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Hum. Reprod. Advance Access originally published online on July 16, 2009
Human Reproduction 2009 24(10):2395-2400; doi:10.1093/humrep/dep256
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© The Author 2009. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

OPINION

Do etiologies of premature ovarian aging (POA) mimic those of premature ovarian failure (POF)?

Norbert Gleicher1,2,3,8, Andrea Weghofer1,2,4, Kutluk Oktay1,2,5 and David Barad1,2,6,7

1 Center for Human Reproduction, 21 East 69th Street, New York, NY 10021, USA 2 Foundation for Reproductive Medicine, New York, NY, USA 3 Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA 4 Department of Obstetrics and Gynecology, Vienna University School of Medicine, Vienna, Austria 5 Department of Obstetrics and Gynecology, New York Medical College, Valhalla, NY, USA 6 Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine, Bronx, NY, USA 7 Department of Obstetrics, Gynecology and Women's Health, Albert Einstein College of Medicine, Bronx, NY, USA

8 Corresponding author. Tel: +1-212-994-4400; Fax: +1-212-994-4499; E-mail: ngleicher{at}thechr.com

BACKGROUND: It is unknown whether etiologies differ between milder forms of premature ovarian senescence (the acronym given here ‘premature ovarian aging, POA’), and premature ovarian failure (POF).

METHODS: We assessed presumed pathophysiologies in 74 consecutive POA patients, diagnosed based on elevated age-specific baseline follicle stimulating hormone and/or abnormally low anti-Müllerian hormone levels (<1.5 ng/ml). A genetic etiology was presumed with ≥34 triple CGG expansions on the FMR1 gene. An autoimmune etiology was assumed with at least one abnormality in a laboratory panel, involving antinuclear, antiphospholipid and thyroid antibodies, total immunoglobulin levels and anti-ovarian as well as anti-adrenal autoantibodies. A combined etiology was presumed with both autoimmune and genetic etiologies, and a patient was considered idiopathic when no abnormalities were found.

RESULTS: Twelve of 74 (16.2%) women demonstrated a genetic, 28 (37.8%) an autoimmune, 9 (12.2%) combined and 25 (33.8%) idiopathic etiologies.

CONCLUSIONS: Presumed underlying etiologies with POA follow a similar distribution pattern as reported for POF. POA and POF may, therefore, represent a continuum in phenotypical expression of different etiologies of premature ovarian senescence. Like POF, POA should be considered reason to investigate underlying etiologies.

Key words: diminished ovarian reserve/premature ovarian failure (POF)/premature ovarian aging (POA)/FMR1 gene/autoimmunity


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