OBJECTIVE: To compare the immunological response to highly active antiretroviral therapy (HAART) in treatment-naive patients with a baseline CD4 count of <200 cells/mm(3). DESIGN AND METHODS: We identified treatment-naive human immunodeficiency virus (HIV-1)-infected individuals who had commenced HAART since 1996 and who had a starting CD4 count of <200 cells/mm(3). Immunological success was defined as achieving a CD4 count of >200 cells/mm(3) and treatments were compared using univariate and multivariate Cox's proportional hazards models in order to establish whether protease inhibitor (PI)-based regimens were significantly different to regimens based on non-nucleoside reverse transcriptase inhibitors (NNRTIs). Both regimens utilize a nucleoside analogue (NA) backbone. RESULTS: A total of 599 patients were identified. When the variables were entered into a multivariate analysis, no significant differences between HAART regimens were found. We showed that compared with efavirenz regimens a two NA plus one PI regimen was not significantly less likely to achieve immunological success (adjusted HR: 0.65, 95% CI 0.41-1.03, P=0.07). Two NA and boosted PI (adjusted HR: 1.33, 95% CI 0.81 to 2.16) or two NA and nevirapine (adjusted HR: 0.93, 95% CI 0.67-1.29) regimens were also not significantly different from efavirenz-based regimens, based on the endpoint of immunological success. CONCLUSION: PI-, boosted PI- and NNRTI-based HAART regimens are not significantly different in achieving increased CD4 counts in individuals who commence therapy with a low CD4 count.
OBJECTIVE: To compare the immunological response to highly active antiretroviral therapy (HAART) in treatment-naive patients with a baseline CD4 count of <200 cells/mm(3). DESIGN AND METHODS: We identified treatment-naive human immunodeficiency virus (HIV-1)-infected individuals who had commenced HAART since 1996 and who had a starting CD4 count of <200 cells/mm(3). Immunological success was defined as achieving a CD4 count of >200 cells/mm(3) and treatments were compared using univariate and multivariate Cox's proportional hazards models in order to establish whether protease inhibitor (PI)-based regimens were significantly different to regimens based on non-nucleoside reverse transcriptase inhibitors (NNRTIs). Both regimens utilize a nucleoside analogue (NA) backbone. RESULTS: A total of 599 patients were identified. When the variables were entered into a multivariate analysis, no significant differences between HAART regimens were found. We showed that compared with efavirenz regimens a two NA plus one PI regimen was not significantly less likely to achieve immunological success (adjusted HR: 0.65, 95% CI 0.41-1.03, P=0.07). Two NA and boosted PI (adjusted HR: 1.33, 95% CI 0.81 to 2.16) or two NA and nevirapine (adjusted HR: 0.93, 95% CI 0.67-1.29) regimens were also not significantly different from efavirenz-based regimens, based on the endpoint of immunological success. CONCLUSION: PI-, boosted PI- and NNRTI-based HAART regimens are not significantly different in achieving increased CD4 counts in individuals who commence therapy with a low CD4 count.