Uterine neoplasia

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Chapter 20 Uterine neoplasia

Benign tumours of the uterus

Uterine polyps

Polyps in the uterine corpus (the commonest site) may be part of a hyperplastic endometrium and present with changes in the menstrual cycle. Presenting symptoms include vaginal discharge and intermenstrual bleeding.

Uterine fibroids (leiomyomas)

These are present in 20%–30% of women and the aetiology is uncertain. Risk factors include nulliparity, family history, African race and hormonal influences, especially oestrogen.

Pathology

• macroscopic: firm, round, whorled masses

• sites: intramural, subserous, submucous, also in cervix and broad ligament

• microscopic: smooth muscle proliferation, fibrous tissue

Degenerative changes

These occur because of poor vascularity, and include:

• hyaline degeneration

• cystic degeneration

• calcification

• red degeneration/necrobiosis

• sarcomatous degeneration, rarely (<0.5%)

Clinical features

• often asymptomatic or variable in presentation; usually shrink after menopause

• presentation: menorrhagia, intermenstrual bleeding, infertility, abdominal swelling, pressure effects on the bladder or on large pelvic veins, which can result in oedema of legs or deep venous thrombosis

• in pregnancy, may grow in size, undergo red degeneration and may obstruct labour

Management

• conservative with small or asymptomatic fibroids

• medical treatment

• progesterone

• gonadotrophin-releasing hormone (GnRH) analogues: cause rapid shrinkage of fibroids in the first 3 months, but they regrow to pretreatment size within 3 months of stopping therapy; reduction in volume is proportional to degree of oestrogen suppression; side effects include menopausal symptoms, pelvic pain from acute necrosis of fibroids, reduced bone density (6% trabecular bone loss in lumbar vertebrae after 6 months, but reversed 6 months after stopping therapy)

• surgery: hysterectomy; hysteroscopic resection, myomectomy with or without pretreatment GnRH analogues

Endometrial hyperplasia

Definition. Hyperplasia is an increase in the number of cells in an organ/tissue; it may be pathological or physiologically normal.

Endometrial hyperplasia consists of a variety of changes in endometrial glandular and stromal elements. It is characterised by proliferation of endometrial glands resulting in greater gland-to-stroma ratio than in normal endometrium. These glands vary in size and shape and may show cytological atypia.

World Health Organization classification of endometrial hyperplasia

• glandular/stromal architectural pattern

• simple (cystically dilated glands with occasional outpouching)

• complex (back to back crowding of glands with minimal intervening stroma)

• presence or absence of nuclear atypia

Risk factors

Endometrial hyperplasia is oestrogen-dependent but its precise role is unknown. Conditions such as polycystic ovarian syndrome, unopposed oestrogen therapy, ovarian tumours (oestrogenic or virilising) and obesity are associated with an increased risk of hyperplasia. Other risk factors are infertility, nulliparity and medical conditions (liver disease, hyperthyroid).

Malignant potential

• Cytological atypia is the most useful predictor of the likelihood of cancer progression.

• Simple hyperplasia without atypia: about 1% will progress to cancer; 80% regress after curettage and other treatment.

• Complex hyperplasia without atypia: 3% progress to cancer.

• Simple hyperplasia with atypia: 8% progress to cancer.

• Complex atypical hyperplasia: 29% progress to carcinoma; up to 25% of women have well-differentiated cancers when hysterectomies are done within 1 month of curettage.

Diagnosis and screening

• common presentations: menorrhagia and abnormal bleeding per vagina

• investigations: ultrasound scan to assess thickness of the endometrium; hysteroscopy and endometrial curettage; endometrial sampling; cytological sample from the cervix and/or vagina (sensitivity is low: 35% for atypical hyperplasia, and 20% for adenomatous hyperplasia)

Management

• oral progesterone: by providing a more complete sloughing of the endometrium, reducing the number of oestrogen receptors on endometrial cells and by affecting the metabolism of oestrogen; when using cyclical therapy, the duration of therapy is important (i.e. at least 12 days per month)

• levonorgestrel-releasing intrauterine system (Mirena)

• stop unopposed oestrogen

• surgical treatment: dilatation and curettage; hysterectomy

Guides to treatment

• treatment dependent on the type/grading of hyperplasia, the age of the woman and her desire for future fertility

• simple hyperplasia: dilatation and curettage, hormone therapy, monitoring with yearly endometrial sampling

• complex hyperplasia: if fertility required, treatment with progesterone and induction of ovulation; if fertility not required, or in the older woman, treatment with progesterone or hysterectomy with or without oophorectomy; if conservative management used, an endometrial sample recommended in 3–6 months

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