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Warts (verrucae
vulgaris) are common, benign epidermal lesions caused by human papillomavirus
infection. They can appear anywhere on the body in a variety of
morphologies. Diagnosis is by examination. Warts are usually self
limited but may be treated by excision, cautery, cryotherapy, liquid
nitrogen, and topical or injected agents.
Warts are almost universal in the population; they affect all ages but are most common among children and are uncommon among the elderly.
Etiology
Warts are caused by human papillomavirus (HPV) infection; there are over 100 HPV subtypes. Trauma and maceration facilitate initial epidermal inoculation. Spread may then occur by autoinoculation. Local and systemic immune factors appear to influence spread; immunosuppressed patients (especially those with HIV infection or renal transplants) are at particular risk of developing generalized lesions that are difficult to treat. Humoral immunity provides resistance to HPV infection; cellular immunity helps established infection to regress.
Symptoms and Signs
Warts are named by their clinical appearance and location; different forms are linked to different HPV types (for unusual manifestations, see
Table 1: Viral Skin Diseases: Wart Variants ).
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Table 1
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Wart Variants
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Clinical Form
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Human Papillomavirus
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Description
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Bowenoid papulosis*
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16, 18, 33, 39
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Flat brown verrucous papules on the vulva and penis (benign)
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Buschke-Löwenstein tumor
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6, 11
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Large cauliflower-like tumors
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Butcher's (meat handler's) wart
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7
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Common warts, usually benign
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Cutaneous squamous cell carcinoma
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38, 41, 48
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In early stages, resembles warts
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Epidermodysplasia verruciformis
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1–5, 7–9, 10, 12, 14, 15, 17–20, 23–25, 36, 47, 50
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May develop into a cutaneous malignancy such as squamous cell carcinoma
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Keratoacanthoma
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77
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Thought to be a well-differentiated squamous cell carcinoma
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Oral focal epithelial hyperplasia (Heck's disease)
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13, 32
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Benign
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Warts in renal transplant patients
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75–77
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Often multiple and difficult to treat
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*Affected women and female partners of affected patients should be frequently evaluated for cervical cancer.
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Common warts: Common warts (verrucae vulgaris) are caused by HPV 1, 2, 4, 27, and 29. They are usually asymptomatic but sometimes cause mild pain, especially when they are located on a weight-bearing surface (eg, bottom of the feet). They are sharply demarcated, rough, round or irregular, firm, and light gray, yellow, brown, or gray-black nodules 2 to 10 mm in diameter. They appear most often on sites subject to trauma (eg, fingers, elbows, knees, face) but may spread elsewhere. Variants of unusual shape (eg, pedunculated or resembling a cauliflower) appear most frequently on the head and neck, especially the scalp and beard.
Filiform
warts: These warts are long, narrow, frondlike growths, usually located on the eyelids, face, neck, or lips. They are usually asymptomatic. This morphologically distinct variant of the common wart is benign and easy to treat.
Flat warts: Flat warts, caused by HPV 3, 10, 28, and 49, are smooth, flat-topped, yellow-brown papules, most often located on the face and along scratch marks; they are more common among children and young adults and develop by autoinoculation. They generally cause no symptoms but can be difficult to treat.
Palmar
and plantar warts: These warts, caused by HPV 1, occur on the palms and soles; they are flattened by pressure and surrounded by cornified epithelium. They are often tender and can make walking and standing uncomfortable. They can be distinguished from corns and calluses by their tendency to pinpoint bleeding when the surface is pared away. Classically, warts hurt with side-to-side pressure, and calluses hurt with direct pressure; in reality, this is not a reliable sign.
Mosaic warts: Mosaic warts are plaques formed by the coalescence of myriad smaller, closely set plantar warts. As with other plantar warts, they are often tender.
Periungual
warts: These warts appear as thickened, fissured cauliflower-like skin around the nail plate. Patients frequently lose the cuticle and are susceptible to paronychia. Periungual warts are more common among patients who bite their nails.
Genital
warts: Genital warts (see Sexually Transmitted Diseases (STD): Genital Warts) manifest as discrete flat to broad-based smooth to velvety papules on the perineal, perirectal, labial, and penile areas. Infection with high-risk HPV types (most notably types 16 and 18) is the main cause of cervical cancer. These warts are usually asymptomatic.
Diagnosis
Diagnosis is based on clinical appearance; biopsy is rarely needed. A cardinal sign of warts is the absence of skin lines crossing their surface and the presence of pinpoint black dots (thrombosed capillaries) or bleeding when warts are shaved. Differential diagnosis includes corns (clavi), lichen planus, seborrheic keratosis, skin tags, and squamous cell carcinomas. DNA typing is available in some medical centers but is generally not needed.
Prognosis
Many warts regress spontaneously; others persist for years and recur at the same or different sites, even with treatment. Factors influencing recurrence appear to be related to the patient's overall immune status as well as local factors. Patients who subject themselves to local trauma (eg, athletes, mechanics, butchers) may have recalcitrant and recurrent HPV infection. Genital HPV infection has malignant potential, but malignant transformation is rare in HPV-induced skin warts, except among immunosuppressed patients.
Treatment
Treatment is aimed at eliciting an immune response to HPV. In most instances, this is achieved by applying an irritant (eg, salicylic acid [SCA], trichloroacetic acid, 5- fluorouracil , podophyllum resin, tretinoin , cantharidin).
These compounds can be used in combination or with a destructive method (eg, cryosurgery, electrocautery, curettage, excision, laser). Direct antiviral effects can be achieved with bleomycin and interferon-α2b, but these treatments are reserved for the most recalcitrant warts. Topical imiquimod 5% cream induces skin cells to locally produce antiviral cytokines. Topical cidofovir , HPV vaccines, and contact immunotherapy (eg, squaric acid dibutyl ester and Candida allergen) have been used to treat warts. Oral treatments include cimetidine , isotretinoin , and oral zinc. In most instances, modalities should be combined to increase the likelihood of success.
Common warts:
In immunocompetent hosts, common warts usually spontaneously regress within 2 to 4 yr, but some linger for many years. Numerous treatments are available. Destructive methods include
Which method is used depends on the location and severity of involvement. For example, 17% liquid SCA can be used on the fingers, and 40% plaster SCA can be used on the soles.
The most common topical agent to be used is SCA. SCA is available in a liquid, plaster, or impregnated within tape. Patients apply SCA to their warts at night and leave on for 8 to 48 h depending on the site.
Cantharidin can be used alone or in combination (1%) with SCA (30%) and podophyllum (5%) in a collodion base. Cantharidin alone is removed with soap and water after 6 h; cantharidin with SCA or podophyllum is removed in 2 h. The longer these agents are left in contact with the skin, the more brisk the blistering response.
Cryosurgery is painful but extremely effective. Electrodesiccation with curettage, laser surgery, or both is effective and indicated for isolated lesions but may cause scarring. Recurrent or new warts occur in about 35% of patients within 1 yr, so methods that scar should be avoided as much as possible.
Filiform
warts:
Treatment is removal with scalpel, scissors, curettage, or liquid nitrogen. Liquid nitrogen should be applied so that up to 2 mm of skin surrounding the wart turns white. Damage to the skin occurs when the skin thaws, which usually takes 10 to 20 sec. Blisters can occur 24 to 48 h after treatment with liquid nitrogen. Care must be taken when treating cosmetically sensitive sites, such as the face and neck, because hypopigmentation frequently occurs after treatment with liquid nitrogen. Patients with darkly pigmented skin can develop permanent depigmentation.
Flat
warts:
Treatment is daily tretinoin (retinoic acid 0.05% cream). If peeling is not sufficient for wart removal, another irritant (eg, 5% benzoyl peroxide ) or 5% SCA cream can be applied sequentially with tretinoin . Imiquimod 5% cream can be used alone or in combination with topical drugs or destructive measures. Topical 5- fluorouracil (1% or 5% cream) can also be used. Spontaneous resolution may follow unprovoked inflammation of the lesions; however, flat warts are frequently recalcitrant to treatment.
Plantar
warts:
Treatment is vigorous maceration with 40% SCA plaster kept in place for several days. The wart is debrided while damp and soft, then destroyed by freezing or using caustics (eg, 30 to 70% trichloroacetic acid). Other destructive treatments (eg, CO2 laser, pulsed-dye laser, various acids) are often effective. Duct tape is effective when applied for 6-day intervals, followed by debridement of macerated tissue.
Periungual:
Combination therapy with liquid nitrogen and imiquimod 5% cream, tretinoin , or SCA is effective.
Refractory:
Several methods whose long-term value and risks are not fully known are available for recalcitrant warts. Intralesional injection of small amounts of a 0.1% solution of bleomycin in saline often cures stubborn plantar and periungual warts. However, Raynaud's syndrome or vascular damage may develop in injected digits, especially when the drug is injected at the base of the digit, so caution is warranted. Interferon, especially interferon-α, administered intralesionally (3 times/wk for 3 to 5 wk) or IM, has also cleared recalcitrant skin and genital warts. Extensive warts sometimes improve or clear with oral isotretinoin or acitretin . Cimetidine at doses up to 800 mg po tid has been used with success but is more effective when combined with another therapy.
Last full review/revision October 2008 by James G.H. Dinulos, MD
Content last modified October 2008
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