Current Update on the Treatment of Genital Warts

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

Disclosures

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

In This Article

Abstract and Introduction

Abstract

External genital warts (EGW) are currently the most common form of viral sexually transmitted disease found in the general population. EGW have been shown to occur as a direct result of infection with the human papillomavirus (HPV). Malignancy is typically associated with high-risk types of HPV; however, low-risk type association has been observed. Numerous therapies are presently indicated for use in the treatment of EGW, which can target lesions through multiple modalities including topically, surgically or via immune modulation. Therapies often differ dramatically with respect to cost, side-effect profiles, dosing schedules, duration of treatment and overall effectiveness. Routine HPV vaccination may play a powerful role in reducing the burden of disease by preventing viral infection and transmission. As HPV vaccination continues to gain widespread approval, it may prove instrumental in decreasing the incidence of HPV infection and eventually eradicating genital warts.

Introduction

External genital warts (EGW), also termed condylomata acuminata (CA), are at present the most prevalent form of viral sexually transmitted disease found within the general population.[1] It is estimated that approximately 3 to 6 million cases present each year in the USA alone, representing approximately 1% of the sexually active population.[2,3] EGW have been shown to occur as a direct result of infection with human papillomavirus (HPV).[4] Although EGW may present in both genders, there is thought to be a slight preponderance for females, with females accounting for 67% of the presenting population.[1] However, recent data from the UK has contraindicated this, with males being suggested to have a higher EGW prevalence than females.[101] In addition to genital warts, oncogenic HPV infection has been linked to the development of a variety of malignant and premalignant lesions of the anogenital and oropharyngeal regions. This helps to account for the tremendous economic burden imposed by HPV, which was estimated at US$4 billion in 2004 in the USA when considering both the direct costs of genital wart treatment as well as those associated with HPV-related invasive cervical cancer.[5]

There are currently over 160 distinct types of HPV that have been identified, with over 40 of these capable of infecting the anogenital tract.[1,6] These can be grossly subdivided into three separate categories based upon their phenotypic association with the development of intraepithelial cancers: low risk, intermediate risk and high risk. Low-risk types comprise those viral strains that rarely give rise to cervical cancers, such as HPV types 6 and 11. Infection by these genotypes, however, accounts for 90% of genital wart lesions. In contrast, HPV types 16 and 18 are strongly associated with cervical, vulvar, vaginal and anal dysplasia, and evidence of infection with these genotypes can be found in up to 70% of squamous cell carcinomas (SCC) of the cervix. They are therefore considered to be high-risk oncogenic types.[7] Intermediate-risk types, such as HPV types 29, 31, 33, 45, 51, 52, 56, 58 and 59, are often found in association with squamous neoplasms; however, some are thought to have a more indolent course of rare progression to cervical SCC.[7] Patients with CA may additionally be infected with multiple HPV strains, and the precise nature of the infection may be a critical prognostic indicator of cervical cancer. This does not play a major role, however, in the diagnosis or treatment of genital warts.[8]

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