E Martín-Echevarria1, S Serrano-Villar2, T Sainz3, A Moreno2, J L Casado2, F Dronda2, M J Pérez Elías2, E Navas4, M Rodríguez Zapata1, S Moreno2. 1. Department of Internal Medicine, Hospital Universitario de Guadalajara, Guadalajara, Mexico. 2. Department of Infectious Diseases, Hospital Universitario Ramón y Cajal, Madrid, Spain. 3. Laboratory of Molecular Immune Biology, Hospital Universitario Gregorio Marañón, Madrid, Spain. 4. Department of Infectious Diseases, Hospital Universitario Ramón y Cajal, Madrid.
Abstract
BACKGROUND: It is unclear whether optimal immunological recovery reduces the risk of tuberculosis (TB) in human immunodeficiency virus (HIV) infected patients receiving antiretroviral therapy (ART), in whom it is still significantly higher than in the general population. METHODS: Retrospective cohort study in ART-treated patients without a previous diagnosis of TB. TB was microbiologically proven. Multivariate analyses were performed to identify risk factors associated with TB. RESULTS: This study included 1824 patients; the median follow-up was 473 days. The median CD4 count was 207 cells/μl (90-363.8); 339 (18.6%) were tuberculin skin test positive. Increased CD4 count gain after ART initiation was a protective factor against active TB (per each 100 cells/μl increase, OR 0.683, 95%CI 0.522-0.894). Maximal protection was observed in patients reaching increments ⩾150 cells/μl after 12 months of ART (OR 0.29, 95%CI 0.11-0.8) or ⩾300 cells/μl after 24 months (OR 0.73, 95%CI 0.71-0.75). There was no association between achieving HIV RNA <50 copies/ml and risk of active TB (OR 1.43, 95%CI 0.68-2.49). CONCLUSIONS: The risk of TB in patients starting ART is reduced among those with better immunological response, and is unrelated to the virological response. Our results emphasise the need for adjunctive strategies in immunological non-responders to minimise any residual risk of TB.
BACKGROUND: It is unclear whether optimal immunological recovery reduces the risk of tuberculosis (TB) in human immunodeficiency virus (HIV) infectedpatients receiving antiretroviral therapy (ART), in whom it is still significantly higher than in the general population. METHODS: Retrospective cohort study in ART-treated patients without a previous diagnosis of TB. TB was microbiologically proven. Multivariate analyses were performed to identify risk factors associated with TB. RESULTS: This study included 1824 patients; the median follow-up was 473 days. The median CD4 count was 207 cells/μl (90-363.8); 339 (18.6%) were tuberculin skin test positive. Increased CD4 count gain after ART initiation was a protective factor against active TB (per each 100 cells/μl increase, OR 0.683, 95%CI 0.522-0.894). Maximal protection was observed in patients reaching increments ⩾150 cells/μl after 12 months of ART (OR 0.29, 95%CI 0.11-0.8) or ⩾300 cells/μl after 24 months (OR 0.73, 95%CI 0.71-0.75). There was no association between achieving HIV RNA <50 copies/ml and risk of active TB (OR 1.43, 95%CI 0.68-2.49). CONCLUSIONS: The risk of TB in patients starting ART is reduced among those with better immunological response, and is unrelated to the virological response. Our results emphasise the need for adjunctive strategies in immunological non-responders to minimise any residual risk of TB.
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