Transient Elastography for Predicting Liver-Related Events in Cirrhotic HIV-Infected PatientsMontes ML1*, Berenguer J2, Miró JM3, Quereda C4, Hernando A5, Sanz J6, Ortega E7, Tural C8, Wichmann MA9, Zamora FX1and Gónzalez-García JJ1
- *Corresponding Author:
- M. Luisa Montes
Hospital Universitario La Paz
Internal Medicine, HIV Unit
Madrid, Madrid 28002, Spain
E-mail: [email protected]
Received date: February 28, 2017; Accepted date: March 08, 2017; Published date: March 15, 2017
Citation: Montes ML, Berenguer J, Miró JM, Quereda C, Hernando A, et al. (2017) Transient Elastography for Predicting Liver-Related Events in Cirrhotic HIV-Infected Patients. J AIDS Clin Res 8:675. doi:10.4172/2155-6113.1000675
Copyright: © 2017 Montes ML, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Aim: We assessed liver stiffness measurement (LSM) for the prediction of mortality and decompensation in HIVinfected patients with compensated liver cirrhosis. Method: A prospective cohort study of HIV-infected patients with confirmed liver cirrhosis from 9 hospitals in Spain. LSM was undertaken for each patient; clinical events were collected prospectively after the baseline visit, and patients were followed until death or the censoring date. We used univariate/multivariate Cox proportional hazard models to evaluate the utility of LSM for predicting the first hepatic decompensation or overall mortality. The sensitivity (SEN), specificity (SPE), positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratio (LR+) and negative likelihood ratio (LR-) were calculated. The LSM cutoff was selected using ROC curves. Results: We included 102 patients with compensated liver cirrhosis; median [interquartile, (IQR)] follow-up was 36 (21-46) months, median (IQR) CD4+ cell count was 415 cells/μL (307-624) and 94% were receiving antiretroviral therapy. The median (IQR) LSM was 17 kPa (11.7-26). Nineteen events were recorded during follow-up. Multivariate analysis showed that time to hepatic decompensation was associated with CD4+ <200 cells/μL (HR, 26; 95% CI, 1.8- 377; p<0.02) and LSM ≥ 25 kPa (HR, 7.2; 95% CI, 1.1-47; p=0.04) and that time to overall mortality was associated with LSM ≥ 25 kPa (HR, 14.3; 95% CI, 1.5-138; p=0.02). The predictive values for decompensation (LSM ≥ 25 kPa) were as follows: SEN, 67%; SPE, 78%; NPV, 96%; PPV, 23%; LR+, 3; LR-, 0.4. The predictive values for overall mortality with this LSM cutoff were as follows: SEN, 86%; SPE, 79%; NPV, 99%; PPV, 23%; LR+, 4; LR-, 0.2. Conclusion: Our data suggest that LSM is an accurate method for the prediction of mortality and decompensation in HIV-infected patients with liver cirrhosis.