Bowenoid papulosis (BP) is an uncommon squamous
intraepithelial neoplasia, which manifests as an eruption
of flesh colored or hyperpigmented verrucous
papules that may become confluent plaques, involving the
genitalia and anogenital regions.
A 39-year-old Chinese gentleman with a past medical history of
Human Immunodeficiency Virus (HIV) infection on antiretroviral
therapy, presented to our center with a one-year history of
biopsy proven BP. Physical examination revealed widespread
disease with multiple hyperpigmented verrucous papules,
patches and confluent plaques over the perianal area (Figure 1).
Given the extent of his disease, conventional therapy with
liquid nitrogen and topical 5% imiquimod would necessitate
multiple treatments; the patient was commenced on oral
acitretin 25 mg daily (0.38 mg/kg/day) in combination with
topical 5% imiquimod, to be applied every alternate day.
His BP regressed after eight weeks of treatment to flattened
pigmented patches. No adverse effects were reported. His
medication was tapered with continued clinical response to
a maintenance regime of oral acitretin 25 mg three times a
week and topical 5% imiquimod twice a week. After 6 months
of treatment, the lesions had cleared with post-inflammatory
depigmentation (Figure 2).
Bowenoid papulosis is associated with infection by oncogenic
human papillomaviruses (HPV),1 which spread by skin-to-skin
contact during coitus. BP typically runs an indolent course with
the risk of malignancy reported to be at 1%.2 Histologically,
BP is characterised by acanthosis with full-thickness dysplasia,
making it challenging to distinguish from other variants of
squamous carcinoma in-situ. Hence, the diagnosis is clinched
by establishing a clinicopathological correlation.
The treatment for BP is conservative as it usually regresses
spontaneously. For persistent, extensive or symptomatic
lesions, therapy is similar to the options for condylomata acuminata,
which is directed at local destruction via keratolysis (eg, podophyllotoxin), immunomodulation (eg, topical 5%
imiquimod and 5% 5-fluorouracil), cryotherapy ablation, photodynamic
therapy (PDT) or other surgical methods (eg, laser
or electrocurettage).
BP’s link to HIV infection is two-fold; patients with HIV infection
are at higher risk for developing BP from exposure during
sexual contact; there is a greater risk of malignant transformation
of BP due to their concurrent immunocompromised state.
In light of the latter, BP in HIV patients need to be managed
with urgency through regular post-treatment checks monitor
for disease recurrence. Our patient’s CD4 count at therapy initiation
was 178 cells/mm3 (reference interval 500 – 1000 cells/
mm3) indicating immunodeficiency.
Therapeutic options for our patient were limited as he was not
keen for surgery. Sole application of topical therapies, though
proven to be effective in BP in HIV patients,3,4 may cause discomfort
owing to the development of ulcerations at the sensitive
anatomical area of affliction. Moreover, an immunosuppressed
constitution may engender treatment failure when imiquimod5
is used to achieve immunomodulation. PDT is a viable option
