Diagnosis: Condylomata acuminata

Condylomata acuminata, also known as genital warts, manifest with a variety of appearances. They may be flesh-
colored, brown, or purple papules, plaques, or nodules on the skin or mucous membranes of the genitals. The warts can appear hyperplastic, pedunculated, verrucous, or flat. Genital warts are caused by human papillomavirus (HPV), most commonly types 6 and 11. The lesions can manifest as flat, usually white, macerated endocervical anal or penile condylomata. Whereas genital warts on dry skin and on the circumcised penis tend to manifest with discrete polyplike papules that cluster, genital warts on moist skin and on the uncircumcised penis tend to coalesce into confluent flat papules.

Genital warts are among the most common skin infections and the most common STDs. Each year 1 million new cases of genital warts are diagnosed, 33% of them in men. The estimated prevalence in the U.S. population is 15%. Usually transmitted sexually, HPV can cause anogenital warts after an incubation period of one to six months. Many patients infected with HPV never manifest a condyloma, but they are infectious nonetheless.

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The most common infectious agents causing condylomata acuminata are low-risk HPV 6 and 11; high-risk HPV types 16 and 18 are associated with premalignant and malignant lesions, which can degenerate into squamous cell carcinoma (SCC). Epithelial moisture surrounding genital warts enhances their maceration and whitening. This clinical appearance is not unique to condylomata. Maceration on the glans penis of the uncircumcised male causes a host of dermatoses with inflammatory, neoplastic, and infectious origins to appear as white moist patches and plaques that are difficult to distinguish.

Common skin diseases manifesting on the genitals can resemble genital warts. Penile psoriatic papules and plaques lack the typical psoriatic scale because they are moist and macerated. Similarly, both allergic contact dermatitis and irritant dermatitis due to condoms, lubricants, feminine hygiene deodorant spray, and spermicides manifest without the scale that marks these conditions on other body sites. Zoon’s plasma cell balanitis also lacks scale and does not have a macerated appearance. On the other hand, SCC in situ, e.g., erythroplasia of Queyrat and Bowen’s disease, can manifest with maceration and concurrent erythema. Tinea of the glans penis is extraordinarily rare but could in theory look like genital warts. Almost all patients with penile tinea have associated foci of fungal infection, with only occasional crural involvement.

Genital warts are usually diagnosed on clinical grounds alone. Magnified examination of the genital skin following application of acetic acid has been advocated as a tool to detect grossly inapparent, flat condylomata acuminata, but a number of studies have shown this to be an unreliable tool for diagnosis.

Topical treatments include podophyllin resin, imiquimod, trichloroacetic acid, podophyllotoxin, and sinecatechins (Veregen), a recently approved herbal-derived agent. Surgical or destructive therapies may also be used, e.g., carbon dioxide laser, surgical excision, loop excision, cryotherapy, and electrodesiccation. Whereas podophyllotoxin is more effective than imiquimod against dry warts, imiquimod is more effective than podophyllotoxin in treating moist or macerated
genital warts, indicating that imiquimod’s effectiveness is enhanced by its penetrance. Clinicians contemplating the use of imiquimod must take into consideration that its efficacy numbers are based on up to 16 weeks of use.

A vaccine for HPV types 6, 11, 16, and 18 (Gardasil) is thus far indicated only for females, aged 9-26, as the prime associated morbidity and mortality of HPV 16 and 18 is SCC of the cervix. The vaccine does not clear pre-existing infection.

The patient underwent cryotherapy and was given imiquimod cream to be used three times a week. The freezing procedure was repeated monthly for three months, and the imiquimod was continued for 12 months, leading to complete resolution of the plaques.

Dr. Scheinfeld is assistant clinical professor of dermatology at Columbia University in New York City, where he has a private practice.