Left Field by Patricia Nell Warren
The return of Kaposi’s sarcoma spurs a new wave of research & rethinking.
Following its grim flare-up starting in 1981, early in the AIDS epidemic, Kaposi’s sarcoma had seemed to burn itself out, like a wildfire. Its sudden and super-aggressive appearance was attributed to the low CD4 counts of people with AIDS—their destroyed immune systems simply couldn’t resist. And KS’s subsequent disappearance, after the advent of antiretroviral therapy, was attributed to positive effects of the new antiretroviral drugs on patients’ immune systems. Then, in October 2007, the San Francisco Chronicle broke an unsettling story. KS is back. Experts were noting a cluster of new KS cases among gay men.
More recently, in February 2010, Skin & Allergy News published an updated report. SAN author Sherry Boschert wrote: “Kaposi’s sarcoma in HIV patients is turning up again—sometimes in a surprisingly deadly form and other times in an indolent, non-threatening form.” The same story was breaking in the UK. In May 2010, Oxford University’s Journal of the National Cancer Institute published a ten-year study of 9,473 HIV-positive gay men in Europe, Australia, Canada, and sub-Saharan Africa. Between 1986 and 2006, 555 of these men were diagnosed with Kaposi’s sarcoma, and, despite receiving combination antiretroviral treatment, 319 of them—over fifty percent—died.
Young people today don’t remember that first dramatic rampage of AIDS-related KS in the 1980s. As yet, nobody had any idea what caused those disfiguring purplish skin tumors to invade almost every crevice of a human body. Some medical institutions refused to treat AIDS patients with KS. A doctor friend of mine still has unsettling memories of the most heartbreaking cases that he treated in the mid-eighties. “They were treated with whatever we had then,” he told me, “which wasn’t much, because there were no retrovirals yet. One case in particular—when I was called to the hospice to pronounce him dead, I was deeply shocked. He was so loaded with tumors that he didn’t even look human. Those were dark days.”
MedicineNet describes KS as “[a] highly vascular tumor of the skin characterized by soft purplish plaques and papules that form nodules, which typically start on the feet and ankles and then slowly spread across the skin of the legs, hands, and arms. In AIDS patients, these tumors can also develop internally.” Vascular means focused in vessels that carry fluids like blood and lymph. When KS goes internal, it can be life-threatening. If lesions invade the lungs, breathing becomes difficult or impossible. In the digestive tract or liver, KS can cause severe bleeding. Internal involvement often includes the hard and soft palate inside the mouth, making it painful or impossible for the patient to eat.
Today, despite much that has been learned about this disease, it still confronts medicine with serious questions. Several different types of this cancer have now been identified.
KS has been around for over 3,000 years—the distinctive skin tumors were mentioned in an Egyptian papyrus dating 1600 B.C. Modern clinical medicine first described it in 1872 when Hungarian dermatologist Moritz Kaposi wrote up a cluster of cases among his patients. They were mostly elderly men with an Eastern European and Mediterranean ethnic background, leading to an initial assumption by many that Kaposi’s sarcoma had a way of genetically targeting old men in these ethnic groups. That original form of KS was usually mild and benign, involving skin tumors on the feet and legs.
A century later, when Kaposi’s and HIV intersected in the U.S., resulting in a new and shockingly virulent form of KS, there was some speculation that KS was kick-started by gay men’s use of poppers. But this didn’t explain cases of KS among non-gay men who didn’t use poppers. Finally, in 1994, researchers identified a new herpesvirus—HHV-8—as the probable cause of KS. In short, this is a transmissible cancer. HHV-8 joined several other herpesviruses—herpes simplex, Epstein-Barr virus and cytomegalovirus—that were being identified as the cause of serious, even lethal, opportunistic AIDS-related infections.
Eventually the experts realized that KS infection was actually widespread across a broad arc of the West and many of its demographics—from Italy and Eastern Europe, across the eastern Mediterranean, including Israel and Egypt, and deep into sub-Saharan Africa, where it strikes women and children as well. Indeed, KS may have originated in Africa, and spread from there into the Middle East and Europe.
HHV-8 infection can be lifelong, as infections by other herpesviruses can be—including the relatively benign HSV-1 that causes those now-and-then cold sores on your lip. There is no known drug that can completely clear herpesviruses from the human system. But the person with a long-time infection of HHV-8 laying latent in the system may never develop KS unless his or her immune system becomes gravely weakened, either due to aging or the presence of other diseases or conditions.
After the AIDS epidemic got going in the 1980s, different types of KS were identified. The “epidemic AIDS-related” form of KS is virulent and fast-moving, often lethal, and the skin lesions invade the body’s internal surfaces and organs on a grand scale. It is found everywhere that AIDS is now found, including Africa. But across Africa, another type—now called “endemic African KS”—is rampant among HIV-negative Africans. This one may be the result of HHV-8 taking opportunistic advantage of immune systems weakened by malaria, TB, cholera, parasites, chronic malnutrition, and other health threats that dog poorer Africans—not to mention the deep stresses of constant civil war and extreme violence that many Africans experience daily. One aggressive sub-type of African KS goes into the bones. Another form of African KS targets children, and spreads through the lymph nodes.
Today, in the U.S., the old “classic Mediterranean” benign KS is turning up for the first time in youngish HIV/AIDS patients. “They develop what looks to us like ‘old man’s Kaposi’s sarcoma,’” was the comment from Toby A. Maurer, associate professor of clinical dermatology at UCSF. In other words, these patients develop small areas of tumors, usually on the legs and feet, after being HIV-positive for some years. “We think that they are showing signs of immune aging,” Dr. Maurer adds, pointing out that in several years of follow-up, none of these parents have developed any internal lesions. “This Kaposi’s sarcoma seems very indolent and is not going anywhere.”
But today’s AIDS-related KS is also showing signs that it may have gotten stronger. According to the Oxford-published study, KS may no longer need a bottomed-out CD4 count to get going—it is appearing in patients who have a healthier count. Dr. Maurer commented on the surprisingly high mortality rate among sixty-five patients that she and her colleagues had treated. Maurer said, “We were shocked to find out that 25% of that cohort died of their Kaposi’s sarcoma, even when they had chemotherapy.” In another group of patients treated with ARVs and chemotherapy, twenty-three percent of them died of KS anyway. “This is quite alarming,” Maurer added.
The fact that KS has such a chimeric nature, and is still not completely understood, gives it a spooky reputation with the American public. Worse, an urban myth now associates KS exclusively with gay and bi men. In the early years of the epidemic, there was a lot of lurid media publicity around the lethal, fast-moving KS that wiped out thousands of American gay men in the 1980s. Hence the San Francisco Chronicle’s hurry in 2007 to report new KS cases among gay men. Yet, globally speaking, taking all the types of KS together, the greatest burden of AIDS-related KS cases is found among non-gay people in Africa, where it affects women and children as well as men.
Some AIDS activists insist that “safe sexual practices” can protect against KS infection. Indeed, some assert that, in gay and bi men, KS is spread by sexual routes, whereas among other groups, KS moves via non-sexual transmission. This distinction is nonsensical, not to mention phobic against gay and bi sex, when you consider the fact that KS also occurs among elderly people and children, who may not be engaging in sex at all. Indeed, based on what we now know about lifelong infections with HHV-8, a gay or bi man might have been infected with HHV-8 as a child, through some form of non-sexual transmission. He may have remained a healthy HHV-8 carrier for many years before he contracted HIV and developed AIDS, at which time his dropping CD4 count would trigger the latent herpesvirus into aggressive activity.
Some research suggests that HHV-8 might be spread merely by intimate contact involving saliva, such as sharing toothbrushes or food dishes. In developing countries, where processed baby food may not be available, mothers often pre-chew the first solid food for an infant. These circumstances could explain non-sexual transmission to children. In DNA classification of viruses, HHV-8 is similar to Epstein-Barr virus (EBV), which causes infectious mononucleosis. “Mono” is known to college students as the “kissing disease” because it can be spread by kissing. In short—“safer sex” as currently defined by the AIDS establishment may or may not protect against KS.
Healthy HHV-8 carriers who get organ transplants are also at risk. KS may develop afterwards as a result of the drugs used to suppress the immune system and keep it from rejecting the new organ. This type of KS is now designated as iatrogenic, or “transplant-associated” KS.
Last, but not least, there are reports of KS in HIV-negative gay men. These cases tend to be the mild “classic” variety of KS, and may be triggered by other types of immune-system problems. Indeed, the majority of KS cases, the world over, are found among males—for reasons that are not yet understood. Yet, when the long list of some 100 other immune-related diseases is looked at, mostly women are affected.
Current KS treatment practice is summarized by MedLinePlus: “How this condition is treated depends on: how much the immune system is suppressed, [the] number and location of the tumors, and [the] symptoms. Treatments include: antiviral therapy against the AIDS virus, combination chemotherapy, freezing, and radiation therapy. Lesions may return after treatment. Treating Kaposi’s sarcoma does not improve the chances of survival from AIDS itself.”
So the research jury is still out on this viral chimera. Some research suggests that another herpesvirus, namely HHV-6, is also involved in KS. AIDS experts insist that antiretroviral HIV treatment has been a positive factor in making KS disappear for a time. If this is true, then why—with all the ARVs being pumped into people now—is KS making a comeback? Are mutating resistant strains of HHV-8 or HIV becoming a factor? Clinical trials are being planned to actually measure KS response to ARV and chemotherapy.
Researchers also hope to improve on methods of early diagnosis. “By the time you find internal involvement, it may be quite late,” one expert says.
“Kaposi’s Sarcoma is back in HIV patients,” by Sherry Boschert, Skin & Allergy News, February 1, 2010 (International Medical News Group).
Copyright ©2011 by Patricia Nell Warren. All rights reserved