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INTRODUCTION

Viral warts are caused by human papillomaviruses (HPV). Various types of HPV-induced warts exist including common warts (70% of all warts), palmoplantar warts, plane warts, and genital warts.

EPIDEMIOLOGY

Incidence: common

Age: children and adults

Precipitating factors: skin trauma, immunosuppression (HIV and transplant patients), genetic predisposition (epidermodysplasia verruciformis)

PATHOGENESIS

HPVs are nonenveloped double-stranded DNA viruses that produce infection and induction of hyperproliferation when the virus enters proliferating basal epithelial cells. Avoidance of host immune surveillance occurs. Exact mechanisms of infection, latency, and reactivation of HPV are unknown.

PHYSICAL EXAMINATION

Warts present as single or multiple hyperkeratotic, exophytic, skin-colored papules, nodules or plaques. They can have finger-like projections (filiform warts) or can be flat-topped (plane warts). Black punctate dots representing thrombosed capillaries are observed frequently. They most commonly present on fingers, dorsal hands, plantar surfaces, and pressure areas.

DIFFERENTIAL DIAGNOSES

Hypertrophic actinic keratosis, seborrheic keratosis, squamous cell carcinoma, verrucous carcinoma, and acral amelanotic melanoma. Plantar warts can also be mistaken for corns or calluses.

DERMATOPATHOLOGY

The epidermis features hyperkeratosis, acanthosis, papillomatosis, with tiers of parakeratosis, valleys of hypergranulosis and koilocytosis. The dermis features dilated capillary loops and hemorrhage.

COURSE

They generally resolve spontaneously in immunocompetent patients, but this may take years. They tend to persist and resist treatment in immunosuppressed patients. Autoinoculation by scratching may occur.

MANAGEMENT

There is no current specific antiviral therapy for HPV. There are multiple treatment options that either induce local physical destruction of the warts or stimulate the immune response against HPV infection or both. Squamous cell carcinoma can arise from some lesions, that is, condylomata and epidermodysplasia verruciformis and require continuous monitoring. Histological evaluation should be considered for warts that are unresponsive to multiple treatment modalities to rule out malignancy.

Topical Treatment

Patients should be educated as to the viral, infectious, and recurrent nature of HPV despite therapeutic intervention. Patients must also be informed of the need for repetitive treatments for all treatment modalities employed. Multiple effective topical treatments exist. There is no current treatment of choice.

  • Localized tissue destruction: salicylic acid, 5% cantharone, trichloracetic acid, and 0.5% podophyllotoxin are employed daily. Localized wart occlusion with duct tape has demonstrated efficacy in a study. Surrounding normal tissue may demonstrate temporary maceration during treatment.

  • Viral cell division alteration: intralesional bleomycin (0.4 mg/mL) in normal preserved saline; 5-fluorouracil cream.

  • Immune modulation: topical imiquimod has demonstrated efficacy.

Surgical Treatment

Lasers (Table 39.1)

TABLE 39.1Laser Treatment of Warts

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