Squamous intraepithelial lesion (LSIL / HSIL)

Vulva & female urethra
Squamous tumors and precursors
Squamous intraepithelial lesion (LSIL / HSIL)

Author: Sarah Strickland, M.D.

Topic Completed: 1 August 2016

Revised: 10 October 2019

Copyright: 2003-2019, PathologyOutlines.com, Inc.

PubMed Search: Usual type vulvar intraepithelial neoplasia

Page views in 2018: 8,374

Page views in 2019 to date: 8,576

Table of Contents

Cite this page: Strickland S. Squamous intraepithelial lesion (LSIL / HSIL). PathologyOutlines.com website. http://www.pathologyoutlines.com/topic/vulvaVIN.html. Accessed December 12th, 2019.

Essential features

Squamous cell carcinoma precursor lesion of the vulva
Distinct oncogenic pathway compared to differentiated type vulvar intraepithelial neoplasia (dVIN)

Terminology

The 2015 International Society for the Study of Vulvovaginal Disease (ISSVD) classifies vulvar squamous intraepithelial lesions as follows:
- Low grade squamous intraepithelial lesion (LSIL) (vulvar LSIL, flat condyloma or HPV effect)
- High grade squamous intraepithelial lesion (HSIL) (vulvar HSIL, VIN usual type)
- Differentiated type VIN (J Low Genit Tract Dis 2016;20:11)

The 2014 World Health Organization Classification of Tumors of the Vulva classification is as follows:

Low grade squamous intraepithelial lesion (LSIL)
High grade squamous intraepithelial lesion (HSIL)
Differentiated type VIN

Epidemiology

Younger women (30 - 50 years)
Risk factors include HPV infection, smoking, immunosuppression, history of genital herpes and increased number of sexual partners
Rate has increased over the last three decades while rate of vulvar squamous cell carcinoma has stayed relatively stable (J Reprod Med 2000;45:613, Obstet Gynecol 2006;107:1018)

Sites

Labia majora, labia minor and posterior fourchette are most frequent sites
May also affect clitoris, mons pubis, perineal and perianal areas

Etiology

Human papillomavirus (HPV) driven process (high risk subtypes HPV 16 and 18 are most common)

Clinical features

Multifocal and multicentric
Pruritus, dysuria, pain, ulceration
20% asymptomatic but abnormal self examination
White or erythematous macules or papules
Can coalesce to form verrucous plaques and can be pigmented
Multicentric intraepithelial or invasive squamous neoplasia of cervix, vagina or anus in 25 - 66% (J Pediatr Adolesc Gynecol 2004;17:45, Cancer 1995;75:2879, Obstet Gynecol 2006;108:1361, Br J Cancer 2009 Jul;101:27)

Diagnosis

Vulvar biopsy: optimally a punch or small incisional biopsy taken from the edge of the lesion including a small piece of normal tissue (Crit Rev Oncol Hematol 2008;68:131)

Prognostic factors

Low risk (3 - 5%) of malignant transformation after treatment (Gynecol Oncol 2005;97:645, Obstet Gynecol 2005;106:1319)
Risk factors for malignant progression include advanced age, radiotherapy and immunosuppression (Gynecol Oncol 1988;31:154)
Can progress to basaloid or warty squamous cell carcinoma
Small percentage undergo spontaneous regression (Gynecol Oncol 2005;97:645,Obstet Gynecol 2000;96:470)
Recurs in 13 - 36% (Cancer 1984;54:1429, Obstet Gynecol 1994;84:741, Gynecol Oncol 1995;56:276, J Reprod Med 1986;31:808)
Studies are conflicting on if positive surgical margins are a risk factor for recurrence (Gynecol Oncol 2005;97:645, Obstet Gynecol 2005;106:1319, Int J Gynecol Cancer 2002;12:490, Obstet Gynecol 1999;93:633)

Treatment

Local excision, imiquimod, cidofovir, photodynamic therapy or laser ablation

Clinical images

Images hosted on other servers:

Various images

Microscopic (histologic) description

Hyperkeratosis and parakeratosis
Acanthosis with club shaped rete ridges
Disorientation of the cells above the basal cell layer with variable extension to the surface
Nuclear clumping with mitotic figures
Intact basement membrane
Variable extension into skin appendages

Microscopic (histologic) images

Images hosted on other servers: