSTRACT It has been known that most cases of ovarian hyperstimulation syndrome (OHSS) are associated with the use of exogenous gonadotropins to induce multiple ovulation. However, OHSS is infrequently associated with a spontaneous ovulatory cycle, usually in the case of multiple gestations, hypothyroidism, or polycystic ovarian syndrome. We report a case of severe OHSS in a spontaneously pregnant woman with no underlying disease.

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    ABSTRACT: Spontaneous ovarian hyperstimulation syndrome is an extremely rare condition that occurs in the absence of ovarian hyperstimulation treatment. It can lead to significant morbidity and mortality, and therefore early diagnosis and supportive treatment are essential. We report an affected mother and her daughter with a previously reported heterozygous activating mutation in the FSHR gene. We performed a literature review with particular regard to pathogenesis, with a view to suggesting a pathophysiological classification system and a diagnostic algorithm to assist in the management of this rare condition.
    European journal of obstetrics, gynecology, and reproductive biology 04/2013; · 1.97 Impact Factor
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    ABSTRACT: The ovarian hyperstimulation syndrome is a major complication of ovulation induction for in vitro fertilization, with severe morbidity and possible mortality. Whereas its pathophysiology remains ill-established, the VEGF may play a key role as well as coagulation disturbances. Risk factors for severe OHSS may be related to patients characteristics or to the management of the ovarian stimulation. Two types of OHSS are usually distinguished: the early OHSS, immediately following the ovulation triggering and a later and more severe one, occurring in case of pregnancy. As no etiologic treatment is available, the therapeutic management of OHSS should focus on its related-complications. Thrombotic complications that can occur in venous or arterial vessels represent the major risk of OHSS, possibly conducting to myocardial infarction and cerebrovascular accidents. Once the OHSS is diagnosed, prevention of thrombotic accidents remains the major issue.
    Journal de Gynécologie Obstétrique et Biologie de la Reproduction 11/2011; 40(7):593–611. · 0.62 Impact Factor
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    ABSTRACT: The pituitary gonadotropin follicle-stimulating hormone (FSH) interacts with its membrane-bound receptor to produce biologic effects. Traditional functions of FSH include follicular development and estradiol production in females, and the regulation of Sertoli cell action and spermatogenesis in males. Knockout mice for both the ligand (Fshb) and the receptor (Fshr) serve as models for FSH deficiency, while Fshb and Fshr transgenic mice manifest FSH excess. In addition, inactivating mutations of both human orthologs (FSHB and FSHR) have been characterized in a small number of patients, with phenotypic effects of the ligand disruption being more profound than those of its receptor. Activating human FSHR mutants have also been described in both sexes, leading to a phenotype of normal testis function (male) or spontaneous ovarian hyperstimulation syndrome (females). As determined from human and mouse models, FSH is essential for normal puberty and fertility in females, particularly for ovarian follicular development beyond the antral stage. In males, FSH is necessary for normal spermatogenesis, but there are differences in human and mouse models. The FSHB mutations in humans result in azoospermia; while FSHR mutations in humans and knockouts of both the ligand and the receptor in mice affect testicular function but do not result in absolute infertility. Available evidence also indicates that FSH may also be necessary for normal androgen synthesis in males and females.
    Reproductive sciences (Thousand Oaks, Calif.) 11/2012; · 2.18 Impact Factor

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