Human reproduction (Oxford, England) · 2009
Do etiologies of premature ovarian aging (POA) mimic those of premature ovarian failure (POF)?
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Gleicher Norbert, Weghofer Andrea, Oktay Kutluk, Barad David
Аннотация
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 > or = 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.
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 > or = 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.