934 
Clinical Progression of Hepatitis C Virus-related Chronic Liver Disease in HIV-infected Patients Undergoing HAART
José A. García-García*1, M Aguilar-Guisado2, M Ríos-Villegas3, M González-Serrano4, A Rivero5, J Del Valle1, R Luque2, J Ruiz-Morales4, J Macías1, J Pineda1, and Grupo Andaluz para el Estudio de las Enfermedades Infecciosas (GAEI)
1Hosp Univ de Valme, Seville, Spain; 2Hosp Univ Virgen del Rocio, Seville, Spain; 3Hosp Univ Virgen de la Macarena, Seville, Spain; 4Hosp Virgen de la Victoria, Malaga, Spain; and 5Hosp Univ Reina Sofía, Cordoba, Spain
Background: HAART
seems to improve the outcome of hepatitis C virus (HCV) -related chronic liver diseases
in HIV-co-infected patients. However, little is known about the rate and
clinical features of hepatic decompensation and the predictors of end-stage
liver disease and liver-related death in this setting. The aim of this study
has been to provide information about the incidence and characteristics of
hepatic decompensation, the mortality as well as the factors associated with
these events in HCV/HIV-co-infected patients undergoing HAART.
Methods: We prospectively followed until
death, lost to follow-up, or the censoring date (July 1, 2005), 1011
ART-naive, HIV/HCV-co-infected patients who started HAART in 5 hospitals. The time
to the first hepatic decompensation and survival were assessed.
Results: After a median (Q1-Q3) follow-up of 5.3 (2.9
to 7.1) years, 59 (5.83%) patients developed a hepatic decompensation. Of the
69 (6.82%) who died, 30 (43%) patients died of liver disease, 15 (22%) of AIDS,
and 24 (35%) of other causes. Ascites was the most common presentation of
decompensated liver disease, followed by hepatic encephalopathy and jaundice
(61%, 27%, and 12%, respectively, of the total cases of decompensation). The
factors independently associated (hazard ratio, 95%
confidence of interval) with the emergence of hepatic decompensation were age
older than 33 years (2.11, 1.18 to 3.78),
female (2.1, 1.07 to 4.15),
CDC stage C (2.14, 1.24 to 3.70),
baseline cirrhosis (10.86, 6.02 to 19.6),
a CD4 cell gain <100/mm3 (4.10, 2.18
to 7.69), and a time with undetectable HIV
viral load shorter than 60% of the follow-up (5.23,
2.5 to 10.93). Older age (2.97,
1.18 to 7.50), lack of HCV therapy (11.32,
1.44 to 89.05), hepatitis D virus (HDV) co-infection
(16.15, 2.45 to 106.48),
baseline cirrhosis (13.69, 5.55 to 34.48),
hepatic encephalopathy (62.5, 21.27 to 200),
and a lower CD4 cell gain (3.63,
1.45 to 9.09) were associated with mortality due
to liver failure.
Conclusions: The overall rate of clinical progression of
liver disease in HIV/HCV-infected patients under HAART is relatively low. In
spite of that, end stage liver disease is the main cause of death in this
population. Older age, a
diagnosis of liver cirrhosis, and a lower CD4 cell gain after starting HAART
are the factors more consistently associated with the emergence of hepatic clinical
events.
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