Skin Disorders Guide

Diagnostic Hallmarks

1. Distribution: face and legs (flat warts); genitalia and perirectal area (genital warts)
2. Tendency for clustering or confluent growth when more than one is present

Clinical Presentation

Genital warts (condylomata acuminata, venereal warts) and flat warts lack visible or palpable surface keratin, and both demonstrate a marked tendency for clustering and a lesser tendency for confluent growth.

Genital warts come in three types. The first type appears as thin, flexible, stalk-like papules. These papules are taller than they are wide. The distal tip of these warts sometimes has a fine filiform appearance. Multiple adjacent lesions may develop a confluent growth pattern forming large clusters. The second type is a flat-topped papule several millimeters in diameter; these are quite similar to the flat warts that occur elsewhere on the body. The third type is a large nodular lesion with a somewhat pebbly surface. These latter lesions, called Buschke­Lowenstein tumors, can reach a diameter of 2-4 cm. Genital warts can grow on any moist surface, but they are most commonly found on the glans and shaft of the penis, at the vaginal introitus, and at the anal orifice. Since in almost all instances they are transferred through sexual activity, they are found most often in young and middle-aged sexually active adults. Condylomata acuminata are asymptomatic. Diagnosis is made on a clinical basis.

Flat warts (verruca plana) appear as barely elevated, square-shouldered, flat-topped papules 1-3 mm in diameter. These lesions may be almost inapparent on visual examination. New flat warts appear rapidly, and by the time patients are first examined, dense clusters of the lesions are usually present. Linear arrangements are sometimes seen because of implantation of viral particles into scratch marks. Flat warts are generally skin colored, but some may be lightly tan. Flat warts in children are most commonly found on the face or on traumatized surfaces of the arms and legs. In adults the distribution assumed is often related to shaving: flat warts frequently develop on the face in men, whereas they are found on the lower legs in women. As noted above, they may also be located on the genitalia. Flat warts are asymptomatic. The diagnosis is made on a clinical basis.

Course and Prognosis

Genital warts appear to be more contagious than other types of warts. Not only are they spread easily on the patient’s own skin through autoinoculation, but they also can be passed on to sexual partners. Left untreated, there is the same tendency for eventual, spontaneous disappearance as is found in verruca vulgaris. However, evidence is currently accumulating to suggest that under certain circumstances the papilloma viruses affecting the genitalia may playa role in the development of genital malignancy. This evidence is particularly strong in the case of HPV 16-induced and HPV IS-induced flat-topped warts involving the cervix. Flat-topped warts elsewhere on the genitalia, especially those that become hyperpigmented, can also demonstrate severe dysplasia or even carcinoma in situ. These latter lesions are often termed Bowenoid papulosis.

Flat warts occurring in children have a short period of growth when they spread like “wild fire.” This is followed by a plateau period involving little change in size or number. The plateau period is succeeded, in turn, by a phase of spontaneous resolution. Flat warts occurring in adults are much more stubborn; left untreated they tend to persist for years.

Flat warts occurring on nongenital surfaces are considered as totally benign lesions, but here, too, evidence is accumulating to suggest that at least one subtype of flat wart virus has some oncogenic potential. That potential is now recognized only in the very rare syndrome of epidermodysplasia verruciformis. Overall, the oncogenic potential of the human wart viruses seems to depend on the specific subtype of virus involved, on the presence of depressed cell-mediated immune responsiveness, and probably on the exposure to certain tumor promoters.

Pathogenesis

Flat warts occurring on nongenital surfaces are caused by HPV type 3. Genital warts of all kind are primarily caused by HPV 6 and HPV 11. Less commonly, HPV 16 and HPV 18 infections are encountered. These latter infections appear to have some oncogenic potential, but unfortunately, they cannot be separately identified on a clinical basis. The implantation and growth of these viruses seem to require some degree of preceding minor skin trauma.

Therapy

Genital warts of the filiform type are most often treated with 20-25% podophyllin in tincture of benzoin. This compound is applied to the entire surface of the wart; care is taken to avoid contact with normal surrounding skin. Generally, instructions are given to wash the painted area 4-8 hours later, but I do not find that this reduces the degree of inflammation and discomfort. Weekly applications for a month will clear 60-80% of these lesions. Podophyllin is, however, a very toxic product; only small amounts should be applied, and its use should be avoided during pregnancy.

A new purified podophyllin product, Condylox, has recently become available. This product is suitable for use at home by the patient. It is applied for three consecutive nights and is followed by four nights without treatment. This weekly cycle of therapy can be continued for 4-6 weeks. Cure rates are similar to those obtained with office application of the older podophyllin; patients describe somewhat less irritation.

The flat-topped genital warts can better be treated with weekly applications of trichloroacetic acid or liquid nitrogen. Large nodular warts should be either excised or destroyed with electrosurgical or laser therapy.

Anoscopy and speculum examination of the vagina are generally desirable and must be carried out if warts are visible at the rectal or vaginal orifice. Intrarectal and intravaginal warts can be treated with podophyllin, cryotherapy, or laser therapy.

Flat warts on nongenital surfaces are best treated with peeling agents such as Retin-A or benzoyl peroxide. These products are applied once or twice daily just as in acne therapy. Most patients will require 4-6 weeks of continuous therapy. Individual lesions can also be treated with daily applications of 16% salicylic acid (Duoftlm or Occlusal). Clyotherapy, trichloroacetic acid, light electrosurgery, and curettage without electrosurgery are also effective but must be used carehllly to avoid pigmentation and scarring.