Ovaires polykystiques en 2001 : physiologie et thérapeutique

Caractéristiques cliniques du syndrome OPK

Deux caractéristiques essentielles : anovulation et hyperandrogénisme, avec, éventuellement, oligo ou aménorrhée, hirsutisme, obésité de type androïde, acanthosis nigricans et anomalies métaboliques (insulino-résistance avec hyperinsulinémie, intolérance au glucose ou diabète de type II).

Examens complémentaires

Échographie : augmentation de volume des ovaires et du stroma central avec présence de kystes folliculaires périphériques (8 à 10) d'environ 8 mm de diamètre.

Histologie : multiplication par 2 à 3 des follicules aux stades de développement précoce jusqu'au stade mi-antral.

Physiopathologie

Approches thérapeutiques

• contraceptifs oraux ± anti-androgènes,
• réduction de l'excès pondéral et entraînement physique,
• agents sensibilisateurs à l'insuline.

Clinical characteristics of PCOS Syndrome

Two fundamental characteristics: hyperandrogenism and anovulation which lead to hirsutism and oligo-or amenorrhea. Other features include obesity, acanthosis nigricans , and metabolic disruption (insulin resistance with hyperinsulinemia, glucose intolerance, or type II diabetes mellitus).

Complementary tests

Serum testosterone and DHEA-S levels: to exclude androgen-producing tumors.

Serum 17-hydroxyprogesterone level: to exclude congenital adrenal hyperplasia, 21-hydroxylase deficiency.

Ultrasound: increased size of the ovaries and central stroma with presence of peripheral follicular cysts (8-10) measuring about 8 mm in diameter.

Pathophysiology

• Alteration of the hypothalamic-pituitary-ovarian axis with increased secretion of LH stimulating increased ovarian androgen production. Pituitary FSH secretion is reduced resulting in a failure of ovulation. These abnormalities appear to be influenced by insulin resistance and hyperinsulinemia.
• Mechanisms of anovulation
  • decreased secretion of FSH and/or anomalous follicular response to FSH stimulation,
  • possible inhibitory role of co-gonadotropins (insulin, IGF).
• Mechanisms of hyperandrogenism
  • increased secretion of LH and/or increased theca cell responsiveness to LH stimulation,
  • possible facilitory role of co-gonadotropins (insulin).
• Hypothesis concerning morphogenesis of follicular development at the mid-antral stage of growth
  • premature acquisition of LH receptors by small-sized follicles,
  • excess LH inducing granulosa cell death at the early antral stage.

Therapeutic approaches

• weight loss and physical exercise,
• oral contraceptives ± anti-androgens,
• insulin-sensitizing agents.
• premature acquisition of LH receptors by small-sized follicles ?

Therapeutic approaches

• oral contraceptives ± anti-androgens,
• weight loss and physical exercise,
• insulin-sensitizing agents.