| Description | Caniglia EC1, Phillips A2, Porter K2, Sabin CA2, Winston A3, Logan R1, Gill J4, Vandenhende MA5, Barger D6, Lodi S1, Moreno S7, Arribas JR8, Pacheco A9, Cardoso SW10, Chrysos G11, Gogos C12, Abgrall S13,14, Costagliola D13, Meyer L15,16, Seng R15,16, van Sighem A17, Reiss P17,18,19, Muga R20, Hoyos SP21, Braun D22, Hauser C23, Barrufet P24, Leyes M25, Tate J26, Justice A27, Hernán MA1,28,29. From the 1
Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA; 2
University College London, London, United Kingdom; 3
Imperial College, London, United Kingdom; 4
Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA; 5
Southern Alberta HIV
Clinic, University of Calgary, Calgary, Alberta, Canada; 6
MCU-PH Service Médecine Interne et Maladies Infectieuses—Pr Bonnet Hôpital Saint-André CHU
Bordeaux, Bordeaux, France; 7
Université de Bordeaux, Bordeaux, France; 8
Ramón y Cajal Hospital, IRYCIS, University of Alcalá de Henares, Madrid, Spain;
Madrid, Spain; 9
Hospital La Paz, Spain; 10Programa de Computação Científica, FIOCRUZ, Rio de Janeiro, Madrid, Brazil; 11INI—Fiocruz, Rio de Janeiro,
Brazil; 12Infectious Diseases Unit, “Tzaneion” General Hospital of Piraeus, Athens, Greece; 13University of Patras, Athens, Greece; 14INSERM, Institut Pierre
Louis d’épidémiologie et de Santé Publique (IPLESP UMRS 1136), Sorbonne Universités, UPMC Univ Paris 06, Paris, France; 15Service de Médecine Interne,
Assistance Publique-Hopitaux de Paris (AP-HP), Hopital Antoine Béclère, Clamart, France; 16Université Paris Sud, INSERM CESP U1018, Paris, France; 17Service de Santé Publique, AP-HP, Hopital de Bicêtre, le Kremlin Bicêtre, France; 18Stichting HIV Monitoring, Amsterdam, the Netherlands; 19Division of
Infectious Diseases, Department of Global Health, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands; 20Amsterdam Institute for
Global Health and Development, Amsterdam, Netherlands; 21Servei de Medicina Interna, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de
Barcelona, Barcelona, Spain; 22Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain; 23Universitätsspital Zürich, Zürich, Switzerland; 24Department of
Infectious Diseases, Bern University Hospital, University of Bern, Bern, Switzerland; 25Hospital de Mataró Mataró, Barcelona, Spain; 26HUSE (Son Espases
Universitary Hospital), Palma de Mallorca, Spain; 27Yale University School of Medicine, New Haven, CT; 28Yale University, New Haven, CT; 29Department of
Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA; 30Harvard-MIT Division of Health Sciences and Technology, Boston, MA. | pt_BR |
| Abstract | BACKGROUND:
The differential effects of commonly prescribed combined antiretroviral therapy (cART) regimens on AIDS-defining neurological conditions (neuroAIDS) remain unknown.
SETTING:
Prospective cohort studies of HIV-positive individuals from Europe and the Americas included in the HIV-CAUSAL Collaboration.
METHODS:
Individuals who initiated a first-line cART regimen in 2004 or later containing a nucleoside reverse transcriptase inhibitor backbone and either atazanavir, lopinavir, darunavir, or efavirenz were followed from cART initiation until death, lost to follow-up, pregnancy, the cohort-specific administrative end of follow-up, or the event of interest, whichever occurred earliest. We evaluated 4 neuroAIDS conditions: HIV dementia and the opportunistic infections toxoplasmosis, cryptococcal meningitis, and progressive multifocal leukoencephalopathy. For each outcome, we estimated hazard ratios for atazanavir, lopinavir, and darunavir compared with efavirenz via a pooled logistic model. Our models were adjusted for baseline demographic and clinical characteristics.
RESULTS:
Twenty six thousand one hundred seventy-two individuals initiated efavirenz, 5858 initiated atazanavir, 8479 initiated lopinavir, and 4799 initiated darunavir. Compared with efavirenz, the adjusted HIV dementia hazard ratios (95% confidence intervals) were 1.72 (1.00 to 2.96) for atazanavir, 2.21 (1.38 to 3.54) for lopinavir, and 1.41 (0.61 to 3.24) for darunavir. The respective hazard ratios (95% confidence intervals) for the combined end point were 1.18 (0.74 to 1.88) for atazanavir, 1.61 (1.14 to 2.27) for lopinavir, and 1.36 (0.74 to 2.48) for darunavir. The results varied in subsets defined by calendar year, nucleoside reverse transcriptase inhibitor backbone, and age.
CONCLUSION:
Our results are consistent with an increased risk of neuroAIDS after initiating lopinavir compared with efavirenz, but temporal changes in prescribing trends and confounding by indication could explain our findings. | pt_BR |
