Also, it is possible that patients may have a store of drugs not previously used. By its nature, this adherence measure does not provide any
information about short-term adherence patterns and whether the GSK126 mouse antiretroviral drugs were taken at the correct times. However, a gold standard for measuring adherence does not exist [47]. A feature that makes adherence particularly difficult to accurately quantify is that rates may vary not just between individuals, but also within the same individual over time. This is the reason why we decided to evaluate drug coverage on the last 6 months immediately previous to time-zero, at every DCVL episode rather than assess it only in one point over time. The second limitation is that the risk of viral rebound may be overestimated, as a result of the definition of VL rebound as a single VL >200 copies/mL. Thus, it represents a relatively low threshold and is not necessarily confirmed by a subsequent VL >200 copies/mL, but our aim Transferase inhibitor was to detect even transient increase of plasma VL. It should be noted that patients may spontaneously re-suppress the VL after a single episode of viraemia >200 copies/mL. Finally, because this study included only subjects who had achieved
viral suppression, the results regarding the relationship between adherence and outcome can only be generalized to HIV-infected subjects on HAART who achieved VL suppression, who represent approximately 90% of HIV-infected patients on HAART [48]. To conclude, although it is well established that most patients on ART nowadays achieve VL suppression, full and long-term maintenance of this suppression, which is the current accepted goal of therapy [49], can be problematic [16]. In this study we have confirmed the importance of ART adherence, as evaluated by drug coverage, to predict VL rebound. Therefore, objective, simple and easy-to-use adherence measures, such as
the one proposed here, could help to identify, together with other known predictors, Sodium butyrate patients at risk of viral rebound, thereby guiding corrective interventions to prevent and promptly manage viral rebound. This work was funded in part by NEAT (European Commission). Royal Free Centre for HIV Medicine Clinical: S. Bhagani, P. Byrne, A. Carroll, I. Cropley, Z. Cuthbertson, A. Dunleavy, A. M. Geretti, B. Heelan, M. Johnson, S. Kinloch-de Loes, M. Lipman, S. Madge, T. Mahungu, N. Marshall, D. Nair, B. Prinz, A. Rodger, L. Swaden, M. Tyrer and M. Youle. Data management: C. Chaloner, H. Grabowska, J. Holloway, J. Puradiredja, S. Scott and R. Tsintas. Biostatistics/Epidemiology: W. Bannister, L. Bansi, V. Cambiano, A. Cozzi-Lepri, Z. Fox, E. Harris, T. Hill, A. Kamara, F. Lampe, R. Lodwick, A. Mocroft, A. Phillips, J. Reekie, A. Rodger, C. Sabin and C. Smith. Laboratory: E. Amoah, C. Booth, G. Clewley, A. Garcia Diaz, A. M. Geretti, B.