CARCINOMA OF THE

ENDOMETRIUM

2003-10-27

Carcinoma of the Endometrium

One of the commonest gynecological

cancers especially in white
Americans
it occurs most often in postmenopausal

women up to 80 of cases with less

than 5 diagnosed under 40 years of
age

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Carcinoma of the Endometrium

There is no effective screening

programme but occasionally
cervical smears contain endometrial
cancer cells or double thickness
endometrial ultrasonic thickness of
4mm or more indicates a need for
endometrial sampling

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Carcinoma of the Endometrium

Risk Factors
The actual cause of this cancer is unknown

Estrogen
given estrogen alone as
postmenopausal hormone replacement
therapy
Estrogen secreting tumors of the
ovary are associated with an increased
incidence of endometrial carcinoma

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There can be no doubt that oestrogen

can alter the behaviour of this tumour but
there is still a question about oestrogen as a
primary causal agent
Approximately 75 of cases of
endometrial cancer occur in the
postmenopausal period when estrogen values
are low and progesterone is
absent Nulliparity and PCO
syndrome with defective progesterone
synthesis carry an increased risk

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Carcinoma of the Endometrium

Only a proportion of obese diabetic and

hypertensive women develop endometrial
cancer and similarly only a proportion of
women with endometrial cancer are
obese diabetic or hypertensive The
question remains whether estrogen is a
causal agent or is acting in its normal
capacity as a growth factor and is really to
be regarded as a co carcinogen

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Carcinoma of the Endometrium

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Oral contraception especially after

long term use reduces the
incidence of both endometrial and
ovarian carcinomas

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The endometrial hyperplasia induced

by Tamoxifen produces endometrial
polyps A report in the Lancet in
1999 suggested a four-fold increase
in endometrial carcinoma

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Carcinoma of the Endometrium

Symptomatology

The usual presenting symptom of endometrial

carcinoma is postmenopausal bleeding which
carries a 10 risk of associated malignancy in
the absence of hormone replacement therapy.
Curettage or endometrial sampling is
mandatory. Postmenopausal discharge from
pyometra carries a 50 risk of associated
malignancy. Pain may occur with pyometra or
metastatic spread

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Diagnosis
Hysteroscopy with endometrial curettage

or endometrial sampling curettage

alone or outpatient endometrial sampling
alone are essential Curettage is not
infallible On the other hand if a Pipelle
has been correctly introduced record
how many cm and the pathology is benign,
or no tissue is obtained it is most unlikely
that malignancy exists
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Hysteroscopy cervical smear >1

risk of concurrent cervical
malignancy and vaginal or abdominal
ultrasound for ovarian pathology are
advised when endometrial
malignancy is found

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Further groups have been described.

Adeno-squamoid group
This has been divided into two groups:
1. If the squamous cells are well
differentiated the tumour is termed
adeno-acanthoma (Histological Grade 1)
2.Poorly differentiated squamous cells
merit the name adeno-squamous carcinoma
(Grade 2).

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Staging

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In general this cancer is slow to

spread from the uterine cavity,
probably because the endometrium
lacks lymphatics. A chest X-ray helps
detect lung metastases. Magnetic
resonance imaging is preferable to
ultrasound for detection of
myometrial invasion and pelvic spread.
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Local Spread
Slow invasion of the myometrium is
the commonest spread. It may
produce
considerable
uterine
enlargement; or spread may involve
the vaginal vault.

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Venous Spread
This pathway might account for the
occasional appearance of a low vaginal
metastasis; but venous spread is not a
common feature of uterine cancer.

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Lymphatic Spread

The incidence of this (it is much debated)

seems to be somewhere between 10 and
30%. All pelvic nodes, including the internal
iliacs, the parametrium, the ovaries, and the
vagina may be involved, probably with equal
frequency. Lymphatic spread is more likely
to occur when the tumour is anaplastic and
the uterine wall is deeply invaded.

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Tubal Spread
Malignant cells can pass along the
tube in the same way that peritoneal
spill may occur during menstruation.
This may account for isolated ovarian
metastases.

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PROGNOSIS OF ENDOMETRIAL CARCINOMA

With the exception of stage 1 tumors

of histological grades I and II, the
prognosis is less favourable than
many gyaecologists believe with an
overall 5 year survival of 70
approximately Fortunately over
80 of cases are dagnosed at stage
1

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Staging diagnosis, extent of myometrial

invasion and histological
grading differentiation are the
most important prognostic factors
apart from competence of treatment.

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Stage
I
II
III
IV

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5 year survival
85%
68%
42%
22%

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Using both methods on similar cases we

and that the 5-year survival rates for
Stage I are the only ones altered
significantly
Stage and histology 5-years survival
I, G1 and 2
80%
I G3
60%

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TREATMENT OF ENDOMETRIAL CARCINOMA

This is essentialy surgical with

postoperative radiotherapy added when
unfavourable prognostic features are found
at surgery Pre-operative clinical Staging
is inaccurate Progestogen therapy is
probab1y only of value in recurrent
disease

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Few women are unfit for

surgery and caesium insertion
radioactive therapy may be employed
for these,but radiation alone is less
effective than combined surgical and
radiation treatment

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Stage I
Total abdominal hysterectomy and bilateral
salpingo-oophorectomy without partial
removal of vagina. Peritoneal saline
washings are taken for cytology on opening
the abdomen and the Abdominal contents
carefully examined Vaginal hysterectomy
with removal of ovaries, sometimes
laparoscopy-assisted has equal 5 year
survival and lower operative mortality in
appropriate hands

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Stage II

Stage IIa carries a similar prognosis to

Stage I and may be treated as stage I

Stage IIb with clinical invasion of the
cervix has a poorer prognosis than Stage
I and radical hysterectomy pelvic
lymphadenectomy and para-aortic lymph
node sampling are indicated with a
combination of local and external radio
therapy as an alternative treatment
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Stage III
Following the Staging laparotomy radical
hysterectomy lymphadenectomy paraaortic node sampling and removal of as
much malignant tissue as
possible omentectorny is carried out
Stage III diseases limited to the pelvis
may be treated by radiotherapy

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Stage IV
Treatment of this Stage is designed
to control tumour growth and alleviate
symptoms Surgery radiation
therapy cytotoxic therapy and
adjuvant progestogen therapy all have
a place

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The overall results are better than

for carcinoma of the cervix not
because it is less malignant tumour
but because treatment is usually given
earlier Post menopausal
bleeding is much more difficult to
ignore than the irregular bleeding of
the younger woman
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RECURRENCE OF ENDOMETRIAL CARCINOMA

The incidence of recurrence within

5years is in the region of 30 and is
accepted along with the 5-year
survival rate as a measure of the
effectiveness of the various systems
of treatment The majority
recurrences appear within 3 years of
treatment. Early recurrence has a
poor Prognosis.
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PROGESTOGENS
Many endometrial carcinomata are
hormone dependent and progestogens
have been used as part of a combined
primary treatment as well as for
recurrent or metastatic growths

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Between 15 and 50 of recurrences

will respond Medroxyprogesterone
acetate 400 mg to 600 mg
daily is most commonly employed
and the addition of tamoxifen may
improve the response.

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Chemotherapy
Cytotoxic chemotherapy has a limited
place in advanced recurrence Single
agent therapy with adriamycin,
cisplatinum ,cyclophosphamide and
hexamethylmelamine gives response
rates between 20 and 40

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Surgery gives poor results but

chernotherapy using vincristine
actinomycin D and cyclophosphamide
has been reported as curative in
80 of children treated

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