9TH EUROPEAN AIDS CONFERENCE (EACS)
1st EACS RESISTANCE & PHARMACOLOGY WORKSHOP

October 25 - 29, 2003 Warsaw, Poland

7.4 Treatment Failure and Salvage Therapy

F7/1 - BIOLOGICAL RESPONSES AND CLINICAL PROGRESSION AND IN PATIENTS WITH VIROLOGIC FAILURE TO MULTIPLE CLASSES OF ANTIRETROVIRALS (ARV)
Potard V.1, Duval X.2, Dupont C.3, Pradier C.4, Duvivier C.5, Salmon D.6, * Costagliola D.1
 
(1) INSERM E0214 Universite Pierre et Marie Curie Paris,2 Bichat CHU Paris,3 Ambroise Paré CHU Paris,4 L'Archet hospital Nice,5 Pitié-Salpétrière Paris,6 Cochin CHU Paris, France
 

Background: Multiple treatment failure in HIV patients is difficult to manage.

Objective: We studied factors associated with clinical progression and biological responses in patients from the French Hospital Database on HIV with virologic failure after exposure to 3 classes of ARV.

Methods: We selected 1092 patients previously exposed to at least 2 NRTI, 2 PI, 1 NNRTI, with viral load (VL)>5000 copies/ml and treatment change occurring between 1998 and 2001. We evaluated new AIDS defining event (ADE) or death, VL and CD4 changes between baseline and last follow-up.

Results: Baseline characteristics were AIDS 49%, median CD4 181 cells/mm3, VL 71009 copies/ml, duration of ARV 5.0 years, exposure to 9 ARV. Patients were followed-up for a median of 13 months during which 187 new ADE or death occurred. The crude rates of progression were 20.1/100 patient-years for patients included in 1998, 15.1 in 1999, 11.1 in 2000 and 8.6 in 2001. After adjustment for baseline characteristics, year was associated with clinical progression (p<0.001). When new drugs at baseline or during follow-up were introduced in the model, calendar year was no longer associated with clinical progression (p=0.26), while exposure to Amprenavir, Lopinavir/rtv, Abacavir or Tenofovir were. Prescription of these drugs was also associated both with a drop of at least one log in VL and an increase of at least 50 CD4 cells/mm3.

Conclusion: Prognosis of patients highly pre-exposed to ARV with virologic failure has improved between 1998 and 2001, mainly because of availability of new drugs with a more favourable resistance.

Presenting Author: PhD Costagliola Dominique, INSERM E0214, 56 boulevard Vincent Auriol, 75625, Paris cedex 13, France, Phone: 33(0)1 42 16 42 82

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