OBJECTIVES: To evaluate the virological, immunological and clinical responses to the boosted double protease inhibitor (PI) regimen combination of lopinavir/ritonavir and saquinavir ('LOPSAQ') without reverse transcriptase inhibitors (RTI) in HIV-positive patients who have few viable RTI treatment options. METHODS: Cohort study of 128 heavily pre-treated patients who were experiencing therapy failure on their current regimen due to RTI resistance and/or systemic toxicities. Patients with PI-resistance mutations or RTI toxicity underwent a structured treatment interruption (STI) (n=76) until virus reverted to wild-type or until resolution of toxicity symptoms. Baseline was defined as the time point when lopinavir/ritonavir plus saquinavir therapy was initiated. Virological response was defined as viral load<400 copies/mL at week 48. RESULTS: A total of 78 (61%) patients experienced a virological response to therapy (ITT). Median viral load at baseline was 5.06 log10 copies/mL; at week 48 median was 2.16 log10 copies. Median CD4 at week 48 was 280 cells/mm3 compared with 172 cells at baseline. At week 48, 78/128 patients were still on therapy. In univariable analyses, significant predictors of virological response included higher CD4 count (P<0.001), lower viral load (P=0.002), less PI-experience (P=0.006) at baseline and fewer PI-resistance mutations (P=0.043) at end of prior failing regimen; in the multivariable analysis only higher CD4 count at baseline (P=0.009) and fewer number of drugs previously taken (P=0.003) could be specified as independent predictors for response. CONCLUSIONS: The combination of lopinavir/ritonavir and saquinavir without RTIs is a potential option as salvage therapy for patients experiencing therapy failure due to RTI resistance or toxicity. This regimen may not be suitable for patients with very low baseline CD4 cell counts, very broad antiretroviral therapy experience or extensive PI-resistance mutations.
OBJECTIVES: To evaluate the virological, immunological and clinical responses to the boosted double protease inhibitor (PI) regimen combination of lopinavir/ritonavir and saquinavir ('LOPSAQ') without reverse transcriptase inhibitors (RTI) in HIV-positivepatients who have few viable RTI treatment options. METHODS: Cohort study of 128 heavily pre-treated patients who were experiencing therapy failure on their current regimen due to RTI resistance and/or systemic toxicities. Patients with PI-resistance mutations or RTI toxicity underwent a structured treatment interruption (STI) (n=76) until virus reverted to wild-type or until resolution of toxicity symptoms. Baseline was defined as the time point when lopinavir/ritonavir plus saquinavir therapy was initiated. Virological response was defined as viral load<400 copies/mL at week 48. RESULTS: A total of 78 (61%) patients experienced a virological response to therapy (ITT). Median viral load at baseline was 5.06 log10 copies/mL; at week 48 median was 2.16 log10 copies. Median CD4 at week 48 was 280 cells/mm3 compared with 172 cells at baseline. At week 48, 78/128 patients were still on therapy. In univariable analyses, significant predictors of virological response included higher CD4 count (P<0.001), lower viral load (P=0.002), less PI-experience (P=0.006) at baseline and fewer PI-resistance mutations (P=0.043) at end of prior failing regimen; in the multivariable analysis only higher CD4 count at baseline (P=0.009) and fewer number of drugs previously taken (P=0.003) could be specified as independent predictors for response. CONCLUSIONS: The combination of lopinavir/ritonavir and saquinavir without RTIs is a potential option as salvage therapy for patients experiencing therapy failure due to RTI resistance or toxicity. This regimen may not be suitable for patients with very low baseline CD4 cell counts, very broad antiretroviral therapy experience or extensive PI-resistance mutations.
Authors: Lucile Larrouy; C Chazallon; R Landman; C Capitant; G Peytavin; G Collin; C Charpentier; A Storto; G Pialoux; C Katlama; P M Girard; P Yeni; J P Aboulker; F Brun-Vezinet; D Descamps Journal: Antimicrob Agents Chemother Date: 2010-05-03 Impact factor: 5.191
Authors: Maximilian Donath; Timo Wolf; Martin Stürmer; Eva Herrmann; Markus Bickel; Pavel Khaykin; Siri Göpel; Peter Gute; Annette Haberl; Philipp de Leuw; Gundolf Schüttfort; Annemarie Berger; Christoph Stephan Journal: Med Microbiol Immunol Date: 2016-07-28 Impact factor: 3.402
Authors: Nils von Hentig; Axel Müller; Carsten Rottmann; Timo Wolf; Thomas Lutz; Stephan Klauke; Michael Kurowski; Bruno Oertel; Brenda Dauer; Sebastian Harder; Schlomo Staszewski Journal: Antimicrob Agents Chemother Date: 2007-02-12 Impact factor: 5.191
Authors: Brian L Robbins; Edmund V Capparelli; Ellen G Chadwick; Ram Yogev; Leslie Serchuck; Carol Worrell; Mary Elizabeth Smith; Carmelita Alvero; Terence Fenton; Barbara Heckman; Stephen I Pelton; Grace Aldrovandi; William Borkowsky; John Rodman; Peter L Havens Journal: Antimicrob Agents Chemother Date: 2008-07-14 Impact factor: 5.191
Authors: Christoph Stephan; Valentin Bartha; Eva Herrmann; Nils von Hentig; Pavel Khaykin; Gaby Knecht; Peter Gute; Hans-Reinhard Brodt; Martin Stürmer; Annemarie Berger; Markus Bickel Journal: Med Microbiol Immunol Date: 2012-09-15 Impact factor: 3.402
Authors: Nils von Hentig; Pavel Kaykhin; Christoph Stephan; Errol Babacan; Martin Stürmer; Schlomo Staszewski; Jörn Lötsch Journal: Antimicrob Agents Chemother Date: 2008-04-14 Impact factor: 5.191
Authors: Heekyoung Choi; Su Jin Jeong; Han Sung Lee; Bum Sik Chin; Suk Hoon Choi; Sang Hoon Han; Myung Soo Kim; Chang Oh Kim; Jun Yong Choi; Young Goo Song; June Myung Kim Journal: J Korean Med Sci Date: 2008-08 Impact factor: 2.153