Warts on the genitals and anus are caused by a sexually transmitted virus called HPV (human papilloma virus). There are many varieties or strains of HPV. Some strains can cause abnormal growths and even cancer inside the body (in the cervix in women and in the anus in both men and women). On the outside of the body, warts on the genitals or anus are usually not harmful but can be disfiguring.
Genital warts can sometimes disappear without treatment. In other cases, they may grow bigger, forming small clusters. Depending on a variety of factors (number of warts, their size and location), different treatment options are available and can include the following:
These treatments can get rid of the warts but don't deal with the underlying problemweakened immunity and HPV infection. Thus, although the wart may be removed, it can recur because HPV is lurking in healthy-looking skin nearby. Also, although HAART reduces HIV's ability to replicate and eventually raises CD4+ cell counts, strengthening the immune system, HAART users can still develop genital warts caused by HPV.
Another possible treatment is the immune booster imiquimod (Aldara). This drug, available in a cream, is applied several times a week to skin affected by warts. Imiquimod seems to work by stimulating cells of the immune system in the skin, including macrophages, to produce chemical messengers such as interferons-alpha and gamma. Imiquimod-stimulated immune cells can then help to destroy warts.
Researchers in Milan, Italy, recently conducted a study comparing the effectiveness of imiquimod in two groups of peopleHIV negative and HIV positivewith genital warts. According to the research team, the use of imiquimod resulted in about 55% of HIV positive subjects having "at least a partial reduction of genital warts." Among HIV negative people, the equivalent figure was 86%.
Between March and October 2001, researchers recruited 125 adult subjects for their experiment:
Both groups of people (HIV negative and HIV positive) were of similar age and had a similar severity of genital warts.
Among the HIV positive subjects, the average age was 28 years and the average CD4+ count was 327 cells (none had a CD4+ count below the 200 cell mark). All subjects were taking HAART and their viral loads were as follows:
No subject had a viral load greater than 100,000 copies.
The number and extent of genital warts was as follows:
Before bedtime, subjects applied imiquimod 5% cream to all visible warts and left it on for eight hours. The next morning the cream was removed by washing with mild soap and water. Subjects used imiquimod three times weekly until the warts cleared or for up to four months. If treated skin became red or swollen, imiquimod was used only twice weekly.
Doctors monitored subjects once a month during the study.
Among the HIV positive subjects the following occurred:
Among the HIV negative subjects the results were somewhat different:
In general, researchers reported that imiquimod was well tolerated and no one stopped using it during the study. However, 77% of subjects developed mild swelling of the skin where they had applied imiquimod. A total of 24% of subjects had to temporarily reduce their application of the drug to a twice-weekly schedule for two to three weeks.
The researchers are not sure why some of their subjects did not respond to imiquimod. In a previous study of imiquimod non-responders, doctors found that there were less-than-normal levels of immune cells in the skin near warts. Moreover, those few cells present may not have been functioning normally. In the current study, the researchers speculate that these factors may have affected the reponse to imiquimod.
Overall, the team found that 55% of HIV positive subjects experienced "at least a partial reduction in genital warts," a response they call clinically meaningful.
REFERENCES
1. Dahl MV. Imiquimod: a cytokine inducer. J Am Acad Dermatol. 2002 Oct;47(4 Suppl):S205-8.
2. Cusini M, Salmaso F, Zerboni R, et al. 5% imiquimod crem for external anogenital warts in HIV-infected patients under HAART therapy. Int J STD AIDS. 2004 Jan;15(1):17-20.
3. Arrese J, Paquet P, Claessens N, et al. Dermal dendritic cells in anogenital warty lesions unresponsive to an immune-response modifier. J Cutan Pathol. 2001 Mar;28(3):131-4.
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