ARTICLE
Auteur(s) : Christian Aquilina, Roland
Viraben
Service de dermato-vénéréologie, Hôpital La Grave, place Lange
31052 Toulouse cedex
accepté le 20 Février 2005
There is a well documented association between LSA and carcinoma in
women with a risk assessed between 5 and 7% [1, 2], but in men,
this fact is until recently a matter of discussion [3]. We report
an observation of acute and invasive penile squamous-cell carcinoma
arising within a short time during evolution of LSA.
Observation
A 56-year-old uncircumcised man initially presented with an
asymptomatic erythematous scaly patch with whitish and atrophic
areas on the dorsal aspect of the glans penis, present for two
years. Histologic changes were compatible with lichen sclerosus and
atrophicus (LSA): hyalinization of collagen in the papillary
dermis, hyperkeratosis with acanthosis without cellular atypia (
(figure 1) ).
The patient had no history of HPV infection. The eruption failed to
respond to topical steroids (betamethasone) and androstanolone
applied together for three months. Nearly 1 year later, he
developed in three weeks an acute tumor at the site of the LSA (
(figure 2) ).
Pathological examination of the excised tumor confirmed the
diagnosis of a well-differentiated invasive squamous cell carcinoma
(SCC) ( (figure
3) ). PCR analysis on sections of biopsy tissue (Technique:
Amorces consensus MY 9/11) and DNA in situ hybridization on a
formalin-fixed paraffin-embedded sample, with three HPV probes for
type-6,11; -16,18; -31,33 were negative. Treatment consisted of
partial penectomy, and bilateral inguinal curettage was negative.
Discussion
Squamous cell carcinoma constitutes at least 95% af all penile
malignancies [4]. Two different growth patterns are described :
flat, the most common presentation that ulcerates early, and
nodular lesions or verrucous papules that eventually become
necrotic, ulcerative, as in our patient. The glans was the most
commonly affected area [5]. Histopathologic classification into
four different groups are described with increasing aspect of
atypia of squamous cells and decreasing keratinization, from
low-grade (I-II) well-differenciated lesions to more poorly
differentiated SCC (III-IV).
At present, similarly to the vulvar site, several papers have
reported malignant changes in men with genital LSA, as anecdotal
cases [6-14] and analyses of series [15-17]. Powell [18] reports 11
of 20 patients with penile SCC who had clinical and histological
evidence of LSA; the interval from the diagnosis of previous LSA
was up to 12 years; three had node involvement and four had
documented metastases. Nasca [5] reports malignant changes as SCC
in 5.8% of a cohort of 86 white uncircumcised males with penile LSA
with a lag time of 10-23 years from diagnosis of LSA to diagnosis
of SCC. In our observation, the delay between the two diseases was
very short (3 years) and the carcinoma was rapidly acute and
invasive. In the literature, only one case describes a rapid
development (within 2 months) of SCC on LSA in 3 years [9]. The
origin of genital LSA remains unclear [19]. Among risk factors for
invasive SCC of the penis, oncogenic HPV infection is discussed
[20]. Table 1( Table 1 ) reports the
main studies concerning the possible relationship between LSA and
HPV [21-25]. Observations indicate that long-lasting topical
corticosteroid therapy may occasionally be associated with
opportunistic reactivation of a latent HPV type infection [26].
However, it is probable that, like in the general population, HPV
carriage is very common during the prolonged time course of LS
before SCC develops. Perceau [25] demonstrated that LS-associated
penile SCC did not tend to be frequently associated with oncogenic
HPV infection, compared with non-LS-associated penile SCC.
Today there is no proof of the preventive role of corticotherapy
on the development of SCC. Circumcision appears the better
treatment for localization on the distal foreskin; although,
corticotherapy does not appear to be effective in other
localizations such as glans and balano-preputial fold [27]. In our
case, at least three months of topic corticotherapy were
ineffective.
In conclusion, similarly to vulvar localization, a likely
malignant evolution of penile LSA should be admitted. Our
observation is unusual because the evolution from SLA to an acute
penis cancer was made in a short time. Careful and systematic
histopathological evaluation of any ulcerated or indurated lesions
developing within SLA is therefore strongly recommended.
Table 1 Main studies concerning the possible
relationship between LSA and HPV
|
Author and reference
|
Number of cases (SLA)
|
Number of cases with Positivity for HPV
|
|
Kiene 1991 [21]
|
18
|
4 (type 16/PCR)
|
|
Lau 1995 [22]
|
24
|
0
|
|
Drut 1998 [23]
|
23
|
70% (PCR and in situ hybridisation)
|
|
Simonart 1998 [24]
|
1
|
0 (PCR)
|
|
Nasca 1999 [5]
|
16
|
4 (type 16/PCR)
|
|
Perceau 2003 [25]
|
8
|
0 (type 16/PCR)
|
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