The Body Covers: The 8th Clinical Care Options for HIV Symposium
Conference Summaries: Day Two
May 2, 1998
The success of antiretroviral therapy has caused major decreases in most of the significant opportunistic infections and has led to new questions being posed by clinical investigators interested in this area.
On the second day of the 8th Annual Clinical Care Options for HIV conference held in Scottsdale, Arizona, Dr. Richard Chaisson of the Johns Hopkins University reviewed the changing epidemiology of opportunistic infections in the era of more potent antiretroviral therapy.
Using data from the Johns Hopkins clinic he compared the incidence of new opportunistic diseases in the years 1993-5 and 1996-7. For all illnesses there has been a dramatic reduction in new cases. This was particularly striking for CMV infections, toxoplasmosis, disseminated MAC and cryptosporidiosis. When the Hopkins investigators examined risk factors for new opportunistic events, they found that patients in their clinic with CD4 counts less than 200 were more likely to develop an opportunistic event if they were not on a protease inhibitor and if they had higher baseline viral loads. The use of protease inhibitors decreased the risk by 60% and having an undetectable viral load reduced the risk by 80%. Thus as Dr. Chaisson stated the key to prevention of opportunistic infections was to maximize antiretroviral therapy and try and keep the viral load as low as possible.
If this is done and patients' viral loads are undetectable, then can one stop prophylaxis for opportunistic infections such as PCP or MAC? Dr. Chaisson reviewed the biphasic nature of the CD4 cell response to potent antiretroviral therapy -- an initial phase in the first 3 months that seems to represent expansion of existing cells, and a second phase after that which appears to represent new immune cells. He suggested that all the available clinical evidence indicates that patients do have restored immunity in this phase, since new infections are extraordinarily rare. As a result he suggested that, in patients whose viral load is undetectable and whose CD4 count has risen, that the calculated risk of stopping prophylaxis was a reasonable one and might be considered in an informed patient. Indeed, as he showed, there have been instances where stopping maintenance treatment for established infections such as CMV has been accomplished with apparent success in patients whose CD4 count has risen with antiretroviral therapy.
One interesting phenomenon that is increasingly recognized is that of a changed presentation of opportunistic infection that occurs in patients if they get an infection shortly after initiation of antiretroviral therapy. It has been most commonly described with mycobacterial infections, which are more localized often to lymph nodes causing significant enlargement and pain. This appears to be an inflammatory reaction associated with a recovering cell-mediated immunity and has been likened to the reversal reaction seen in lepromatous leprosy. The importance of recognizing this is that it probably does not represent failure of antiretroviral treatment which should therefore be continued.
Unlike Kaposi's sarcoma whose incidence has clearly decreased in the current era, there is much more uncertainty about non-Hodgkin's lymphoma, with some investigators reporting decreased incidences and other increased. As Dr. Levine pointed out, either could theoretically occur -- more potent treatment could lead to decreased B cell stimulation and less oncogenesis, or it could lead to longer survival with more time for continued B cell stimulation to lead to lymphoma development. Only time will tell.
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