Liver Failure/Cirrhosis/Portal Hypertension
Liver stiffness predicts clinical outcome in human immunodeficiency virus/hepatitis C virus-coinfected patients with compensated liver cirrhosis†
Article first published online: 6 JUN 2012
DOI: 10.1002/hep.25616
Copyright © 2012 American Association for the Study of Liver Diseases
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How to Cite
Merchante, N., Rivero-Juárez, A., Téllez, F., Merino, D., José Ríos-Villegas, M., Márquez-Solero, M., Omar, M., Macías, J., Camacho, Á., Pérez-Pérez, M., Gómez-Mateos, J., Rivero, A., Antonio Pineda, J. and on behalf of the Grupo Andaluz para el Estudio de las Hepatitis Víricas (HEPAVIR) de la Sociedad Andaluza de Enfermedades Infecciosas (SAEI) (2012), Liver stiffness predicts clinical outcome in human immunodeficiency virus/hepatitis C virus-coinfected patients with compensated liver cirrhosis. Hepatology, 56: 228–238. doi: 10.1002/hep.25616
- † Potential conflict of interest: Nothing to report.
Publication History
- Issue published online: 3 JUL 2012
- Article first published online: 6 JUN 2012
- Accepted manuscript online: 25 JAN 2012 05:08AM EST
- Manuscript Accepted: 15 JAN 2012
- Manuscript Received: 13 JUL 2011
Funded by
- Consejería de Salud de la Junta de Andalucía. Grant Number: Reference PI-0008/2007
- Servicio Andaluz de Salud. Grant Number: Reference SAS/111239
- Fundación para la Investigación y la Prevención del SIDA en España (FIPSE). Grant Number: Reference 36-0799-09
- Fundación Progreso y Salud of the Consejería de Salud de la Junta de Andalucía. Grant Numbers: Reference AI-0011-2010, Reference AI-0021
- Ministerio de Sanidad y Consumo, Instituto de Salud Carlos III, Red de SIDA from Spain. Grant Number: ISCIII-RETIC RD06/006
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Abstract
Our aim was to assess the predictive value of liver stiffness (LS), measured by transient elastography (TE), for clinical outcome in human immunodeficiency virus / hepatitis C virus (HIV/HCV)-coinfected patients with compensated liver cirrhosis. This was a prospective cohort study of 239 consecutive HIV/HCV-coinfected patients with a new diagnosis of cirrhosis, done by TE, and no previous decompensation of liver disease. The time from diagnosis to the first liver decompensation and death from liver disease, as well as the predictors of these outcomes, were evaluated. After a median (Q1-Q3) follow-up of 20 (9-34) months, 31 (13%, 95% confidence interval [CI]: 9%-17%) patients developed a decompensation. The incidence of decompensation was 6.7 cases per 100 person-years (95% CI, 4.7-9-6). Fourteen (8%) out of 181 patients with a baseline LS < 40 kPa developed a decompensation versus 17 (29%) out of 58 with LS ≥ 40 kPa (P = 0.001). Factors independently associated with decompensation were Child-Turcotte-Pugh (CTP) class B versus A (hazard ratio [HR] 7.7; 95% CI 3.3-18.5; P < 0.0001), log-plasma HCV RNA load (HR 2.1; 95% CI 1.2-3.6; P = 0.01), hepatitis B virus coinfection (HR, 10.3; 95% CI, 2.1-50.4; P = 0.004) and baseline LS (HR 1.03; 95% CI 1.01-1.05; P = 0.02). Fifteen (6%, 95% CI: 3.5%-9.9%) patients died, 10 of them due to liver disease, and one underwent liver transplantation. CTP class B (HR 16.5; 95% CI 3.4-68.2; P < 0.0001) and previous exposure to HCV therapy (HR 7.4; 95% CI 1.7-32.4, P = 0.007) were independently associated with liver-related death; baseline LS (HR 1.03; 95% CI 0.98-1.07; P = 0.08) was of borderline significance. Conclusion: LS predicts the development of hepatic decompensations and liver-related mortality in HIV/HCV-coinfection with compensated cirrhosis and provides additional prognostic information to that provided by the CTP score. (HEPATOLOGY 2012;56:228–238)
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