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자궁내막 증식증 (Endometrial Hyperplasia)

원인

Endometrial hyperplasia almost always results from excess estrogen exposure. This may be caused by obesity, anovulation, estrogen therapy without a progestin, or estrogen producing ovarian tumors

경과

Type progression to cancer (%)
Simple (cystic without atypia) 1
Complex (adenomatous without atypia) 3
Simple (cystic with atypia) 8
Complex (adenomatous with atypia) 29

[Ref]1)

Treatment

Medroxyprogesterone acetate 10–20 mg daily or cyclic 12–14 d/mo
Depot medroxyprogesterone 150 mg intramuscularly every 3 mo
Micronized vaginal progesterone 100–200 mg daily or cyclic 12–14 d/mo
Megestrol acetate 40–200 mg per d, usually reserved for women with atypical hyperplasia
Levonorgestrel-containing intrauterine device 1–5 y

em

without atypia

  • Cyclical progestin therapy: medroxyprogesterone acetate, 10-20 mg/day for 14 days per month
  • Continuous progestin therapy: megestrol acetate, 20-40 mg/day

With atypia

  • Continuous progestin therapy: megestrol acetate (40-160 mg/day)
  • For women with atypical complex hyperplasia who no longer desire fertility, hysterectomy is recommended.
  • 메게시아 Megestrol Acetate 40mg / 1 tablet /246원

내막증이 있다고 판단되면 이 듀파스톤이 자궁내막의 증식을 억제하므로 복용하셔도 되고 또 다른 황체호르몬제도 있어서 다른 약을 복용하셔도 된다. 자궁내막증을 치료하기 위해 듀파스톤이란 프로게스테론 제제를 먹고 있는바 이는 자궁내막의 증식을 막고 배란도 억제 한다.

F/U

  • Therapy should be continued for 2 to 3 months, and endometrial biopsy should be performed 3 to 4 weeks after completion of therapy to assess response.
  • Periodic endometrial biopsy or transvaginal ultrasonography d/t undiagnosed cancer in 25% of cases, progression rate to cancer
1)
The behavior of endometrial hyperplasia. A long-term study of "untreated" hyperplasia in 170 patients. AUKurman RJ, Kaminski PF, Norris HJ SOCancer. 1985;56(2):403.

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