The second group of HIV-infected patients consists of those at the other extreme, the ones who are least likely to die from AIDS or its complications. These individuals were diagnosed with HIV after the advent of HAART and have taken their medications religiously ever since. In these cases, HAART is likely to suppress their virus for decades, and they’re now significantly more likely to die of heart disease or cancer than of anything related to AIDS. To get an idea of the mortality rate among these patients, consider Alexander McMeeking’s practice, on East 40th Street. McMeeking ran the HIV clinic at Bellevue from 1987 to 1989 and then left to start a private practice. To the best of his knowledge, only three of his 300-odd Bellevue patients survived long enough to get on HAART. They are still alive today. “Fortunately, thank God, all three are doing great,” says McMeeking. “I tell them they will essentially die of old age.”
McMeeking’s practice now includes 600 HIV-infected patients, and last year he lost only two of those—one to lung cancer, another to liver cancer.
Now the question is whether these patients doing well with HAART are actually more susceptible to the kind of chronic diseases that kill the uninfected. Are they more likely to die from heart disease, cancers, liver and kidney failure, and other chronic diseases either because of the HIV itself or the anti-retroviral regimen keeping it under control? One observation made repeatedly in studies—including the 2006 report from the Department of Health and Mental Hygiene—is that these HIV-infected individuals appear to have higher rates of several different cancers, in particular lung cancer among smokers, non-Hodgkins lymphoma, and cancers of the rectal area. These cancers appear both more precocious and more aggressive in HIV-infected patients—they strike earlier and kill quicker. The reason is not yet clear, although a likely explanation is that the ability of the immune system to search out and destroy incipient malignancies is sufficiently compromised from either the anti-retroviral drugs, the virus, or the co-existence of several viruses—squamous-cell cancers of the rectal area are caused by the same human papilloma virus that causes cervical cancer in woman—that the cancers get a foothold they don’t get in non-HIV-infected individuals.
“I still expect most of my patients to live a normal life expectancy,” says an AIDS doctor, “but they may do so with a bit more nips and scrapes.”
One finding that’s considered indisputable is that HAART, and particularly the protease inhibitors that are a critical part of the anti-retroviral cocktail, can play havoc with risk factors for heart disease. They raise cholesterol and triglyceride levels; they lower HDL, and they can cause increased resistance to the hormone insulin. These changes often accompany a condition known as HIV-related lipodystrophy, which afflicts maybe half of all individuals who go on HAART. Subcutaneous fat is lost on the face, arms, legs, and buttocks, while fat accumulates in the gut, upper back (a condition known as a buffalo hump), and breasts. The question is whether these metabolic disturbances actually increase the likelihood of having a heart attack. It’s certainly reasonable to think they would, but it’s remarkably difficult to demonstrate that the drugs or the virus itself is responsible: The fact that a relatively young man or woman with AIDS has a heart attack does not mean that the heart attack was caused by HIV or the disturbance in cholesterol and lipid levels induced by the therapy.
Any difference in disease incidence between HIV-infected and uninfected individuals, explains John Brooks, leader of the clinical-epidemiology team within the CDC’s Division of HIV/AIDS Prevention, can be due to the infection itself, to the therapy—HAART—or to “the host, the person who has HIV infection, both physiologically and socioculturally.” It’s the last factor—the host—that complicates the science. Until recently, for instance, physicians saw little reason to worry about heart-disease risk factors in their HIV-infected patients and so didn’t bother to aggressively treat risk factors in those patients, as they did the HIV-negative. “Think about it,” says Brooks, “if it’s 1988, 1989, and I have a patient with HIV disease and hypertension, he’s not going to live long enough to die of hypertension. I want to treat the disease.”
The rate of cigarette smoking among HIV-infected individuals is also twice as high as the national average. The rate of intravenous drug use is far higher, as is the rate of infection with hepatitis B or C, because intravenous drug use is a common route to getting both HIV and hepatitis. So the fact that an HIV-infected patient may seem to be suffering premature heart disease, diabetes, or liver or kidney disease earlier than seems normal for the population as a whole—or the fact that a study reports such a finding about a population of HIV-infected individuals—only raises the issue of whether the population as a whole is the relevant comparison group. “Since one of the major risk factors for HIV is intravenous drug use,” says Brooks, “you have to ask, what’s the contribution of heroin to somebody’s kidney disease versus the HIV versus untreated high blood pressure versus smoking?”