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Does elevated human chorionic gonadotropin alone trigger spontaneous ovarian hyperstimulation syndrome?
Rachel Michaelson-Cohen1, Gheona Altarescu, Uziel Beller
1Department of Obstetrics and Gynecology, Shaare Zedek Medical Center, Hebrew University, Jerusalem, Israel. drraymico@hotmail.com
Fertility and Sterility
|January 2, 2008
Summary
Elevated human chorionic gonadotropin (hCG) alone does not cause spontaneous ovarian hyperstimulation syndrome (sOHSS). Additional factors beyond the hCG-FSH-receptor interaction are involved in sOHSS development.
Area of Science:
- Reproductive Endocrinology
- Medical Genetics
Background:
- Spontaneous ovarian hyperstimulation syndrome (sOHSS) is a rare condition with an unclear pathophysiology.
- The role of human chorionic gonadotropin (hCG) as a sole trigger for sOHSS requires further investigation.
Observation:
- A case of sporadic, nonfamilial sOHSS was analyzed.
- Patients with elevated hCG levels (>150,000 IU/L) were evaluated, excluding those with gestational trophoblastic diseases, multiple pregnancies, or iatrogenic OHSS.
Findings:
- Genetic sequencing of the follicle-stimulating hormone (FSH) receptor gene revealed no known mutations associated with OHSS.
- Thyroid-stimulating hormone (TSH) levels were normal, ruling out hypothyroidism.
- Despite extremely high hCG levels, none of the selected patients developed sOHSS.
Implications:
- Elevated hCG alone is insufficient to cause sOHSS.
- The pathogenesis of sOHSS likely involves a complex interplay of factors beyond the hCG-FSH-receptor pathway.
- Further research is needed to elucidate the multifaceted mechanisms underlying sOHSS.
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