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• wart treatment
• Sexually Transmitted Diseases
  

Background: Infections dueness to papillomaviruses are common and lead to a wide variety of clinical manifestations involving the epidermal surfaces.

Manifestations include common warts (verrucae vulgaris) , palmo-plantar warts, flat warts (verrucae plana) , oral warts, focal epithelia hyperplasia, epidermodysplasia verruciformis (EDV) , genital warts (condyloma acuminata) , Bowen papulosis, Bowen disease, papillomas of the mucosal surfaces, and intraepithelial neoplasias.

Very strong evidence indicates that certain papillomaviruses are involved in cervical and genital cancers.

Pathophysiology: Papillomaviruses are small (55 nm) , double-stranded DNA viruses.

Over 200 genotypes of papillomaviruses infect the skin and mucosal surfaces.

These viruses are highly species specific.

More than 70 genotypes are known to infect humans.

Papillomaviruses have never been cultured in vitro but have been characterized by molecular methods.

These viruses are classified by the molecular resemblance of their genetic raw material and are assigned a genotype number.

The viruses infect the basal keratinocyte of the epidermis, presumably through disruptions of the skin or mucosal surface.

At this location, the virus remains latent in the cell as a circular episome.

As the epidermal cells differentiate and migrate to the surface, the virus is triggered to undergo replication and maturation.

The process of virus replication alters the character of the epidermis, resulting in cutaneous or mucosal excrescences known as warts.

Human papillomaviruses (HPVs) are grouped broadly into cutaneous and mucosal types, based on the clinical location of the lesion.

Although some overlap exists, most papillomaviruses have distinct anatomic predilections, infecting only certain epidermal sites, such as skin or genital mucosa.

A number of genotypes of virus have the potential to transform cells and are associated with epidermal malignancies.

The mechanism for transformation is not known, but viral DNA apparently integrates into the genome of the host cell.

Table 1.

Association of HPV Types with Morphology and Site of Skin Lesions

Lesion Location HPV Genotype

Common wart Mostly hands 2, 4

Plantar wart Bottom of feet 1

Mosaic wart Hands and feet 2

Flat wart Arms, face, knees 3, 10, 28, 41

Butcher wart Hand 7

Extragenital Bowen disease Upper and lower extremities, head 2, 3, 5, 16, 18, 20, 31, 33, 34, 54, 56, 58, 61, 62, 73

Macular plaques of epidermodysplasia verruciformis Light-exposed areas 5, 8, 9, 12, 14, 15, 17, 19, 20, 21, 22, 23, 24, 25, 36, 47, 50

Table 2.

HPV Types Associated with Anogenital Lesions

Lesions HPV Genotype

Genital warts 6, 11

Flat condylomata 6, 11, 16, 18, 31

Cervical intraepithelial neoplasia 16, 18, 31, 33, 35, 39, 42, 43, 44, 45, 51, 52, 56

Bowen disease 6, 11

Buschke-Löwenstein tumors 6, 11

Vulvar intraepithelial neoplasia 16 (occasionally 6, 11)

Cervical cancer 16, 18 (strong association)

31, 33, 35, 45, 51, 52, 56 (moderate association)

6, 11, 42, 43, 44 (weak association)

Penile intraepithelial neoplasia 16, 18

Anal intraepithelial neoplasia 16 (rarely 6, 11, 18, 33)

Because no medications currently available eradicate the virus itself, there are no cures for HPV infection.

Aggressive or prolonged therapies usually produce long-lasting or permanent eradication of the wart tumor, yet the wart virus may linger for years in normal-appearing skin in a dormant form.

Patient education is extremely important, and therapy should begin with careful counseling about the infectious nature of warts, the current unavailability of a cure, the often prolonged therapy required to eliminate the wart bump, and the possibility of recurrence later, even in the absence of re-exposure.

These issues are especially important for patients with anogenital warts.

An additional concern for women with anogenital warts is the association of cervical carcinoma with some HPV infections, Dr.

Edwards cautioned.

Most wart treatments eliminate the virus by destroying the skin that contains the virus.

The subsequent disappearance of the wart may occur because the virus was removed as the destroyed skin sloughs, or because the disruption of cells and release of the virus stimulates the patient’s immune system to eradicate the virus.

The only patients whose infections are truly cured are probably those whose immune system recognize and eliminate the virus.

Patients with immune system deficiencies due to HIV infection, cancer, or medications such as cortisones, usually experience regrowth of warts following treatment.

The most common treatment for warts are those that physically destroy the skin.

The choice for treatment depends partially upon the location of the wart, and the success of treatment depends upon the location and number of warts, the number of treatments, and the aggressiveness of the caregiver.

The common treatments include: salicylic acid; liquid nitrogen; laser surgery or electrocautery (electric needle) ; cantharidin; trichloroacetic and bichloroacetic acids; and interferon alpha.

An important recent advance in the treatment of anogenital warts includes imiquimod.

This cream which can be applied topically at home and eliminates warts, not by destroying skin, but by prompting the patient’s immune system to attack the virus itself.

About half of the patients experience removal of all treated warts, and warts shrink dramatically on most other patients.

Most exciting is an apparent, but not yet proven, lower recurrence rate than that seen with other treatments.

The other new medication is a gel form of podofilox, a purified and less irritating form of podophyllin, an old standby caustic office therapy for anogenital warts.

This gel is easier to apply than the liquid, and podofilox is gentle enough for home use by a patient.

wart treatment , Sexually Transmitted Diseases

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