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