JCU - January 2022 - 20

20
Journal of Clinical Urology 15(1)
To elaborate these misgivings. Firstly, carcinoma in situ/
penile intraepithelial neoplasia (PeIN) or any of its clinical
manifestations (erythroplasia of Queyrat, Bowenoid papulosis
or Bowen's disease of the penis) are not mentioned at
all either clinically or histologically in this paper. It seems
curious to us that 508 circumcisions for significant penile
dermatoses presenting to urologists would not yield any
cases of PeIN. Admittedly PeIN is rare but, regardless,
PeIN is often misdiagnosed or unsuspected. Also, the differentiated,
lichen-sclerosus subtype, can be a very challenging
diagnosis even for an experienced pathologist.2
The diagnosis of PeIN is certainly not going to be achieved
if it is not included in the clinical differential diagnosis in
the first place and if histology is not subsequently routinely
undertaken except for 'suspicious' lesions. In approximately
45% of our 345 patients with PeIN, the diagnosis
was not made clinically and in ~8% a confident clinical
diagnosis (warts, psoriasis, lichen sclerosus, lichen planus
or cancer) was made prior to biopsy or circumcision.2
Secondly, we have to question the 'clinical diagnosis'
of 'physiological phimosis'. This is an oxymoron. We
aver, and teach, that phimosis in the adult male is always a
pathological situation. It is a physical sign. It is not a diagnosis.
It is not a variant of normal. The (pathological)
causes of phimosis are lichen sclerosus, lichen planus,
non-specific balanoposthitis, hidradenitis suppurativa,
Crohn's disease, cicatricial (mucous membrane) pemphigoid,
chronic penile lymphoedema (with or without cellulitis),
sexually transmitted diseases, squamous carcinoma
and Kaposi's sarcoma; lichen sclerosus would be the most
common of all of these.2 Therefore, it cannot pass criticism
that 69 patients clinically diagnosed with 'physiological
phimosis' did not have histology.
Thirdly, and intimately related to the above, we are
bewildered because the histological diagnosis in these
cases of 'physiological phimosis' is not clearly spelled out.
Table 1 in the article cannot possibly mean the authors are
promulgating a histological entity of 'physiological phimosis'
in 147 patients. We have never seen it on a histological
report or made that diagnosis histologically. It is
not clear how these patients are accounted for in the data
presented in Table 2 in the article. We would purport that
certainly most, if not all, of these patients with 'physiological
phimosis' would have actually had lichen sclerosus,
had they been sedulously evaluated and accurately diagnosed.
Indeed, the authors themselves write that:
[Lichen sclerosus] is consistently diagnosed clinically. . .
[and]. . . Other benign inflammatory conditions including
balanitis, zoons [sic] and fibrosis appear to have poor clinical
diagnosis [sic], however 57.6% of cases clinically diagnosed
as non-specific inflammatory conditions were shown to be
early [lichen sclerosus].
Putting aside the criticisms that 'balanitis' and 'fibrosis'
are not actually diagnoses and that Zoon's balanoposthitis
probably does not exist and is almost always part of the
presentation of lichen sclerosus,4 the point the authors are
making here is that lichen sclerosus can be present even
when not suspected clinically. We make the additional
converse point that it is crucial to understand that the prepuce
is not always the site or seat of clinically or histologically
evident disease (although the foreskin is a pivotal
factor in the pathogenesis of lichen sclerosus).5 The implication
made by the authors that histology of the foreskin is
the gold standard in the diagnosis of lichen sclerosus has,
therefore, to be vigorously rebuffed as does, equally, their
paradoxical conclusion that 'clinical diagnosis is consistently
accurate' and their conclusion that 'routine histology.
. . is not required unless a clinical suspicion of
malignancy exists'. None of these arguments hold any
water in militating for the abandonment of routine histology
at circumcision. Quite the opposite.
Next, the authors write that 'previous studies have
suggested histology should be requested [at circumcision]
if [lichen sclerosus] is suspected but this is not
based on evidence'. Not 'studies' actually, but it is manifestly
good clinical practice borne out by evidence published
by us, e.g. (a) in an account of 329 cases of lichen
sclerosus, 177 (53.8%) had biopsies or circumcisions and
in 120 there was corroborative histology from biopsy
(n=49) or circumcision (n=71) specimens; five (2.8%)
had lichen sclerosus in conjunction with PeIN); 57
(17.3% of the total cohort; 32.2% of the number biopsied)
showed non-specific balanoposthitis; of those men
with histopathological evidence of lichen sclerosus, six
(5%) had histopathological evidence of concurrent
human papillomavirus (HPV) infection,6 (b) from another
series of 301 cases, in 260 patients with isolated lichen
sclerosus, clinical diagnosis was achieved in ~95% of
cases; in 41 patients with lichen sclerosus and PeIN combined,
~85% were diagnosed histologically on biopsy
and the remaining ~15% confirmed retrospectively following
histology after circumcision; in those patients
with isolated male genital lichen sclerosus (MGLSc) who
were diagnosed clinically, 93 had histological results
available from subsequent circumcision; histology confirmed
the diagnosis in 87 patients (93.5%), but did not
show evidence of MGLSc in six (6.5%) where the findings
were non-specific,5 (c) in 88 cases three (3.4%)
reported no apparent history of genital warts but koilocytosis
was seen in the penile biopsies; however 33/88
(37.5%) showed the presence of HPV DNA (although
HPV is not thought to be directly pathogenic in lichen
sclerosus),7 and (d) as stated in our fifth paragraph above,
in some patients where lichen sclerosus alone was suspected,
biopsy or circumcision showed PeIN;2 it is not
uncommon in our practice to be 'surprised' by a histological
diagnosis of invasive squamous carcinoma in
patients circumcised for clinically evident lichen sclerosus.
We do not apologise for the detail recounted above;
these findings clearly demonstrate that the differential

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