Activate Windows

Go toSettingsto activate Windows.

GY51 Gynaecology Toronto Notes 2023

Fallopian Tube

•least common site for carcinoma of female reproductive system (0.3%)

•usually serous epithelial carcinoma

•new evidence shows thatsome serous ovarian cancers originate in the fallopian tube

•more common in fifth and sixth decade

Clinical Features

•classic triad present in minority of cases, but very specific

watery discharge (most specific): “hydrops tubae prolluens"

vaginal bleeding or discharge in 50% of patients

crampy lower abdominal/pelvic pain

•most patients present with a pelvic mass (see Pelvic Mass,GY42 and Ovary,GY44 for guidelines

regarding diagnosis/investigation)

Treatment

•same as for malignant epithelial ovarian tumours,see Table 25,GY45

•salpingectomy (removal of fallopian tubes to prevent ovarian cancer)

Vulva

BENIGN VULVAR LESIONS

Non-Neoplastic Disorders of Vulvar Epithelium

• biopsy is often necessary'to make diagnosis and/or rule out malignancy:

1.Lichen sclerosus

subepithelial fat becomes diminished; labia become thin, atrophic, with membrane-like

epithelium and labial fusion

pruritus, dyspareunia, burning, bleeding, ulceration, excoriations

‘figure of 8'

distribution

most common in postmenopausal women but can occur at any age

patients should be monitored for malignancy, due to increased risk ofSCC

treatment: high- potency topical steroid (dobetasol), likely long-term treatment necessary

2.Lichen simplex chronicus

surface of labia majora is thickened and hyperkeratotic,leather-like in appearance

pruritus and burning, often at night most common symptoms

typically occursin postmenopausal women

treatment:medium- or high-potency steroid cream based on symptom severity + nighttime

antihistamines

3.Lichen planus

autoimmune disorder where T cells attack basal keratinocytes

peak incidence at age 30-60

3 variants including erosive, papulosquamous,and hypertrophic

can extend into vaginal canal and cause loss ofstructure (desquamative vaginitis)

can have oral lichen planus in oral cavity

treatment: ultrapotent steroid cream BID until plaques resolve, vaginalsuppositories, or

immunosuppressive therapies(e.g. cyclosporine) are all accepted

Any suspicious lesion ot the vulva should

be biopsied

Tumours

• papillary hidradenoma, nevus,fibroma, hemangioma

MALIGNANT VULVAR LESIONS

Epidemiology

• 5% of genital tract malignancies

• 90% SCC;remainder melanomas, basal cell carcinoma, Paget’

s disease, Bartholin’

s gland carcinoma

Type 1 disease:HPV-related (50-70%)

more likely in younger women

90% of vulvar intraepithelial neoplasia (VIN) contain HPV DNA (usually types 16, 18)

Type 11 disease: not HPV-related, associated with current or previous vulvar dystrophy

usually postmenopausal women n

LJ

Risk Factors

• HPV infection

• VIN: precancerous change which presents as multicentric white or pigmented plaques on vulva (may

only be visible at colposcopy)

• progression to cancer rarely occurs with appropriate management

treatment:local excision (i.e.superficial vulvectomy ± split thickness skin grafting to cover

defects if required) vs.ablative therapy (i.e.laser, cauterization) vs.local immunotherapy

(imiquimod)

+

Activate Windows

GotoSettingstaactivate-WindowsJ

GY52 Gynaecology Toronto Xotes 2023

• history of cervical cancer

• cigarette smoking

• immunodeficiency

• vulvar lichen sderosus

Clinical Features

• most lesions occur on the labia majora, followed by the labia minora (less commonly on the clitoris or

perineum)

• localized pruritus, or white, red, orskin coloured papules, nodules, or plaques most common

• less common: ulcer, bleeding, discharge, pain, and dysuria

• patterns ofspread

local

groin lymph nodes (usually inguinal,then spreading to pelvic nodes)

hematogenous

Investigations

• ± vulvar biopsy

• always biopsy any suspiciouslesion

• do not remove entire lesion during biopsy (allowsfor site identification through sentinel LN

injection if malignant)

Prognosis

• depends on stage: particularly nodal involvement (single most important predictor followed by

tumoursize)

lesions >4 cm associated with poorer prognosis

• overall 5 yr survival rate: 79%

Treatment

• 1

'

KiO Stage I (tumour confined to vulva; no extension to adjacent perineal structures): radical local

excision

• I-

'

IGO Stage 11 (tumour of any size with extension to adjacent perineal structures, no nodal

metastases): modified radical vulvectomy

• 1TGQ stage lll-IV (extension to any of:proximal 2/3of urethra, proximal 2/3of the vagina, bladder

mucosa, rectal mucosa, or fixed to pelvic bone, or large/distant nodal metastases):sentinel lymph node

biopsy followed by surgical resection of residual primary and adjuvant chemotherapy or radiation

Vagina

BENIGN VAGINAL LESIONS

• inclusion cysts

cysts form atsite of abnormal healing of laceration (e.g.episiotomy)

no treatment required

• endometriosis

dark lesions that tend to bleed at time of menses

» treatment:excision

• Gartner’

s duct cysts

remnants of Wolffian duct seen along side of cervix

• treatment:conservative unlesssymptomatic

• urethral diverticulum

can lead to recurrent urethral infection, dyspareunia

• treatment:surgical correction if symptomatic

MALIGNANT VAGINAL LESIONS

Epidemiology

• primary carcinomas of the vagina represent 2-3% of malignant neoplasms of the female genital tract

. 80-90% are SCC

• more than 50% diagnosed between 70-90 yr

Risk Factors

• associated with HPV infection (analogousto cervical cancer)

• increased incidence in patients with prior history of cervical and vulvar cancer

n

L J

Investigations

• cytology

significant false negative rate for existing malignancy (i.e.if grosslesion present, biopsy)

• colposcopy

• Schiller test (normal squamous epithelium takes up Lugol'

siodine)

• biopsy, partial vaginectomy (wide local excision for diagnosis)

• rule out disease on cervix, vulva,or anus(most vaginal cancers are metastatic from one of these sites)

• staging

+

Activate Windows

Go to Settings to activate Window:

GY53 Gynaecology Toronto Notes 2023

Clinical Features

Table 30. Clinical Features of Malignant Vaginal Lesions

Type Clinical Features

Vaginal Intra-Epithclial Neoplasia (VAIN)

Squamous Cell Caicinoma(SCO)

Ciades:analogous to cervical dysplasia

Most common site is upper 113 olposterior wallol vagina

Asymptomatic

Painless vaginal discharge (often foul-smelling) and bleeding

Vaginal bleeding especially during/post- coitus

Urinary and/or rectal symptom 2°to compression

Most are metastatic,usually from cervix,endometrium,ovary,or colon

Most primaries are dear-cell adenocarcinomas

Iwo types:non-DES and OES syndrome

Adenocarcinoma

Treatment

• Stage I

radiation therapy:for tumours >2 cm diameter or tumour involvement of the middle or lower

vagina

surgical excision:radical hysterectomy, upper vaginectomy,and bilateral pelvic

lymphadenectomy

• Stage II-1V:primary radiation with or without chemotherapy

Gestational Trophoblastic Disease/Neoplasia

•refers to a spectrum of proliferative abnormalities of the trophoblast

•GTD = abnormal, can be benign or lead to the malignant form, called GTN

Epidemiology

•1/1000

•marke

l pregnancies

d geographic variation (as high as 1/125 in Taiwan)

•80% benign, 15% locally invasive, 5% metastatic

•cure rate >95%

HYDATIDIFORM MOLE (GTD)

Complete Mole

•most common type of hydatidiform mole

•diffuse trophoblastic hyperplasia,hydropic swelling of chorionic villi, no fetal tissues or membranes

present

•46XX or 46XY, chromosomes completely of paternal origin (90%)

•One sperm fertilizes egg with reduplication or two sperm fertilize empty egg

•15-20% risk of progression to malignant sequelae

•risk factors

• geographic (most common in those of South East Asian background)

others (maternal age >40 yr,

P-carotene deficiency, vitamin A deficiency not proven)

prior molar pregnancy

•clinical features often present during apparent pregnancy with abnormal symptoms/findings

vaginal bleeding (97%)

• hyperemesis gravidarum (26%)

• excessive uterine size for LMP (51%)

hyperthyroidism (7%)

• theca-lutein cysts >6 cm (50%)

- P-hCG >1000001U/L

preeclampsia (27%)

no fetal heartbeat detected,due to absence of fetal parts

With development of HTN early

in pregnancy (i.e.<20 wk).think

gestational trophoblastic disease

Partial (or Incomplete) Mole

•focal trophoblastic hyperplasia and hydropic villi are associated with fetus or fetal parts

•often triploid (XXY, X Y Y, XXX) with chromosome complement from both parents

• usually related to single ovum fertilized by two sperm

•low-risk of progression to malignant sequelae (<4%)

•associated with fetus, which may be growth-restricted, and/or have multiple congenital

malformations

•clinical features

typically presentsimilar to threatened/spontaneous/missed abortion

pathological diagnosis often made after D&C

ri

LJ

+

Activate Windows

Go to Settings to activate Windows.

GYM Gynaecology Toronto Notes 2023

Investigations

• quantitative p-hCG levels (tumour marker) abnormally high for gestational age

• U/S findings

if complete: no fetus(classic “snow storm"

due to swelling of villi)

• if partial: molar degeneration of placenta ± fetal anomalies,multiple echogenic regions

corresponding to hydropic villi,and focal intrauterine hemorrhage

CXR (may show metastatic lesions)

• features of molar pregnancies at high-risk of developing persistent GTN post-evacuation

local uterine invasion as high as 31%

• p-hCG >1000001U/L

excessive uterine size

prominent theca-lutein cysts >6 cm in diameter

Treatment

• for GTD:suction D&C (or rarely hysterectomy)

• Rhogam* if Rh-negative

• for GI N:single agent (i.e. methotrexate, actinomycin D) or multi

-agent (i.e. UMACO, KMA-EP)

chemotherapy based on WHO scoring system

Follow-up

• serial p-hCGs (as tumour marker) every week until negative x 3 (usually takesseveral wk), and then

one month after for incomplete hydatidiform mole or monthly for 6 months if complete hydatidiform

mole

• reliable contraception required to avoid pregnancy during entire follow- up period

• women who become pregnant during the follow-up period should be referred to gynaecologic

oncology and maternal-fetal medicine specialists

• increase or plateau of P-hCG indicates GTN:single or multi-agent chemotherapy based on WHO

scoring system (see Table 31)

Table 31. WHO Prognostic Score for GTD (2011)

Score

Prognostic Factor 0 1 2 4

Maternal Age

Antecedent Pregnancy Mole

Interval(Endol

Antecedent Pregnancy to

Chemotherapy in Months)

HCGIU/L

<40 >40

Abortion Term

<4 46 M3 >13

<103 10310 » 10«-105 »105

Number of Metastases 0

Site of Metastases

largest Tumour Mass

Prior Chemotherapy

14 5-8 >8

Lung Spleen, kidney Gltract Brain, liver

3-S cm >Scm

Single drug two drugs

A score ol C or lessIs considered low-risk CTO.A score ot 7 or more Is considered high-risk GTO.A score ol 213 Is considered ultra high-risk GTO.

The prognostic factor score isrecorded alter the FIGO score stage,separated by a colon

GTN (MALIGNANT GTD)

GTN Diagnosis

• P-hCG plateau: <10% drop in P-hCG over four values In 3 wk (c.g. days 1, 7,!4, and 2 l) OR

• p-h(Xi rise >20% in any two values over 2 wk or longer (e.g. measure at days 1, 7, 14) OR

• P-hCG persistently elevated >6 mo OR

metastases on work-up

Invasive Mole or Persistent GTN

• development of metastases following treatment of documented molar pregnancy

• histology: molar tissue from D&C

• metastases are rare (4%)

Choriocarcinoma

• often presents with symptomsfrom metastases

• highly anaplastic, highly vascular

• no chorionic villi, elements ofsyncytiotrophoblast and cytotrophoblast

• may follow molar pregnancy, miscarriage, therapeutic abortion, ectopic pregnancy, or normal

pregnancy

Placental-Site Trophoblastic Tumour

• rare aggressive form of GTN

• abnormal growth of intermediate trophoblastic cells

• low p-hCG, production of human placental lactogen ( hPL), relatively insensitive to chemotherapy

+

Activate Windows

Go to Settings to activate Windows.

GY55 Gynaecology Toronto Notes 2023

Classification of GTN

• non-metastatic

-15% of patients alter molar evacuation

• may present with abnormal bleeding

all have rising or plateau of P-hCG

negative metastases on staging investigations

• metastatic

4% of patients alter treatment of complete molar pregnancy

• metastasis more common with choriocarcinoma, which tends toward early vascular invasion and

widespread dissemination

ifsigns orsymptomssuggest hematogenous spread, do not biopsy (they bleed)

lungs (80%):cough, hemoptysis, CXR lesion(s)

vagina (30%): vaginal bleeding, “blue lesions” on speculum exam

pelvis (20%): rectal bleeding (if invades bowel), U/S lcsion(s)

liver (10%):elevated Ll'

Ts, U/S, or Cl findings

brain (10%); headaches, dizziness,seizure (symptoms of space-occupying lesion),CiVMRl

findings

• highly vascular tumour, which is more likely to bleed and result in anemia

all have rising or plateau of P-hCG

classification of metastatic GTN

divided into good prognosis and bad prognosis

features of bad prognosis

- long duration (>4 mo from antecedent pregnancy)

- high pre-treatment P-hCG titre:>100000 IU/24 h urine or >400001U/L of blood

- brain or liver metastases

- prior chemotherapy

- metastatic disease following term pregnancy

good prognosis characterized by the absence of each of these features

Investigations (for Staging)

• blood work:CBC, electrolytes, creatinine,

P-hCG,TSH, LPTs

• imaging:CXR, U/S pelvis only

• if CXR showslung metastasis then CT abdomen/pelvis, MRI brain

• if suspect brain metastasis but CT brain negative, consider lumbar puncture for CST p-hCG

• ratio of plasma p-hCGtCSF P-hCG <60 indicates metastases

Lungs are the primary site for malignant

GTN metastases: when pelvic exam

and CXR arc negative, metastases are

uncommon

Table 32. FIGO Staging and Management of Malignant GTN

Stage Findings Management

I Single agent chemotherapy lor low-risk disease (WHO score s6)

1st line: pulsed actinomycin D (Act-0) IV q 2 wk

Alternatives:methotrexate (MIX( based regimen

20% of patients need to switch to alternate single-agent regimen due to failure of

P-hCG to return to normal

Combination chemotherapy (EMA-C0:etoposide.MIX, ACI-D,cyclophosphamide,

vincristine) if high-risk (WHO score >7) or if resistant to single-agent chemotherapy

Can consider hysterectomy il fertility not desired or placental

-site trophoblastic

tumour

Metastatic disease to genitalstructures As above

Metastatic disease to lungs with or without As above

genital tract involvement

Distant metastatic sitesincluding brain, liver, Ultra high-risk patientsshould have low-dose induction chemotherapy weekly lor

1-3 wk,followed by multi-agent chemotherapy

Disease confined to uterine corpus

II

III

IV

kidney.Gl tract

Follow-up (for GTN)

• contraception for all stages to avoid pregnancy during entire follow-up period

• stage 1,11,111

weekly P-hCG until 3 consecutive normal results

• then monthly x 6-12 mo

• stage IV

• weekly P-hCG until 3 consecutive normal results

• then monthly x 24 mo

+

Activate Windows

Go to Settings to activate Windows.

GY56 Gynaecology Toronto Notes 2023

Common Medications

Table 33. Common Medications

Side Effects (S/E), Contraindications

(C/I). Drug Interactions (D/I)

Drug Name (Brand Name) Action Dosing Schedule Indications

S/E:headache.Cl upset

D/I:zidovudine,probenecid

acyclovir (Zovirax!

) Antiviral:inhibits ONA

synthesis and viral replication

First Episode: 400 mg P0 TIO Genital herpes

x 7-10 d

Recurrence: 400 mg P0 TIO *

5 d

Initial:1.25-2.5 mg P0 once Galactorrhea amenorrhea

daily at night with food

then:increase by 2.5 mg every Prolactin-dependent menstrual

2-7 d as needed untiloptimal

therapeutic response

Usual Range:1.5-15 mg once

daily

bromocriptine (Parlodel -

) Dopaminomimebc.agonist at D2

Receptor and antagonist at 01

Receptor:acts directly on anterior

pituitary cells toinhibit

synthesis and release of

prolactin

S/E:N/V,headache,postural

hypotension,somnolence

C/I:uncontrolled KIN.pregnancy-induced HTN.

CAD.breastfeeding

D/I:domperidone,macrolides,octreotide

2" to hyperprolactinemia

disorders and infertility

Prolactin-secreting adenomas

(microadenomas,prior tosurgery of

macroadenomas)

IVF

forIVF:

Initial: 1.25 mg/d P0 between

days 4- 6 of follicular phase

Then: 2.5 mg/d until 3 d after

onset menstruation

domiphene citrate (Clomid | Increases output olpituitary

gonadotropins toinduceovulation

50 mg once dailyx 5 d

try 100 mg or 1G0 rng once dally dysfunction (e.g. amenorrhea.PC0S)

who desire pregnancy

Patients with persistent ovulatory S/E:Common:hot flashes,abdominal

discomfort,exaggerated cyclic ovarian

enlargement,accentuation olMittelscbmerz

Rare: ovarian hyperstimulation syndrome,

multiple pregnancy,visual blurring,birth delects

C/I:pregnancy,liver disease,hormone-dependent

tumours,ovarian cyst,undiagnosed vaginal

bleeding

S/E: vulvar/vaginal burning

If Ineffective 3 courses:

adequate Inal

clotrimazole(Caneslen ) Antifungal:disrupts fungal cell

membrane

Tablet:100 mg/d intravaginally Vulvovaginal candidiasis

x 7 d or 200 mg/d x 3 d or 500

mg x 1dose

Cream |1or 2%):1applicator

intravaginally OHS x 3-7 d

Topical:apply BIDx 7 d

combined oral contraceptive

pill (OCP)

Ovulatory suppression by inhibiting

LHandFSH

Decidualication of endometrium

Thickening of cervical mucus lo

prevent sperm penetration

Synthetic progestin

Contraception

Disorders of menstruation

See Tables 7-10,6Y1S-6Wani Table12.6Y18

dienogest (Visanne!

) 2 mgP0 Pelvic pain associated with

endometriosis

S/E:changes to menstrual pattern,VIE

C/I:pregnancy,lactation, liver disease/

malignancy. VIE disorders, cardiovascular disease,

hormone- dependent tumours,undiagnosed AUB

S/E:Gl upset,hepaloloxicity

C/I:pregnancy, severe hepatic dysfunction

D/I:warfarin,dlgoxin

S/E: hot flushing,nausea,headache

C/I:pregnancy, osteoporosis,undiagnosed vaginal

bleeding, severe hepalicdyslunction

D/I:Organic Anion Transport Protein (0ATP) 1B1

inhibitors

S/E:headache, rash.N/V.abdominal pam.diarrhea

D/I:terfenadine,cisapride,astemicole,

hydrochlorothiazide,phenyloin. warfarin,rifampin

See Tables 7-10,GY15- GWand Table 12.GYM

100 mg P0 BI0 xe7 d Chlamydia,gonococcalmlection,

syphilis

doxycydinc Tetracycline derivative:inhibit

protein synthesis

clagolix (Orlissa ) Synthetic GnRH antagonist:induces

reversible hypoestrogemc stale

150 mg P0 daily or 400 mg

P06ID

Endometriosis,emerging evidence

lor libroids.adcnomyosrs

fluconazole (Diflucan -) Antifungal:disrupt fungal cell

membrane

150 mgP0 x1dose Vulvovaginal candidiasis

unresponsive to clotrimazole

Copper IUD:mild foreign body

reaction in endometrium,which

is toxic to sperm and alters sperm

motility

Progesterone-releasing IUD:

decidualization of endometrium and

thickening of cervical mucus,may

suppress ovulation

Synthetic GnRH antagonist:induces 3.75 mg IM q1mo or 11.25 mg

reversible hypoestrogenic stale IM q3 mo

Usually ? 6 mo. cheekbone

density il>6 mo

Rclrcalment with lupron'

alone

not recommended because ol

effects on bone density

Contraceptive effects last 3 yr; Contraception

up to 5 yr (Copper IUD,Mirena8, Disorders of menstruation

Kyleena5)

intrauterine device (IUD)

copper IUD (Nova-T

;

)

progesterone-releasing

IUD (Mirena ,Kyleena )

leuprolide (lupron ) Endometriosis

leiomyomata

S/E:hot flashes,sweats,headache,vaginitis,

reduction in bone density, acne.Glupset

C/I:pregnancy,undiagnosed vaginal bleeding,

breastleeding

DUB

Precocious puberty

r y

L J

+

Activate Windows

Go to Settings to activate Windows.

GY57 Gynaecology Toronto Notes 2023

Table 33. Common Medications

Drug Name (Brand Name) Action Dosing Schedule Indications Side Effects (S/E),Contraindications

(C/I),Drug Interactions (D/I)

mcnotropin (Pergonal ) Human gonadotropin with FSH

and IK effects;induce ovulation

and stimulate ovarian follicle

development

75 -150 IU olFSH and IH IM once Infertility

dally n 7-12 d.then 10000 IDHCG

1d alter last dose

S/E: bloating,irritation at injection site,

abdominal/pelvic pain,headache. N/V. multiple

pregnancy

C/I:primary ovarian failure,intracranial lesion

(e.g.pituitary tumour),uncontrolled thyroid/

adrenal dysfunction,ovarian cyst (not PCOS),

pregnancy,undiagnosed uterine bleeding

metronidazole (Flagyl:

) Bactericidal:forms toxic metabolites 2 g P0 x 1dose or 500 mg P0

which damage bacterial DNA

Bacterial vaginosis,trichomonas

vaginitis

S/E: headache,dizziness. N/ V.diarrhea,disulfiramlike reaction (flushing,tachycardia,N/V)

C/I:pregnancy (1st trimester)

0/1: cisapride,warfarin, cimelrdine,lithium,

alcohol,amiodaionc,milk thistle,caibamarcpinc

Sec tables 7-10.6Y15 CYVand fable 12,6Y18

BID x 7 d

Releases progestin which causes Contraceptive effects last up

decidualization of endometrium and to 3 yr

thickening of cervical mucus,may

suppress ovulation

Anticholinergic:relaxes bladder

smooth muscle,inhibits involuntary

detrusor contraction

Contraception

Disorders of menstruation

nexplanon (etonogestrcl

implant)

5 or 10 rrig/d P0

May increase doses by 5 mg

weekly to a maxof 30 mg/d

Ovciacllvc bladdei (urge

incontinence)

oxybulynin (Ditropan ) S/E: dry mouth/eyes, constipation,palpitations,

urinary retention,dizziness,headache

C/I:glaucoma.Gl ileus,severe colitis,obstructive

uropathy.use with caution if impaired hepatic/

renal function

S/E: anaphylaxis,psychosis,tachycardia,dry

moulh/cyes.headache, constipation, urinary

retention, chest pain,abdominal pain

C/I:glaucoma,gastric/urinary retention,use with

caution if impaired hepatic/renal function

S/E:N/V,diarrhea,dizziness,rare cases ol

thrombosis,abdominal pain. MSK pain

C/I:thromboembolic disease,acquired

disturbances of colour vision,subarachnoid

hemorrhage,age <15 yr

S/E: headache,hoi flushes,constipation,vertigo,

endometrial thickening

C/I:pregnancy,undiagnosed vaginal bleeding,any

gynaecological cancer

S/E:ovarian enlargement or cysts,edema and pain

at injection site,arterial thromboembolism, fever,

abdominal pain,headache,multiple pregnancy

C/I:primary ovarian failure,intracranial lesion

(e.g.pituitary tumour), uncontrolled thyroid/

adrenal dysfunction,ovarian cyst (not PCOS),

pregnancy,abnormal uterine bleeding

tolterodinc (Octroi ) 1- 2 mg P0 BIO Overaclive bladder (urge

incontinence)

Anticholinergic

trancxamic acid

(Cyklokapron )

Anil- fibrinolytic:reversibly inhibits

plasminogen activation

1-1.5 g 110 010 for first 4 d of Menorrhagia

cycle

Max 4 g/d

Ophthalmic check if used for

several wk

5 mg P0 once daily foi max 3 mo: leiomyoma (prcopeialive)

first tablet taken anytime during

first 7 d of menstruation

ulipristal acetate(Fibristal | Selective progesterone receptor

-withdrawn frommarket modulator ISPRM)

in 2020 urofollitropin

(Melrodin )

urofollitropin (Metrodin | FSH 75 lU/d SC x 7-12 d Ovulation induction in PCOS

r m

L J

+

Activate Windows

Go to Settings to activate Windows.

GY58 Gynaecology Toronto Notes 2023

Landmark Gynaecology Trials

Trial Name Reference Clinical Trial Details

Endometrial Cancer

P0RTEC-3 LANCET 2019;20(9):1273 1235 Title:Adjuvant Chemoradiotherapy versus Radiotherapy Alone in Women with High- Risk Endometrial Cancer (PORTEC-3):

Patterns ol Recurrence and Post-Hoc Survival Analysis ola Randomised Phase 3 Trial

Purpose:loinvestigate the benefit ol combined adjuvant chemotherapy and radiotherapy vs.pelvic radiotherapy alone for

women withhigh-risk endometrial cancer.

Methods: Women with high-risk endometrial cancer were randomly assigned to receive radiotherapy alone or

chemoiadiolherapy.The co-primary endpoints were overall survival and failure- free survival. Secondary endpoints included

vaginal,pelvic,and distance recurrence.

Results:At a median of 72.6 mo,Syr overall survival was 81.4% with chemoradiotherapy vs.76.1% with radiotherapy,and 5 yr

failure- free survival was 76.5% with chemoradiotherapy vs.69.1% with radiotherapy.Distant metastases occurred in 78 /330

women in the chemoradiotherapy group vs. 98(330 in the radiotherapy group.

Conclusions: For women with stage 3 or serous endometrial cancers,or both,chemoradiotherapy should be recommended

over radiotherapy alone.

Cervical Cancer

HEJM 2018; 379:1895 1904 Title: Minimally Invasive versus Abdominal Radical Hystercdomy lor Cervical Cancer

Purpose:loinvestigate survival outcomes after laparoscopic or robot-assisted radical hysterectomy (minimally invasive

surgery) vs.open abdominalradical hysterectomy (open surgery).

Methods:Patients with stage At.IA2.or 181cervical cancer and a histologic subtype of squamous- cell carcinoma,

adenocarcinoma,or adenosquamous carcinoma,were randomly assigned toundergo minimally invasive surgery or open

surgery.

Results:The rate of disease- free survival at 4.5 yr was 86% withminimally invasive surgery and 96.5% with open surgery,a

difference of -10.6% (95% confidence interval[Cl],-16.4 to -4.7).Minimally invasive surgery was associated with a lowci rate

of disease-free survival than open suigciy (3 yr rate. 91.2% vs.97.1%) and a lower rate ol overall suivival (3 yr late. 93.8% vs.

99.0%).

Conclusions:Among women with early-stage cervical cancer,minimally invasive radical hysterectomy was associated with

lower rates of disease-free survival and overall survival than open abdominal radical hysterectomy.

UCC

ri

L J

+