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Clinical outcome among HIV-infected patients starting saquinavir hard gel compared to ritonavir or indinavir

Kirk, Olea; Mocroft, Amandab; Pradier, Christianc; Bruun, Johan N.d; Hemmer, Roberte; Clotet, Bonaventuraf; Miller, Veronicag; Viard, Jean-Paulh; Phillips, Andrew N.b; Lundgren, Jens D.*; the EuroSIDA Study Group

Clinical Science

Objective: To compare the clinical response among patients who initiate protease inhibitor therapies with different virological potency.

Design: We analysed patients who started indinavir, ritonavir or saquinavir hard gel capsule (hgc) as part of at least triple therapy during prospective follow-up within the EuroSIDA study.

Methods: Changes in plasma viral load (pVL) and CD4 cell count from baseline were compared between treatment groups. Time to new AIDS-defining events and death were compared in Kaplan–Meier models, and Cox models were established to further assess differences in clinical progression (new AIDS/death). Adjustment was made for differences in baseline parameters, in particular pVL, CD4 cell count, and region of Europe.

Results: A total of 2708 patients (median follow-up: 30 months) were included, of which 556 started ritonavir (21%), 1342 indinavir (50%), and 810 saquinavir hgc (30%). The three groups were fairly evenly balanced at baseline regarding CD4 count, previous diagnosis of AIDS and pVL, After 12 months, the median changes in CD4 cell count were 90, 96 and 74 × 106 cells/l, respectively;P < 0.001, the proportions of patients with pVL < 500 copies/ml were 47, 54 and 41%;P < 0.001, and the proportions with clinical progression were 11.9, 9.2 and 11.9%, respectively;P = 0.20 (log-rank test). In multivariate models the relative risk of clinical progression for indinavir compared with saquinavir hgc was: 0.77 (0.60–0.99);P = 0.043, and for ritonavir 0.83 (0.62–1.11);P = 0.20.

Conclusions: Saquinavir hgc was associated with an inferior long-term clinical response relative to indinavir, which was consistent with the observed differences in virological and immunological responses.

From the aEuroSIDA Coordinating Centre, Department of Infectious Diseases, Hvidovre Hospital, University of Copenhagen, Copenhagen, Denmark, the bRoyal Free Centre for HIV Medicine, Royal Free and University College London Medical School, London, UK, the cDepartment of Infectious Diseases, Hopital de l'Archet, Nice, France, the dDepartment of Infectious Diseases, Ullevål Hospital, Oslo, Norway, the eDepartment des Maladies Infectieuses, Centre Hospitalier, Luxembourg, Luxembourg, the fRetrovirology Laboratory ‘irsiCaixa’ Foundation, Hospital Universitari ‘Germans Trias i Pujol', Universitat Autónoma de Barcelona, Badalona, Spain, the gZentrum der Inneren Medizin, J W Goethe University Hospital, Frankfurt am Main, Germany and the hService d'Immunologie Clinque, Hopital Necker-Enfants Malades, Paris, France. *See Appendix.

Correspondence to Ole Kirk, EuroSIDA Coordinating Centre, Department of Infectious Diseases, Hvidovre Hospital, University of Copenhagen, Kettegaard Alle, 2650 Hvidovre, Denmark. Tel: + 45 36 32 30 15; fax: + 45 36 47 33 40; e-mail:

Received: 8 September 2000;

revised: 5 January 2001; accepted: 8 March 2001.

© 2001 Lippincott Williams & Wilkins, Inc.