AMA unit says ‘no’ to mandatory HIV testing
The American Medical Association reversed its 5-year-old policy that HIV testing should be mandatory for pregnant women. Instead, during the interim meeting of the AMA House of Delegates in San Francisco, California, the representatives of the 290 000-member organization revised the recommendations, substituting ‘universal’ testing for HIV status. “We believe the data show a clear benefit to universal HIV testing,” said Mohammed Khan, MD, a member of the AMA's Council on Scientific Affairs, from Ann Arbor, Michigan. “We believe it prevents the problem in the mandatory approach to testing in which some women may decline prenatal care in order to avoid mandatory testing. If this is enacted we believe this type of approach will reduce further the risk of HIV transmission.”
The change in the policy was approved by the legislative body of the AMA without objection. The change in position moves the AMA in line with other medical organizations, including the American College of Obstetricians and Gynecologists which have shied away from making the testing a mandatory recommendation.
The new policy states: “That there should be universal HIV testing of all pregnant women with notification of the right of refusal as a routine component of prenatal care.”
Paul Gluck, MD, of Miami, Florida, representing ACOG at the AMA meeting, said “This excellent academic, scholarly report balances privacy, ethical concerns about autonomy and self-determination, public health concerns and individual health. We think this approach has been working and will continue to work and will provide universal screening for HIV in our pregnant population.”
Garlic supplements can impede HIV medication
If it's natural it must be good for you, right? That's the cry of the promoters of alternative medications for treatment of a variety of diseases, but increasing evidence suggests that not all natural products are healthy for people with chronic diseases such as HIV infection. Garlic – touted as a wonder drug for preventing heart disease and cancer – appears to adversely affect levels of protease inhibitors in the blood, researchers from the US National Institutes of Health reported in Clinical Infectious Diseases (http://www.journals.uchicago.edu/CID/journal/home.html).
`‘In the presence of garlic supplements, blood concentrations of saquinavir decreased by about 50 percent among our study participants,” said Judith Falloon, MD, an AIDS clinical researcher at the National Institute of Allergy and Infectious Diseases. “We saw a definite, prolonged interaction. The clear implication is that doctors and patients should be cautious about using garlic supplements during HIV therapy,” she said.
For the first 3 days of the study, nine healthy, HIV-negative volunteers received doses of saquinavir. The research team drew samples of the volunteers’ blood to measure their baseline levels of saquinavir. Next, the volunteers took garlic caplets twice daily for 3 weeks. When the researchers again analyzed blood samples, the average overall levels of saquinavir had decreased 51 percent, and the average maximum concentrations had fallen 54 percent.
Even after a 10-day ‘wash-out’ period with no garlic supplements, when the volunteers again used only the protease inhibitor for 3 days, their blood levels of saquinavir still averaged about 35 percent lower than the expected baseline amount.
`‘We set out to learn more about these alternative medicine products because there simply are not a lot of clinical data available on them,” Dr. Falloon said. In an earlier study, the team found a potentially dangerous interaction between the herbal remedy St. John's wort and the protease inhibitor indinavir.
Garlic became the next focus because of its reputation as a natural cholesterol fighter, which has made it particularly popular for patients whose cholesterol levels have risen due to a side effect from HIV medications. The research team suspected a strong possibility of a drug interaction because both garlic and protease inhibitors share the same pathway into the body, a metabolic route known as the CYP450 enzyme system. Exactly how garlic supplements disrupt the uptake of saquinavir is still unclear.
What happens to T-cells explained
Studies conducted independently at the Aaron Diamond AIDS Research Center at The Rockefeller University, New York and at NIAID appear to resolve one of the controversies concerning how HIV depletes CD4-positive T cells. Many scientists have believed that HIV depletes its T cells by preventing new T-cell production. The new studies, published in the Journal of Experimental Medicine, challenge that point of view. Those findings suggest that HIV doesn't block production, but rather accelerates division of existing T cells. The studies also suggest that antiretroviral therapy boosts levels of T cells by slowing the loss of these cells.
`‘These two studies have come to the same conclusion, namely that the primary cause of the immunodeficiency associated with HIV infection is an increase in the rate of CD4-positive T-cell death,” said Anthony Fauci, MD, director of NIAID, which funded both studies. “This research sheds light on how we might best reduce the decline in those cells in the setting of HIV infection and more effectively treat people with HIV.”
David Ho, MD, a coauthor of one of the studies and scientific director at the Aaron Diamond, added, “These two papers should put to rest a controversy that has been part of the scientific debate in HIV research for the past decade.”
Using different sophisticated methods to study directly the growth and death of individual T cells in people infected with HIV, researchers studied the effects of the virus on T-cell dynamics in treated and untreated individuals. In the NIAID study, Joseph Kovacs, MD, and colleagues attached chemical tags to dividing cells to monitor the fates of individual T cells in 17 HIV-infected patients before and after the initiation of HAART. Their results showed that high HIV levels did not block T-cell production, but instead caused those cells to multiply and divide more rapidly. When patients were treated with antiretroviral drugs, T-cell proliferation and death both slowed [Kovacs JA, et al. Identification of dynamically distinct subpopulations of T lymphocytes that are differentially affected by HIV. J Exp Med 2001, 194:1731–1741].
Their findings are in agreement with those published by Dr. Ho, Hiroshi Mohri, MD, and their colleagues. They used a different technique to monitor and compare T-cell proliferation in seven people with HIV infection before and after HAART therapy and in four uninfected individuals. Their studies found the same effect of HIV infection on T-cell production [Mohri H, et al. Increased turnover of T lymphocytes in HIV-1 infection and its reduction by antiretroviral therapy. J Exp Med 2001, 194:1277–1287].
However, Mike McCune, MD, a senior investigator at the University of California, San Francisco, said, “My colleagues and I believe that ‘accelerated destruction’ of mature, effector T cells – those ones measured in the studies from Mohri et al. and Kovacs et al.– represents just part of the story.” His research suggests that the ability of the blood-forming system to replace these cells is also impaired, leading to ‘regenerative failure.’ Dr. McCune said his work indicates that replacement occurs because new T cells are produced from ‘progenitor cells'. “These progenitors – often also positive for CD4 and targets for infection by HIV – are found at varying levels of blood cell maturation and include multilineage hematopoietic stem cells in the bone marrow, early T cell progenitors in the thymus, and memory T cells residing in peripheral lymphoid organs,” he said. These cells, he noted, are not easily measured and are not considered in the studies by Mohri and Kovacs.
`‘We pose the following working hypothesis: in most cases, HIV infection initially results in accelerated destruction in the peripheral lymphoid system; such loss of T-cells prompts increased compensatory renewal from progenitor sources; as long as such compensation can occur, the system remains intact; once HIV destroys the sources of production, the system crashes and immunodeficiency – CD4 T-cell depletion – ensues,” Dr. McCune said.