Hot Topics in Pediatric Dermatology

Lian Sorhaindo; Anthony Rossi; Andrew Alexis; Nanette B Silverberg

Disclosures

Expert Rev Dermatol. 2010;5(3):259-267. 

In This Article

HPV: Prevention, Diagnosis, Treatment

The session 'HPV: prevention, diagnosis, treatment' was presented by Barry L Smith from St Luke's Roosevelt and Beth Israel Medical Centers (NY, USA). Human papillomavirus (HPV) has an estimated incidence of 6.2 million infections per year, with a prevalence of 20 million. The lifetime risk for sexually active men and women is at least 50%, and in sexually active individuals in the 15–24 age range there are 9.2 million currently infected, with 74% of new HPV infections occurring in this demographic. In females less than 25 years of age the prevalence rates range from 28 to 46%.[101] WHO estimates the worldwide prevalence at 9–13%. The taxonomic family is Papillomaviridae, and this diverse virus occurs in almost all mammals and birds. There are over 100 types of HPV identified, 30–40 of those being anogenital types. There are approximately 15–20 oncogenic types, with the major ones being 16, 18, 31 and 33. HPV 16 and HPV 18 account for 54% and 13%, respectively, of worldwide cervical cancers. Non-oncogenic types include 6, 11, 40, 42, 43, 44 and 54, with HPV 6 and 11 most associated with external anogenital warts.[27] They are classified on species specificity and degree of DNA relatedness, with types that are closer together on the phylogenetic tree having similar genomes. HPV types 6 and 11 are almost identical in DNA sequence. HPV is a nonenveloped, double-stranded DNA virus with a shell composed of the L1, major, and L2, minor, proteins. Virus neutralizing antibodies made in response to natural infections recognize conformational epitopes of L1 on the outer surface of the intact virus particle.[28] HPV is able to evade the host immune response by keeping the antigenic L1 capsid protein from causing a strong immune response. E6 and E7 are the two HPV proteins associated with oncogenic properties. The E6 protein associates with the tumor suppressor protein, p53, and promotes complete degradation of the protein, which therefore leads to prevention of p53-induced apoptosis. The E7 protein alters the cell cycle by its association with retinoblastoma protein, p105RB, which is also a tumor suppressor protein. HPV clearance occurs in approximately 80% of women 15–25 years old. 70% of new HPV infections are cleared within 1 year, and 91% in 2 years, with a median duration of infection of approximately 8 months. High-risk HPV types are more likely to persist, which is crucial for the development of precancerous lesions.[29] Common risk factors for infection include: young age – in women the peak age group is 20–24 years, and in men it is 25–29 years; and lifetime numbers of sex partners. For women other risk factors include early age of first sexual intercourse, male partner sexual behavior, smoking, oral contraceptive use and uncircumcised male partners. For men risk factors include being uncircumcised, a sex partner with cervical intraepithelial neoplasm, anal intercourse with men and a history of other sexually transmitted infections.[30] Mechanisms of HPV transmission and acquisition include sexual contact, which encompasses intercourse, manual, oral or nonpenetrative sexual contact. Nonsexual routes include vertical transmission from mother to newborn, fomites including undergarments, surgical gloves and biopsy forceps (but these are not well documented) and autoinoculation. External warts can present as flesh-colored, flat to papular, exophytic or pedunculated or verrucous. They occur on the penis, vulva, scrotum, perineum and perianal region, the latter not always associated with a history of anal intercourse. Internal warts can occur on the mucous membranes of the vagina, urethra, anus, oral cavity, conjunctiva or larynx. The differential diagnosis includes pearly penile papules or angiofibromas, molluscum contagiosum, lichen planus, enlarged sebaceous glands, condylomata lata (secondary syphilis) or a benign or malignant neoplasm. The diagnosis is a clinical one, but biopsy and viral typing are utilized when: the diagnosis is uncertain; the patient is immunocompromised; there is a poor response to therapy; there is a pigmented or atypical lesion; there is a high risk for a HPV-related malignancy; or there is a medical–legal issue.[31] Chromogenic in situ hybridization can be utilized for HPV typing.

Treatment options should be based on the number, size and morphology of lesions, patient preference, cost, convenience and adverse effects. The choice of therapy includes cryotherapy, electrocauterization, carbon dioxide laser, surgical destruction, podophyllin resin and tricholoracetic acid versus patient-applied therapy, which includes imiquimod cream, podofilox gel or sinecatechins. Imiquimod cream is a cell-mediated immune response modifier applied every other day for 16 weeks. Podofilox is cytotoxic and antimitotic, and is applied twice-daily for 3 days then discontinued for 4 days at 1-week cycles for 4 weeks. Sinecatechins is a green tea extract that has antioxidative, antiviral and immune stimulatory properties that is applied three-times per day for up to 16 weeks. During pregnancy, the goal is to reduce the number of lesions. The only approved therapies during pregnancy include trichloroacetic acid, surgical excision, cryotherapy and electrocautery. Education and counseling should always be provided. Two approved vaccinations against HPV are Gardasil®, which is a vaccine against HPV types 6, 11, 16 and 18, and Cervarix®, which is a bivalent vaccine against HPV types 16 and 18. Both showed good efficacy in preventing disease caused by the HPV virus.

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