Pocket ObGyn – Premature Ovarian Insufficiency (POI)

Dec 8, 2019 admin PHỤ KHOA, SẢN KHOA, SINH DỤC 0

Pocket ObGyn – Premature Ovarian Insufficiency (POI)
See Abbreviations

Definition & Epidemiology (Obstet Gynecol 2009;113:1355; Lancet 2010;376:911)

  • Decline in nml ovarian fxn in a woman <40 A form of hypergonadotropic hypogonadism. 0.3% of reproductive age ; 5–10%  w/ secondary amenorrhea.
Etiology
  • Accelerated follicular atresia due to genetic syn (Turner XO ® oocyte apoptosis; fragile X premutation ® oocyte toxic prot). Autoimmune ovarian failure secondary to systemic autoimmune dz (check for type 1 DM, thyroiditis, hypoadrenalism). Ovarian toxins (chemo w/ alkylating agents, XRT, smoking, infxn such as mumps or CMV).
  • Abn follicular stimulation due to defects in steroidogenic enzymes or defects in ovarian gonadotropin receptors (eg, FSH receptor mut)
  • Result is ¯ ovarian estrogen production ® ¯ negative feedback on pituitary ® ­ FSH, LH
Clinical Manifestations
  • Primary or secondary Irreg menses vs. primary or secondary amenorrhea
  • W/ fragile X – mental retardation, ataxia, premature ovarian failure
  • W/ Turner syn – short stature, shield chest, web neck, low hairline, low set ears, aortic coarct, streak ovaries
  • ¯ estrogen w/ primary infertility ® impaired secondary sexual dev, dyspareunia (secondary to vaginal dryness), decreased bone density
  • ¯ estrogen & secondary infertility ® hot flashes, night sweats, emotional lability, dyspareunia, decreased bone density
Initial Workup
  • ¯ estrogen ® ­ FSH, ­ POI if:

FSH >10 mIU/mL (except during the midcycle preovulatory LH surge) FSH > LH w/ E2 <50 pg/mL (´ 2 if ­ FSH) = absent/nonfunctioning follicles

  • Clomiphene citrate challenge test – check FSH on cycle day 3 & 10 after 100-mg clomiphene PO daily on cycle day 5–9; ­ FSH after clomid sugg low ovarian reserve
  • AMH–secretion by small preantral & early antral follicle granulosa cells reflects size of primordial follicle pool, declines w/ age, undetectable at Early marker of ovarian reserve, & AMH level is not cycle dependent. AMH >1 ng/mL – adequate ovarian reserve.
  • AFC by transvaginal US – high variability, useful if equivocal labs
Follow-up Studies
  • Karyotype (identify individuals w/ any form of gonadal dysgenesis characterized by an absent or abn X chromo & those w/ any portion of a Y chromo), genetic testing for FMR1 gene permutations
  • Adrenal autoantibodies by immunofluorescence assay
  • Anti-islet cell Ab (given association w/ type 1 DM)
  • Serum TSH, thyroid-stimulating Ig, thyroid peroxidase antibodies
  • Bone mineral density to detect osteopenia
Treatment and Medications
  • HT to ¯ sx of estrogen deficiency & prevent bone loss
  • Daily calcium (1200–1500 mg) + Vit D (600–800 IU) for bone health
  • Exogenous androgen – unclear role in mgmt; no high-quality evid
  • Clinician sensitivity, additional psychological support
  • IVF using donor oocytes – controversial in women w/ Turner syn
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Polycystic Ovarian Syndrome (PCOS)

Definition (Nat Rev Endocrinol 2011;74:219)

  • A d/o of ovarian fxn characterized by anovulation, elevated androgen levels, & polycystic A/w obesity & insulin resistance (metabolic syn). Different diagnostic criteria used:

1990 NIH – NICHD – hyperandrogenism or hyperandrogenemia, oligoanovulation, & exclusion of other endocrine disorders

2003 Rotterdam criteria – 2 of following 3: Clinical or biochemical hyperandrogen- ism, oligo- or anovulation, polycystic ovaries. Other endocrine disorders must be excluded.

2006 androgen excess – PCOS society – clinical or biochemical hyperandrogenism w/ oligo-/anovulation &/or polycystic ovaries

 

Epidemiology & Pathophysiology
  • 6–10% of women, depending on diagnostic criteria. Uncertain etiology, but hyperandrogenism may cause ovulatory dysfxn & abn gonadotropin
  • Androgen excess ® follicular arrest & ­ Hyperinsulinemia may also ® follicular arrest & phenotypic features.
  • Presentation may include excess body or facial hair, frequent shaving/plucking, irreg menstruation, infertility, alopecia, acne, obesity, metabolic
Physical Exam
  • Assess weight & BMI, hair pattern/growth, thyroid, galactorrhea (prolactin-secreting tumor), acanthosis nigricans
  • Deep voice, male pattern facial/body hair, clitoromegaly may suggest androgen- secreting tumor or congen adrenal hyperplasia
Diagnostic Workup
  • Document oligo- or anovulation by Hx, serum progesterone, or urinary LH testing
  • Labs: Consider testing for serum androgens esp if no clinical hyperandrogenism – or – if frank TSH, FSH, & prolactin if pt anovulatory. 75 g, 2-h oral gluc tol test for women w/ hyperandrogenism w/ anovulation + acanthosis nigricans +

Obesity (BMI > 30 kg/m2, or >25 in Asian pop) + FHx of T2DM or GDM (Fertil Steril

2012;97(1):28)

  • TVUS ovaries: ³12 follicles in each ovary measuring 2–9 mm in diameter, &/or ovarian volume >10 mL indicates polycystic ovaries
  • Endometrial bx if long Hx of oligomenorrhea due to ­ endometrial cancer

Treatment (Fertil Steril 2008;89:505)

  • Exercise & weight loss improve ovulation rate – 1st-line rx
  • In women not attempting Preg, low-dose combination OCP may ¯ hyperandrogenism & risk of endometrial cancer
  • Clomiphene citrate 1st-line ovulation induction in women desiring Preg (see below)
  • Limit to 6 ovulatory cycles before considering 2nd-line rx

Ovulation induction w/ exogenous gonadotropins is 2nd-line therapy. IVF is 3rd-line therapy.

See Abbreviations

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