Mark Dybul, MD; Anthony S. Fauci, MD; John G. Bartlett, MD; Jonathan E. Kaplan, MD; Alice K. Pau, PharmD
Table 1.
Table 2.
Table 3.
complete history and physical (AII);
complete blood count, chemistry profile, including serum transaminases and lipid profile (AII);
CD4+ T lymphocyte count (AI); and
plasma HIV RNA measurement (AI).
*b-Deoxyribonucleic acid; †reverse transcriptase-polymerase chain reaction. Source: Mellors JW, Muñoz A, Gigorni JV, et al. Plasma viral load and CD4+ lymphocytes as prognostic markers of HIV-1 infection. Ann Intern Med. 1997;126:946-54.
Table 4.
Table 5.
Table 6.
Table 7.
Table 8.
Table 9.
Table 10.
Table 11.
Table 12.
Table 13.
Table 14.
Table 15.
Table 16.
Table 17.
Table 18.
Table 19.
Table 20.
results of recent clinical history and physical examination;
results of plasma HIV RNA levels, which have been measured on two occasions;
absolute CD4+ T lymphocyte count and changes in these counts;
assessment of adherence to medications;
remaining treatment options;
potential resistance patterns from previous antiretroviral therapies; and
the patient's understanding of the consequences of the new regimen (e.g., side effects, drug interactions, dietary requirements and possible need to alter concomitant medications).
The patient experiences <0.5–0.75 log10 reduction in plasma HIV RNA by 4 weeks after therapy initiation or <1 log10 reduction by 8 weeks (CIII).
Therapy fails to suppress plasma HIV RNA to undetectable levels within 4–6 months of initiation (BIII). The degree of initial decrease in plasma HIV RNA and the overall trend in decreasing viremia should be considered. For example, a patient with 106 viral copies/mL before therapy, who stabilizes after 6 months of therapy at an HIV RNA level that is detectable but is <10,000 copies/mL, might not warrant an immediate change in therapy.
Virus in plasma is repeatedly detected after initial suppression to undetectable levels, indicating resistance (BIII). However, the degree of plasma HIV RNA increase should be considered. Clinicians should consider short-term observation for a patient whose plasma HIV RNA increases from undetectable to low-level detectability (e.g., 50–5000 copies/mL) at 4 months. In this situation, the patient's health status should be followed closely. The majority of patients who fall into this category will subsequently demonstrate progressive increases in plasma viremia that will probably require a change in the antiretroviral regimen.
Any reproducible substantial increase, defined as ≥ 3-fold, from the nadir of plasma HIV RNA that is not attributable to intercurrent infection, vaccination, or test methodology, except as noted previously (BIII).
Undetectable viremia occurs in the patient receiving dual-nucleoside therapy (BIII). Patients receiving two NRTIs who have achieved no detectable virus have the option of continuing this regimen or modifying it to conform to regimens in the strongly recommended category (Table 12). Previous experience indicates that patients on dual-nucleoside therapy will eventually have virologic failure with a frequency that is substantially greater compared with patients treated with the strongly recommended regimens.
CD4+ T cell numbers decline persistently, as measured on ≥ 2 occasions (CIII).
Clinical deterioration occurs (DIII). A new AIDS-defining diagnosis that was acquired after treatment initiation indicates clinical deterioration, but it might not indicate failure of antiretroviral therapy. If the antiretroviral effect of therapy was inadequate (e.g., <1.0 log10 fold reduction in viral RNA), therapeutic failure might have occurred. However, if the antiretroviral effect was adequate but the patient was already severely immunocompromised, the appearance of a new OI might not be an antiretroviral therapy failure but a persistence of severe immunocompromise that did not improve despite adequate suppression of virus replication. Similarly, an accelerated decline in CD4+ T cell counts indicates progressive immune deficiency, if quality control of CD4+ T cell measurements has been ensured.
Table 21.
Table 22.
decrease the severity of acute disease;
alter the initial viral setpoint, which can affect disease-progression rates;
reduce the rate of viral mutation as a result of suppression of viral replication;
preserve immune function; and
reduce the risk for viral transmission.
adverse effects on quality of life resulting from drug toxicities and dosing constraints;
drug resistance if therapy fails to effectively suppress viral replication, which might limit future treatment options; and
a need for continuing therapy indefinitely.
Table 23.
Table 24.
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Dybul M, Fauci AS, Bartlett JG, Kaplan JE, Pau AK. Guidelines for Using Antiretroviral Agents among HIV-Infected Adults and Adolescents: The Panel on Clinical Practices for Treatment of HIV*. Ann Intern Med. 2002;137:381–433. doi: 10.7326/0003-4819-137-5_Part_2-200209031-00001
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© 2018
Published: Ann Intern Med. 2002;137(5_Part_2):381-433.
DOI: 10.7326/0003-4819-137-5_Part_2-200209031-00001
HIV, Infectious Disease.