Mola Hidatidosa

Jessica Octaviani
 HYSTORY
 Hipocrates (400 BC) : hydatid mole  dropsy of uterus
 Aetius of armida AD 600 : a uterus “filled with bladderlike objects”
 Smellie (1700 ) : first term hydatid dan mole, but not until
 Velpeu and Bovin (1827) first recognized hidatids as cystic dilatation of chorionic villi
 Sanger (1889) : coined the term sarcoma uteri deciduocellulare as a malginant tumor derived from decidua of
pregnancy
 Marchand ( 1895) : demontrated these tumor to be the sequele of pregnancy, abortion or hydatid mole and
describedd the proliferation of the syncytium and cytotrophoblast
 Teacher (1903) : confirmed Marchand’s work and negated Sanger’s theory of sarcomatous degeneration of
decidualis
 Finally Fels, Ernhart, Roessler, and Zondek : demonstrated excessive levels of gonadotropic hormone in the urine
of patient with these process
 Hertz and co : evolution of chemotherapy
 Ross, Lipsett, Delfs, Odell, and Vaiukaitus : application of newer endocrinologic and chemotherapy modalities
 Hetig, Sheldon, Gore, Brewer, and Park L detailed pathologic studies performed
 Bagshawe, Acosta-sison, Goldstein, Lewis, Brewer, Lurain, and other : advancement of diagnostic and
therapeutic effort in these disease
Definisi

 Kehamilan abnormal yang ditandai dengan

perubahan yang tidak normal dari plasenta secara
histologi : (TRIAS Mola)
 Proliferasi trofoblastik
 Avaskular
vili  CLINICAL
PATHOLOGY
 Degenerasi hidrofik villi

Williams Gynecology
Klasifikasi
 Terbagi menjadi 2 secara klinis dan histologi yaitu:
 Mola hidatidosa Complete
 Mola hidatidosa Partial
 Not true neoplasm but rather represent pathologic conceptus
 Molar Pregnancy consider malignant potential :
 Aggressive local proliferation
 Myometria invasion
 Systemic metastasis
 Gestational choriocarcinoma and placenta site tumors : true neoplasm
 All characterized by focal or diffuse proliferation of trophoblast
 Trophoblast : derived from outer cell mass of the preimplantation embryo and has
several unique properties
 Affect the physical implantation of the embryo into endometrium and produces
sufficient amount of human chorionic gonadotropin (hcg)  to maintain pregnancy
 Normal trophoblast : lacks expression of transplantation antigens such HLA and ABO
system  allows escape from maternal immunologic rejection
 Invade into maternal decidua, vessels, and myometrium  furthermore continously
embolizes from endometrial lsinuses into maternal venous system where the
trophoblast cell are filtered by the pulmonary circulation and rarely gain access to
remainder of the systemic circulation
 GTN  normal trophoblast function are exagerated
 Complete and partial mole, invasive mole, and choriocacinoma ; exhibit proliferation
of both cytotrophoblast and syncytiotrophobalst cell  maintain the secretion of HCG
 In contrast : The palcental site tumor derived from the intermediate cytotrophoblast
 produced low level of hCG
Klasifikasi : Gross morphology, Hystopathology, & Kariotype

Perbedaan Mola Hidatidosa Mola hidatidosa Partial

Complete
Jaringan fetus atau Tidak ada Ada
embriogenik
Edema dari vili korialis Diffuse Fokal
Hiperplasia Trofoblastik Diffuse Fokal
Scalloping dari vili korialis Tidak ada Ada

Inklusi stoma trofoblastik Tidak ada Ada

Kariotipe 46,XX (90%) ; 46,XY Triploid
Klasifikasi

Mola hidatidosa Complete Mola hidatidosa Partial

• Pembesaran villi dengan kavitasi • Perbedaan ukuran villi,

sentral • Trophoblastic inclusions (tengah)
• Dikelilingi hyperplasia trofoblastik • Hiperplasia trofoblastik ringan
Klasifikasi
 Complete Mole  Totally
paternally derived diploid genotype
(diandric diploidy)

 Partial Mole  Associated with

complete triploidy that incorporates
an extra haploid paternal
chromosomal complement (diandric
triploidy)
Gejala dan Tanda
Perjalanan Penyakit
 Mola hidatidosa Complete  evakuasi  invasi uterus local 15% dan metastasis 4%
 Tanda pasien mola hidatidosa Complete yang beresiko tinggi :
 hCG level >100,000 milli-IU/mL
 Pembesaran uterus yang berlebihan
 Diameter Kista Theca lutein > 6 cm
 Pasien > 40 tahun  resiko of PTM post mola  53%
 Mola hidatidosa Partial  2–4% berkembang menjadi tumor persisten post mola
Sequelae Dari Mola Hidatidosa Complete
Diagnosis
Ultrasonografi
 Mola hidatidosa Complete   Mola hidatidosa Partial
“swiss cheese” pattern
Penanganan

 Evakuasi:
 Suction Curretage  fungsi reproduksi (+)
 Histerektomi  fungsi reproduksi (-)
 Follow Up: kadar βhCG
 βhCG tiap minggu s/d tidak terdeteksi (<5 milli-IU/mL) sampai 3 minggu berturut-
turut
 βhCG tiap bulan s/d tidak terdeteksi sampai 3 bulan berturut-turut
PTM
PTM
 PSTT
PTM (DIAGNOSIS) CHORIOCARCINOMA
• Sangat jarang
ETT
• Hiperplasia
• Patologi:& anaplasia trofoblastik
• Variasi dari PSTT  jarang
 Mola hidatidosa, Abortus, Hamil Aterm abnormal
• Sel
• Berisidengan
tumor infiltrasi ke miometrium
sel trofoblast neoplastic
• Tidak ada villi invasi vascular/limfatik
 Mola Invasif MOLA
MOLA INVASIF
chorionic-type
HIDATIDOSA intermediate
• Tidak ada villi
• • Invasi
• βhCG Perdarahan
myometrium
(extravilli)
Plateu• dalam dan
Pewarnaan
nekrosis
mengelilingi
sel tumorarteri
4 kali (+) untuk hPL
 Choriocarcinoma • • Hidrofik
Metastasis
pemeriksaan : jauh
• • Kebanyakan
villi,
Klinis
selama
 paru/otak/hati
muncul
hiperpasia
3 minggu setelah hamil
trophoblast
• • 15 % aterm.
• Relatif ke
metastasis kemoresisten
vagina/paru
 βhCG
Placental site trophoblastic tumor (PSTT) meningkat ≥ 10%
• Kadar hCG tidakdalam 3 kali
menjadi indicator
pemeriksaan • selama
Pengobatan2 minggu
utama  operasi
 Epithelioid trophoblastic tumor (ETT)
• βhCG persisten selama 6 bulan
setelah evakuasi mola
Klasifikasi
Clinical Classification of Gestational Trophoblastic Tumors
I. Nonmetastatic : No evidence of disease outside uterus
II. Metastatic
 Hammond A. Good Prognostic
1. Short duration of symptoms (≤4 months)
 FIGO 2. Low hCG level (≤40.000 mIU/ml serum β-hCG)
3. No metastases to brain or liver
 FIGO-WHO 4. No antecedent term pregnancy
5. No prior chemotherapy
B. Poor Prognostic (any high-risk factor)
1. Long duration of symptoms (> 4months)
2. High pretreatment hCG level (>40.000 mIU/ml serum β-hCG)
3. Brain or liver metastases
4. Antecedent term pregnancy
5. Prior chemotherapy (unsuccessful)
PTM
Penatalaksanaan
 Berdasarkan stadium:
 Non metastasis (stadium
1)
 Low risk metastasis Survival
Kemoterapi single-
(Stadium II dan III, FIGO agent
Rate :100%
WHO Skor < 7)
 High risk metastasis Kemoterapi multiagent dengan Survival
(stadium II-IV,FIGO atau tanpa radiasi adjuvant Rate : 80-
WHO skor ≥ 7) dan operasi 90%
Kemoterapi PTM Low Risk  MTX/Act-D

RESISTEN

EMACO
Kemoterapi PTM High Risk  EMACO

RESISTEN

EP-EMA
 Kemoterapi Konsolidasi
 Digunakan untuk
 mengeliminasi sel tumor residu
 meminimalisir kemungkinan relaps.
 Diberikan setelah βhCg normal  jumlah sel maligna <105  sel tumor belum
tereradikasi sempurna  kemoterapi konsolidasi
 Kemoterapi konsolidasi  diberikan 3 siklus

 FIGO : beberapa lokasi metastasis memerlukan terapi spesial

 Lesi otak  MTX 1g/m2 sesuai EMA-CO  level of evidence C
 Untuk mencegah kematian dini pada penderita level advance  etoposide 100mg/m2 dan
cisplatin 20mg/m2 pada hari 1 dan 2  level of evidence D

 ESMO :
 Pengurangan 1 siklus pada kemoterapi konsolidasi  resiko relaps
Respon kadar HCG terhadap kemoterapi
TERIMA KASIH