Current Update on the Treatment of Genital Warts

Valerie R Yanofsky; Rita V Linkner; David Pompei; Gary Goldenberg


Expert Rev Dermatol. 2013;8(3):321-332. 

In This Article

Clinical Presentation

Following initial exposure and infection, HPV requires an incubation period ranging from 3 weeks to 8 months prior to the appearance of clinical symptoms. On average, however, these present approximately 2–3 months after initial contact.[18] The virus can additionally lie dormant within epithelial cells for prolonged periods of time, resulting in subclinical infections that may remain undetected throughout an individual's lifetime. The degree of clinically silent HPV infection within the general population is thought to be as great as 40%, evidenced by the positive identification of viral samples through DNA analysis conducted on unaffected individuals with healthy appearing genital skin.[19]

Clinical manifestations of EGW may vary dramatically based upon the size, number and location of warts. Typically, EGW present on the moist tissues of the anogenital area, although they can sometimes develop in the mouth or throat following oral sexual contact with an infected person.[3] Lesions themselves may be highly variable in appearance, ranging from flat to dome-shaped, cauliflower-shaped or pedunculated.[13] The warty contour can also vary in color and appearance, and has alternatively been described as white, pink, purple, red or brown, and ranges from flat to ceribriform or verrucous.[20] EGW are frequently found in large warty clusters; however, they may also manifest individually as a solitary keratotic papule or plaque. Patients with small numbers of lesions are often asymptomatic. Initial presentation of EGW lesions usually begin as small, nondistinctive, 1–2-mm flesh-colored papules on the skin; this presentation can be retained for the duration of infection, or alternatively grow up to several inches in diameter.

EGW may be asymptomatic and, particularly when found in small numbers, are rarely described as painful. Large numbers of lesions, however, may be associated with severe discomfort, tenderness, burning and pruritus. Furthermore, large lesions may be subject to bleeding and irritation upon contact, which can result in pain during normal intercourse, defecation or childbirth. Initial infection is often believed to be transient in nature, and it is thought that within the first 4 months of infection approximately 30% of all warts regress spontaneously. An additional 20% are estimated to resolve within the next 2 years.[21] Despite this, long-term remission rates remain largely unknown. Even with the appropriate treatments, the majority of EGW are thought to recur within 3 months of infection.[22] Risk factors for long-term wart persistence include host immunosuppression, concurrent infection with HIV, an increased number of sexual partners, infection with high-risk HPV types and increased patient age.[22,23] Conversely, high rates of spontaneous regression have been linked to the presence of CD4+ lymphocytes in the dermis and epidermis, further supporting the critical role played by the immune system in determining the course of viral infection. Additionally, it is believed that persistent infection in the setting of other clinical risk factors, including pregnancy, may be associated with an increased risk of malignant progression.[24]

The vast majority of EGW infections can be accurately diagnosed on the basis of a careful clinical history and physical examination alone. Documenting findings and the extent of involvement is crucial during physical examination, which may be supplemented with vaginal speculum examination, high-resolution anoscopy, sigmoidoscopy, colposcopy or vaginal speculum examination when indicated.[25] In the case of mild or ambiguous infection, a 3–5% acetic acid solution (the acetowhite test) can be used to help visualize lesions by staining them white. Biopsy is almost never needed for diagnosis, yet it is often recommended for high-risk lesions with possible increased malignant potential. This includes lesions that are found in immunocompromised hosts, those that fail to respond to treatment, or those with atypical features such as ulceration, a rapidly changing appearance or fixation to an underlying structure.[13]