September 15, 2003
Dr. Collier opened her session describing the case of a 30-year-old female HIV diagnosed in 1996. At the time, the patient had PCP with a nadir CD4 of 50 cells. She now has a CD4 count of 220 cells and a viral load of 1,950 copies/mL. Of note was that she had been on multiple regimens in the past and has had low-level viremia over the past year. Collier asked the audience how they would treat the patient at this point. When given various choices, in the interactive voting, 47 percent of the audience stated they would obtain a genotype and discuss switching therapy, whereas 26 percent thought the patient should attend an education or counseling course to assist with adherence.
Dr. Collier noted that studies may vary in their end points and that it is critical to know how the study defined the end point. Although HIV-RNA viral load is frequently used as an end point, some studies use a viral load (VL) of 400 copies/mL while others use 500, 50 or 40 copies/mL as the cut-off point. Also, the treatment course may vary in duration (e.g., 24 or 48 weeks) or may use viral rebound after initial suppression. In addition, some studies use immunologic failure defined as a CD4 T-cell count return to baseline or a percent decrease. Others may use clinical failure such as the development of an opportunistic infection three months or longer after antiretroviral therapy (ART) initiation.
The management of patients differs among those with limited resistance, Dr. Collier pointed out: the goal in these cases would be to obtain virologic suppression and improve immune function. In patients with multi-drug resistance, the goal would be to maintain the current CD4 and to attain the lowest HIV RNA level possible.
Dr. Collier presented the genotype of the patient from her initial case. Impressively, 54 percent interpreted the genotype correctly and 28 percent responded that they did not know, which is not surprising given that some of the audience initially responded that they did not treat HIV.
However, what was disturbing was that 19 percent of the audience misinterpreted the genotype. I hope that these individuals were just trying to see what they knew and took their best guess and, in practice, do not interpret genotypes for patient care.
Summarizing the various case scenarios is almost an impossible task, so rather than go through the cases in detail I will briefly discuss Dr. Collier's main teaching points. Dr. Collier brought up the importance of discussing pregnancy with women of child-bearing age and how what you discover about the likelihood of the patient getting pregnant in the coming years may impact your initial decision of which NNRTI or protease inhibitor (PI) to use -- keeping in mind the fact that efavirenz (EFV, Sustiva) is teratogenic as well as the tolerability of PIs.
Dr. Collier also discussed the pros and cons of structured treatment interruptions and maintaining a failing regimen. She pointed out the discouraging results of the CPCRA four-month structured treatment interruption (Lawrence, JAMA) compared with the improved results of the eight-week structured treatment interruption (ARNS 097). Given the conflicting results and limited data, Dr. Collier recommended that these strategies should only be done in the context of a clinical trial and are not recommended in clinical practice.
She recommended that one should assess the reasons for treatment failure(s) and plan accordingly with the patient what would be the right option for that individual. In closing, she briefly reviewed the drugs in development for both the immediate and distant futures.
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