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Editor,—We read with interest the article by Riddel et al on 66 men with penile lichen sclerosus (PLS) attending a department of genitourinary medicine.1 In this study, the authors found no cases of malignancy.
We have previously reported a retrospective study on the incidence of cancer on 86 cases of PLS retrieved from our histopathological files over a 10 year period (1987–97).2 In that study, five cases showed malignant transformation—namely, squamous cell carcinoma (SCC) (three cases), in situ carcinoma (one case), and verrucous carcinoma (one case).
Since that report, we decided to interview all PLS patients in order to rule out any further malignancy that occurred over time. Of 86 patients identified, 60 were evaluated at our clinic. Among these, we found three additional patients treated with partial penectomy for invasive SCC at other institutions. Their medical records were obtained together with paraffin embedded tissue samples to perform polymerase chain reaction (PCR) for human papillomavirus (HPV) testing. Clinical and laboratory information for these cases, together with previously reported patients, are summarised in table 1.
In this current study, eight (9.3%) out of 86 patients with PLS developed an epithelial cancer. Data analysis using the t test confirmed in our series a statistically significant risk of malignant degeneration (p <0.05).
Clinically, the most common presentation of epithelial cancer arising with PLS was that of an infiltrated or ulcerated plaque followed, in decreasing order of frequency, by a nodular lesion or verrucous papules. The glans was the most commonly affected area. The average age of onset of PLS was 45 years, and that of development of cancer was 62 years. The average lag time from onset of PLS to cancer development was 18 years (range 10–34 years). This long latency time might explain the paucity of cases, mostly anecdotal, reported in the literature in the past 22 years (approximately 20)2–5 compared with our study, in which a long follow up disclosed 9.3% malignant degeneration in a series of 86 patients.
Also, the latency time was shorter in the HPV positive patients (average 15 years) compared with the HPV negative patients (average 23 years). The role of HPV in the pathogenesis of penile cancer is not fully understood. Some HPVs, such as type 16 and 18, are likely to play a part, but not all penile carcinomas are HPV positive, as shown in our study. Also, PLS is not commonly associated with HPV infection.5 In our study we found five patients positive for HPV 16 infection, and this may have hastened the progression towards cancer resulting in a shorter lag time. However, routine HPV testing on larger series is necessary in order to draw any definitive conclusion.
Similarly to vulvar lichen sclerosus, which has been observed to undergo malignant degeneration in 3–6% of women,6 a likely malignant evolution of PLS should be considered. Careful and systematic histopathological evaluation of any ulcerated or indurated plaques developing within PLS is therefore strongly recommended. The association between PLS and cancer may very well be underestimated and there is a need for further investigation that includes long term follow up and routine PCR analysis for HPV infection.
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