11
Vulva, Vagina, and Anus
Fig. 11.2 Herpes simplex of the vulva. Herpes-infected cells with
enlarged multinuclei and ground glass-like chromatin (Papanicolaou xHP).
Fig. 11.3 Pemphigus vulgaris of the vulva. Loose aggregates of acantholytic
cells with enlarged nuclei and prominent nucleoli (Papanicolaou xHP).
Vulvar intraepithelial Neoplasia
Vulvar intraepithelial neoplasia is defined as an abnormal
growth of vulvar epithelium exhibiting lack of cell maturation
and crowding of cells within the epithelium.12,15 Nuclear hyper-
chromasia, nuclear pleomorphism, and abnormal mitosis are
usually observed.12,15 The term VIN, in this chapter, encompasses
erythroplasia of Queyrat, bowenoid papulosis, carcinoma in
situ, and Bowen's disease.
VIN lesions are becoming more prevalent in younger age
groups than previously observed (i.e., in women 20 to 35 years
of age). The epidemiologic profile in VIN suggests an impor-
tant role for HPV infection.12,15 Immunodepressive disorders
are present in approximately 5% of patients with VIN. VINs are
graded according to their severity and their potential to progress
into an invasive process as follows: VIN I (mild dysplasia); VIN II
(moderate dysplasia); and VIN III (severe dysplasia and carci-
noma in situ). The Bethesda System terminology of "low grade"
and "high grade" can be applied to the VIN I and VIN II/III
groups, respectively. Histopathologically, VIN lesions are sub-
divided into two major morphologic types: classic (usual) and
differentiated (simplex). The classic (usual) VIN encompasses
two subtypes: warty and basaloid.16,17 Classic VIN cases are char-
acterized by disordered cell maturation, with cellular crowding
and nuclear hyperchromasia and pleomorphism (Fig. 11.5). The
warty type of classic VIN displays koilocytotic atypia toward the
surface with cellular eosinophilia, multinucleation, and hyper-
and/or parakeratosis. The basaloid type of classic VIN is com-
posed of more uniform and crowded basaloid cells with scanty
cytoplasm and no maturation near the surface. The differenti-
ated (simplex) type of VIN has some features that overlap with
a hyperplastic or reactive process (Fig. 11.6). However, there are
certain morphologic features that are helpful in differentiating
simplex VIN from squamous hyperplasia. At the surface, simplex
VIN often shows parakeratosis, whereas squamous hyperplasia
often display hyperkeratosis. At the parabasal zone, the presence
of enlarged cells that have prominent eosinophilic cytoplasm
and large pleomorphic nuclei with prominent nucleoli is the
feature characteristic of simplex VIN. There may be prominent
dyskeratosis even with early keratin pearl formation in para-
basal zone, a phenomenon often described as "paradoxical
maturation."14,18
Fig. 11.4 Hyperplastic dystrophy of the vulva. (A) Hyperkeratotic cells with anuclear orangophilic cytoplasm; (B) parakeratosis (Papanicolaou xMP).
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