Article Figures & Data
Figures
- Figure 1
Timing of ovarian senescence has significant implications for managing symptoms and reducing sequelae related to estrogen deficiency. Currently, women can expect to live one-third of their lifetime after menopause, and the health risks they face are important to address. Women who lose ovarian function 10, 20, or more years before the average age at menopause face even more serious threats from long-term hypoestrogenism if left untreated.
Based on information from reference 1.
Tables
- TABLE 1
Health risks associated with undiagnosed or untreated premature ovarian insufficiency
Associated endocrine disorders
Thyroid disease or Hashimoto thyroiditis
Adrenal insufficiencyLong-term health risks
Osteoporosis and fractures
Cardiovascular disease
Reduced life expectancy due to cardiovascular disease Pregnancy
Unexplained vaginal bleeding
Poorly controlled liver disease
Previous estrogen-sensitive cancer (including breast cancer)
Previous coronary heart disease, stroke, myocardial infarction, or venous thromboembolism
Personal history or inherited high risk of thromboembolic diseaseBased on information from reference 19.
- TABLE 3
Menopausal hormone therapy (MHT) in premature ovarian insufficiency (POI): Principles and recommendations
Systemic MHT is physiologic estrogen replacement in women with POI; oral or transdermal MHT that achieves estrogen replacement levels is recommended as a first-line approach MHT is indicated to reduce long-term health risks associated with POI and to treat symptoms of estrogen deficiency MHT is indicated until age 50 to 51 even if estrogen-deficiency symptoms are absent The need to continue MHT beyond age 50 to 51 should be based on a personalized risk-benefit assessment Systemic MHT does not provide contraception in women with POI Women’s Health Initiative study results should not be extrapolated to treatment decision-making in women with POI or early menopause because these individuals were not included in the study22 Based on information from references 1, 5, and 19.
Classification by cause Idiopathic (90% of cases) Genetic Monosomy X (Turner syndrome) Fragile X premutation (fragile X mental retardation 1 [FMR1]) carrier Autoimmune Isolated In association with polyglandular failure Iatrogenic Cancer treatment with chemotherapeutic agents, stem cell transplantation, or pelvic radiation (exposure > 10–12 Gy highest risk) Bilateral salpingo-oophorectomy Risk factors for POI and early menopause Family history (menopause before age 46 in mother, sister, aunt, or grandmother) Smokinga Earlier onset of menopause Increased prevalence and severity of vasomotor symptoms ↵aIn the Canadian Longitudinal Study on Aging,2 which examined multimorbidity risk in POI, 15.5% of women in the POI group smoked vs 7.3% in the group who experienced menopause at an average age.
Based on information from references 4 and 5.
Irregular menstrual cycles (amenorrhea or oligomenorrhea) for ≥ 4 months
Infertility
Vasomotor symptoms
Urogenital atrophy symptomsBased on information from reference 1.
Criteria for diagnosis of POIa
History of bilateral oophorectomy or other iatrogenic cause of POI
OR
≥ 4-month history of spontaneous amenorrhea or irregular menstrual cycles
FSH > 25 IU/L (repeat in 4 to 6 weeks if diagnostic uncertainty)
Estradiol concentrationb
Negative serum human chorionic gonadotropin testFurther testing for POI causes (specialist evaluation)
Genetic (karyotype, fragile X premutation testing)
Autoimmune (adrenal antibodies, thyroid screening)
Other (additional testing individualized)↵aDiagnosis of POI does not require a specialist, but referral is indicated if there is clinical uncertainty. Note that oral contraceptives can skew follicle-stimulating hormone (FSH) and estradiol values and should be stopped for 1 to 2 weeks before hormone testing.
↵bEstradiol levels are often ordered in conjunction with FSH concentration to assist with test interpretation. Typically, the combination of low estradiol levels and elevated FSH is consistent with POI.
Based on information from reference 1.
