Definition/General

Introduction:
-Molar pregnancy (hydatidiform mole) is an abnormal fertilization resulting in placental tissue with hydropic villous swelling and trophoblastic hyperplasia
-It represents a form of gestational trophoblastic disease
-The condition involves abnormal genomic imprinting
-It occurs in 1-2 per 1000 pregnancies globally
-Higher incidence in Asian populations.
Origin:
-Results from abnormal fertilization events
-Complete moles: diploid androgenetic (all paternal DNA)
-Partial moles: triploid (two paternal, one maternal set)
-Genomic imprinting abnormalities
-Loss of maternal chromosome contribution
-Paternal genome excess drives trophoblastic proliferation.
Classification:
-Two main types: Complete hydatidiform mole (CHM)
-Partial hydatidiform mole (PHM)
-By risk: Low-risk GTD
-High-risk GTD
-By genetics: Diploid complete
-Triploid partial
-Rare: Invasive mole.
Epidemiology:
-Incidence: 1-2:1000 pregnancies
-Higher in Asia (2-10:1000)
-Bimodal age distribution
-Risk <20 years: 1.5x
-Risk >40 years: 5-10x
-Recurrence risk: 1-2%.

Clinical Features

Presentation:
-Irregular vaginal bleeding
-Uterine size-date discrepancy
-Absence of fetal parts
-Hyperemesis gravidarum
-Early preeclampsia
-Hyperthyroidism
-Theca lutein cysts.
Symptoms:
-Vaginal bleeding (95% cases)
-Passage of vesicles
-Excessive nausea and vomiting
-Abdominal pain
-Rapid uterine enlargement
-Respiratory symptoms (trophoblastic embolism).
Risk Factors:
-Extremes of age (<20, >40 years)
-Previous molar pregnancy
-Asian ethnicity
-Dietary factors (low vitamin A)
-ABO incompatibility
-Consanguinity
-Oral contraceptive use.
Screening:
-β-hCG levels (markedly elevated)
-Pelvic ultrasound ("snowstorm" pattern)
-Complete blood count
-Thyroid function tests
-Liver function tests
-Chest X-ray.

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Gross Description

Appearance:
-Grape-like vesicles (complete mole)
-Mixed fetal parts and vesicles (partial mole)
-Hydropic villi
-Absence of fetus (complete)
-Abnormal fetus (partial)
-Clear fluid-filled vesicles.
Characteristics:
-Translucent, cystic structures
-Variable size vesicles
-Soft, friable tissue
-Abundant clear fluid content
-No normal placental architecture.
Size Location:
-Complete mole: entire conceptus abnormal
-Partial mole: mixed normal and abnormal areas
-Vesicle size: few mm to several cm
-Total volume often increased.
Multifocality:
-Diffuse involvement in complete moles
-Focal involvement in partial moles
-Skip areas possible
-Associated with lutein cysts.

Microscopic Description

Histological Features:
-Hydropic villous swelling
-Trophoblastic hyperplasia
-Absence of fetal vessels (complete)
-Central cisterns in villi
-Scalloped villous outlines
-Stromal edema.
Cellular Characteristics:
-Syncytiotrophoblast hyperplasia
-Cytotrophoblast proliferation
-Loss of polar arrangement
-Nuclear atypia
-Increased mitotic activity
-Absence of stromal vessels.
Architectural Patterns:
-Enlarged, rounded villi
-Central cavitation
-Trophoblastic proliferation
-Loss of normal branching pattern
-Circumferential hyperplasia.
Grading Criteria:
-Complete mole: all villi abnormal
-Partial mole: mixed population
-Degree of hyperplasia
-Atypia assessment
-Mitotic index.

Immunohistochemistry

Positive Markers:
-β-hCG (syncytiotrophoblast)
-hPL (human placental lactogen)
-Cytokeratin (trophoblast)
-Inhibin-α
-p57 (maternal genome - absent in complete mole)
-Ki-67 (increased proliferation).
Negative Markers:
-p57 (absent in complete mole)
-CD68 (Hofbauer cells decreased)
-Factor VIII (fetal vessels absent)
-Smooth muscle actin (vessel walls).
Diagnostic Utility:
-p57 staining distinguishes complete from partial mole
-β-hCG confirms trophoblastic origin
-Proliferation markers assess activity
-Genetic studies may be needed.
Molecular Subtypes:
-Complete mole (diploid androgenetic)
-Partial mole (triploid)
-Invasive mole
-Rare genetic variants.

Molecular/Genetic

Genetic Mutations:
-Complete mole: 46,XX or 46,XY (all paternal)
-Partial mole: 69,XXY or 69,XXX (triploid)
-NLRP7 mutations (recurrent moles)
-KHDC3L mutations
-Imprinting defects.
Molecular Markers:
-Loss of maternal alleles (complete)
-Extra paternal genome (partial)
-Microsatellite analysis
-Flow cytometry
-Imprinting gene expression.
Prognostic Significance:
-Complete moles: higher malignant potential (15-20%)
-Partial moles: lower risk (<5%)
-β-hCG levels predict outcome
-Uterine size correlates with risk.
Therapeutic Targets:
-Suction curettage (primary treatment)
-β-hCG monitoring
-Chemotherapy (persistent GTD)
-Hysterectomy (selected cases)
-Contraception during follow-up.

Differential Diagnosis

Similar Entities:
-Hydropic abortion
-Partial mole vs complete mole
-Twin pregnancy with mole
-Placental mesenchymal dysplasia
-Early choriocarcinoma.
Distinguishing Features:
-Complete mole: All villi abnormal
-No fetal parts
-p57 negative
-Partial mole: Mixed villi
-Fetal parts present
-p57 positive
-Hydropic abortion: Focal changes
-Normal genetics.
Diagnostic Challenges:
-Early gestational age
-Small tissue samples
-Distinguishing partial from complete
-Hydropic changes in normal pregnancy
-Genetic studies may be needed.
Rare Variants:
-Invasive mole
-Twin pregnancy with mole
-Recurrent molar pregnancy
-Familial molar pregnancy syndrome.

Sample Pathology Report

Template Format

Sample Pathology Report

Complete Report: This is an example of how the final pathology report should be structured for this condition.

Specimen Information

Products of conception with molar features

Diagnosis

[Complete/Partial] hydatidiform mole

Clinical Correlation

β-hCG: [X] mIU/mL, uterine size [X] weeks

Gross Findings

[Grape-like vesicles/Mixed vesicles and fetal parts]

Microscopic Findings

Hydropic villi with trophoblastic hyperplasia

Immunohistochemistry

p57: [positive/negative], β-hCG: positive

Mole Classification

[Complete/Partial] mole based on morphology and p57 staining

Risk Assessment

[Low/Intermediate/High] risk for persistent GTD

Follow-up Recommendations

Serial β-hCG monitoring, contraception, surveillance

Final Diagnosis

[Complete/Partial] hydatidiform mole