Management of Endometrial Hyperplasia

Question 1

What percentage of women with endometrial hyperplasia without atypia progress to endometrial cancer?

Answer 1

<5% in 20 years

Question 2

What should the first-line medical treatment of hyperplasia without atypia be?

Answer 2

The LNG-IUS should be the first-line medical treatment because compared with oral progestogens it
has a higher disease regression rate with a more favourable bleeding profile and it is associated with
fewer adverse effects.

Question 3

What options are there if a woman declines the LNG IUS?

Answer 3

Continuous progestogens should be used (medroxyprogesterone 10–20 mg/day or norethisterone
10–15 mg/day) - minimum 6 months

Question 4

When is surgical management appropriate for women with endometrial hyperplasia without atypia?

Answer 4

Hysterectomy is indicated in women not wanting to preserve their fertility when
(i) progression to
atypical hyperplasia occurs during follow-up, or
(ii) there is no histological regression of hyperplasia
despite 12 months of treatment, or
(iii) there is relapse of endometrial hyperplasia after completing progestogen treatment, or
(iv) there is persistence of bleeding symptoms, or
(v) the woman declines
to undergo endometrial surveillance or comply with medical treatment.

Question 5

What should the initial management of atypical hyperplasia be?

Answer 5

Women with atypical hyperplasia should undergo a total hysterectomy because of the risk of underlying malignancy or progression to cancer.

Question 6

What is the most common gynaecological malignancy in the Western World?

Answer 6

Endometrial cancer

Question 7

What is the most common presentation of endometrial hyperplasia?

Answer 7

abnormal uterine bleeding– This
includes heavy menstrual bleeding, intermenstrual bleeding, irregular bleeding, unscheduled bleeding
on hormone replacement therapy (HRT) and postmenopausal bleeding.

Question 8

What are the risk factors for endometrial hyperplasia?

Answer 8

Unopposed estrogen:

• increased body mass
  index (BMI) with excessive peripheral conversion of androgens in adipose tissue to
  estrogen;
• anovulation associated with the perimenopause or polycystic ovary syndrome (PCOS);
• estrogen-secreting ovarian tumours, e.g. granulosa cell tumours (with up to 40%
  prevalence of endometrial hyperplasia);
• drug-induced endometrial stimulation, e.g. the
  use of systemic estrogen replacement therapy or long-term tamoxifen

Also
Immunosuppression (2x)
Infection

Question 9

What percentage prevalence of endometrial hyperplasia is there with granuloma cell tumours?

Answer 9

40%