Warts

Warts are caused by infection with human papilloma virus (HPV), a double-stranded DNA virus that is trophic to the skin. There are over 150 serotypes of HPV, and different serotypes have different clinical manifestations. Warts can be transmitted by direct physical contact as well as indirect contact via fomites on object surfaces. Risk factors for warts include immune suppression, immune deficiency syndromes, atopic dermatitis, and direct and indirect contact with other warts.

(Reference: Dermatology, 4th Edition, Elsevier 2018.)

Clinical Manifestations

Types of Warts

(Source: VisualDx 2023.)

(Photograph courtesy of Marcia Hogeling, MD.)

(Source: VisualDx 2023.)

(Source: VisualDx 2023.)

(Source: VisualDx 2023.)

(Source: VisualDx 2023.)

(Source: Oral HPV-Associated Papillomatosis in AIDS. N Engl J Med 2016.)

(Source: Human Papillomavirus Lesions of the Oral Cavity. N Engl J Med 2011.)

(Source: VisualDx 2023.)

Diagnosis

• The diagnosis is made by recognition of characteristic lesions on physical exam.

• Paring of the hyperkeratotic surface results in visible punctate capillary loops. This can help differentiate a wart from a callus or a corn.

  • Paring of plantar wart (figure 11)

  • Punctate pattern of plantar wart after paring (figure 12)

• Biopsy with staining for high-risk types (i.e., HPV-16, -18) is recommended for immunocompromised hosts, extensive disease, and/or warts resistant to substantial treatment.

• In refractory cases, immunosuppressive workup is recommended (e.g., HIV testing).

• In the rare cases of generalized verrucosis (>20 warts distributed in more than one localized area of the body) a limited differential diagnosis should be considered. (See this extensive review on generalized verrucosis.)

Treatment

• Indications for treatment include: functional impairment, discomfort, or high-risk features (e.g., immunosuppressed host, atypia on biopsy).

• Smoking is associated with five times higher rate of wart recurrence after successful clearance.

• For immunosuppressed patients, aggressive therapy is commonly required.

Nongenital Warts

In the immunocompetent host, about 8 out of 10 warts will spontaneously resolve by 2 years without treatment due to host immune recognition.

First-line therapy:

• salicylic acid (SA) 17%

  The following table provides a step-by-step approach for treatment with SA:

  

  (Source: Treatment of Nongenital Cutaneous Warts. Am Fam Physician 2011.)

• aggressive cryotherapy every 4 weeks

  The following table offers a suggested approach for cryotherapy:

  

  (Source: Treatment of Nongenital Cutaneous Warts. Am Fam Physician 2011.)

• Cryotherapy combined with SA may be more effective than either alone, and cryotherapy may be associated with higher cure rates than SA in common warts but not in plantar warts.

>Second-line therapy (refractory to 3 months of first-line treatment):

• Common second-line therapies in dermatologic practice include Candida antigen, cantharidin, podofilox, topical 5-fluorouracil, intralesional bleomycin, topical cidofovir, oral cimetidine, electrodesiccation, carbon-dioxide laser, and pulsed dye laser.

• These therapies have varying evidence and are best summarized in this Cochrane Review and these British Guidelines.

Genital Warts

In the immunocompetent host, one-third of warts will resolve without treatment.

• patient-applied treatments

  • podofilox 0.05% solution or gel

  • imiquimod 5% cream

  • sinecatechins 15% ointment

• clinician-applied treatments

  • cryotherapy every 1-2 weeks

  • podophyllum resin 10%­-25% in compound tincture of benzoin

  • trichloroacetic acid or bichloroacetic acid

  • surgical removal

The following table provides treatment options for the management of external genital warts:

(Source: Management of External Genital Warts. Am Fam Physician 2014.)

Prevention

• Male circumcision results in 34% reduction of high-risk HPV infection.

• The most recent HPV vaccine is 9-valent HPV (Gardasil-9). Data from the Centers for Disease Control and Prevention show at least 64% reduction in vaccine-type HPV infections among teen girls in the United States since introduction of the vaccine (2006).