Human Papillomaviruses

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66

Human Papillomaviruses

Key Points

• Human papilloma viruses (HPV) comprise a large group of at least 200 genotypes of DNA viruses that infect the skin and mucosa.

• Different genotypes cause different skin lesions (Table 66.1).

– Clinical variants differ as to anatomic location, morphology, histopathology, and HPV subtype; correlation of clinical and histopathologic findings is particularly important for bowenoid papulosis and verrucous carcinoma in order to prevent over- or undertreatment, respectively.

Table 66.1

Clinical manifestations of common human papillomavirus (HPV) types.

In clinical practice, subtyping is generally only performed routinely on Papanicolaou smears. Subtyping does not usually change management of cutaneous lesions.

Skin Lesions	Frequently Detected HPV Type
Common, palmar, plantar, myrmecial warts	1, 2, 4
Flat warts	3, 10
Epidermodysplasia verruciformis	5, 8* > others (e.g. 9, 20)
Condylomata acuminata (anogenital warts)	6, 11
High-grade squamous intraepithelial neoplasia (cervical lesions, bowenoid papulosis, erythroplasia of Queyrat)	16, 18, 31, 33 > others (e.g. 35)
Cervical cancer	16, 18

^* Oncogenic, like HPV types 16, 18.

• Nongenital warts.

– Transmitted via person-to-person contact or contact with contaminated surfaces/objects.

– Prevalence of 20% in schoolchildren.

– A third or more self-regress within 1–2 years.

– Numerous warts or persistent/progressive warts should prompt consideration of immunosuppression, defects in cellular immunity, or other syndromes [e.g. HIV infection, epidermodysplasia verruciformis, WHIM syndrome (see Chapter 49)].

• Anogenital infection with HPV.

– Sexually transmitted; in young children may also be acquired perinatally or via the same routes as nongenital warts.

– May be subclinical.

• High-risk HPV types, especially 16 and 18, are a major cause of cervical cancer as well as cutaneous (periungual SCC) and other mucosal intraepithelial neoplasias or SCCs, in particular vaginal, vulvar, penile, and anal; HPV-associated oropharyngeal SCC is a recently identified specific subtype.

• Rx.

– If desired, focuses on destruction of visible lesions or induction of an immune response.

– Effective targeted antiviral treatments are not available.

• Prevention: prophylactic HPV vaccines (e.g. Cervarix^® and Gardasil^®) are available for genital warts and cervical cancer.

Common Warts (Verrucae Vulgares)

• Any site, but commonly on the fingers, dorsal hands, and/or sites prone to trauma (Figs. 66.1 and 66.2).

Fig. 66.1 Verrucae vulgares (common warts). Courtesy, A. Geusau, MD.

Fig. 66.2 Periungual common warts. Destruction of the nail matrix and bed can lead to partial (A) or complete (B) absence of the nail plate. Bowen’s disease may be considered in the differential diagnosis, especially for a single, recalcitrant digital wart. A, B, Courtesy, Reinhard Kirnbauer, MD, and Petra Lenz, MD.

• Hyperkeratotic, exophytic or dome-shaped papules or plaques with punctate black dots (thrombosed capillaries) that may require paring to see (Fig. 66.3).

Fig. 66.3 Verrucae plantares (plantar warts). The photo was taken after shaving of the hyperkeratotic surface; the black dots represent thrombosed capillaries. Courtesy, Reinhard Kirnbauer, MD, and Petra Lenz, MD.

• Histopathology: papillomatosis, acanthosis, hypergranulosis; epidermal keratinocytes have haloes around their nuclei (koilocytes).

• DDx: seborrheic keratosis, actinic keratosis, cutaneous horn, SCC (especially periungual), trichilemmoma, Spitz nevus.

• Rx: outlined in Fig. 66.4; may regress spontaneously within 1–2 years; may be difficult to eradicate.

Fig. 66.4

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