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Kaposi's sarcoma
   Last updated: 21.12.05
 
Kaposi's sarcoma (KS) results in purplish-black lesions on the skin, mucous membranes or internal organs.

It can affect people at all stages of HIV infection, as well as some HIV-negative people, and it is unlikely to be serious as long as the CD4 cell count is above 250. People with lower CD4 counts are more likely to develop KS that affects internal organs, such as the lymph nodes or lungs, with potentially life-threatening consequences.

KS is now believed to be caused by a virus called human herpes virus 8 (HHV-8), which is also known as Kaposi's sarcoma-associated herpes virus (KSHV). In the presence of other factors – such as immune suppression or other effects of HIV in the body – HHV-8 is thought to encourage normal cells to change into tumour cells.

Both HHV-8 and Kaposi's sarcoma itself are much more common among HIV-positive gay or bisexual men, women infected by bisexual men, and people from African communities, than other groups of people with HIV. Earlier ideas about the cause of KS, such as the theory that it was linked to the recreational use of poppers (inhaled nitrites) by gay men, have now been discounted.

HHV-8 appears to be sexually transmitted, although it could also be transmitted in other ways. There is no generally available test for HHV-8 yet; a test might not be useful anyway since no-one knows what proportion of HIV-positive people infected with HHV-8 will go on to develop KS.

Diagnosis and treatment
The best way to diagnose KS is by taking a sample from a skin lesion. Experienced doctors may diagnose KS simply by looking at it. KS inside the body can often be detected using X-rays and fibre-optic viewing instruments.

You and your doctor may decide not to treat your KS if you only have a few lesions on the skin, if
your CD4 count is high and if the lesions are not causing you significant distress or embarrassment. Some AIDS centres or organisations like the Red Cross may be able to advise you about ways of camouflaging lesions using cosmetics.

However, over time KS generally progresses and spreads if left untreated. Doctors will normally recommend treating `poor prognosis' KS (i.e. KS that is likely to develop rapidly), for example, when there are many lesions, when they affect internal organs, or when your CD4 count is low.

In many cases, the best initial approach to treating KS may be to inhibit HIV and boost the immune system using a strong combination of anti-HIV drugs. Like most other opportunistic infections, there have been many reports of people whose KS improved or disappeared once they started taking protease inhibitor-based combinations. Encouraging evidence that triple NRTI combinations and combinations including an NNRTI have an equally powerful effect on KS has recently emerged.

There is also a range of specific KS treatments. If the KS only affects your skin, you may be able to use `topical' therapies such as gels or creams, localised radiation therapy, injections of chemotherapy drugs into the lesions, or methods that freeze or burn them.

For more extensive KS, you may be advised to consider `systemic' treatments that affect the whole body, such as injections of chemotherapy drugs or interferon. Liposomal drugs are just as effective but significantly less toxic than standard chemotherapy drugs.

In the future, drugs that inhibit HHV-8 may be used to treat KS. However, they might not be effective against KS lesions that have already formed. For example, some lymphomas are caused by the common virus EBV, but anti-EBV drugs seem not to be effective against lymphomas once they have started to grow.