Cervical Intraepithelial Neoplasm Speaker: Tseng Jen-Yu
Jan 13, 2016
Cervical IntraepithelialNeoplasm
Speaker: Tseng Jen-Yu
Introduction
• Cervical cancer was the most common malignancy in both incidence and mortality among women prior to the 20th century
• Incidence fallen dramatically in developed nations due to implementation of population based screening, detection, and treatment programs for pre-invasive disease
Epidemiology and Risk Factor
• 500,000 cases of cervical cancer diagnosed
• 2nd leading cause of cancer death• Risk factors
– Sexually transmitted disease– Human papilloma virus– Multiple sexual partners– Intercourse at early age– Poor personal hygine– Immunocompromise– Cigarette smoking
Pathophysiology• Transformation zone
– Area where glandular epithelium undergoes squamous metaplasia
• Metaplasia– Occurs during fetal development / adolescence / and first pregnancy
– Columnar cells replaced by squamous cells
• Cells undergoing metaplasia are vulnerable to carcinogens
Bethesda System
• LSIL– Low grade squamous epithelial lesion
• HSIL– High grade squamous epithelial lesion
• ASCUS– Atypical squamous cells of undetermined significance
• AGUS– Atypical glandular cells of undetermined significance
Terminology and Definition
• CIN I– Mild dysplasia ( lower 1/3 of epithelium )
• CIN II– Moderate dysplasia ( 2/3 of epithelium )
• CIN III– Severe dysplasia ( upper 1/3 of epithelium / CIS )
• Dysplasia– Disorder maturation / Nuclear hyperchromatism– Increased N/C ratio / Pleomorphism / Mitosis
CIN I
• Disease Profile– Self limited sexually transmitted HPV infection
– 60% regress spontaneously– 30% persistent– 10 ~ 15% progress to CIN II / III– 1% progress to invasive cancer
• Treatment– Ablation ( cryotherapy / laser )– Excision ( LEEP / Knife conization )
• Follow up without treatment– Pregnant women– Immunosuppressed women– Adolescents
CIN II / III
• Disease Profile– 43% untreated CIN II spontaneous regression– 32% untreated CIN III spontanenous regression
– 35% CIN II will persist– 56% CIN III will persist
– 22% CIN II progress to CIS or invasive cancer
– 14% CIN II progress to CIS or invasive cancer
• Treatment– Ablation ( cryotherapy / laser )– Excision ( LEEP / Knife conization )
• Follow up without treatment– Pregnant women– Adolescents
ASCUS
• Represent reactive / reparative changes secondary to inflammation
• 5% of routine Pap smears• Treatment
– Repeat Pap smear in 4 ~ 6 months– Colposcopy if repeat Pap shows ASCUS
AGUS
• Suspected glandular lesion that can’t be classified as reactive or neoplastic
• Higher risk of neoplasia ( adenocarcinoma )
• 0.5 ~2.5% of routine Pap smear• Treatment
– Colposcopy– Conization + ECC
Colposcopy• Acetic acid
– coagulation of nuclear protein preventing light to pass through the epithelium
– Higher nuclear density and higher concentration of protein => white intensity increase
• Schiller / Lugol’s Iodine– Normal, mature squamou
s epithelium contains abundant glycogen
– Produce dark brown stain
– Abnormal epithelium contains relatively little or no glycogen
– Remain relative unstained
Cryotherapy • Indication
– Cytology / Colposcopy / ECC => No microinvasion
– Lesion in ectocervix• Criteria
– CIN I / II– Small lesion– Ectocervix – ECC negative– No endocervical gland involvement
Conization• Indication
– Unsatisfactory colposcopy – Evidence of premalignant or malignant glandular epithelium
– Microinvasion on biopsy / colposcopy / Pap smear
– HSIL ( CIN II / CIN III )– Uncertainty regarding presence of microinvsaion or invasion following direct biopsy for CIn
– Inconsistent Pap smear and colposcopy
Cold Knife
• Indication– Lesion extend to endocervical canal and extent not possible to confirm
– Extent exceeds capability of LEEP ( 1.5 cm )– Cytology shows atypical glandular cells – Colposcopy suggest glandular dysplasia or adenocarcinoma
– Abnormal endocervical curretage
Thank You for your attention