1059 
Natural History of Compensated Hepatitis C Virus-related Cirrhosis in HIV-infected Patients
Jose A. Garcia-Garcia*1, M Aguilar-Guisado2, A Rivero3, J Giron-Gonzalez4, M Gonzalez-Serrano5, D Merino6, M Rios-Villegas7, J Macias1, J Gomez-Mateos1, J Pineda1, and for the Grupo para el Estudio de las Hepatitis Víricas de la SAEI
1Hosp Univ de Valme, Seville, Spain; 2Hosp Univ Virgen del Rocio, Seville, Spain; 3Hosp Univ Reina Sofia, Cordoba, Spain; 4Hosp Puerta del Mar, Cadiz, Spain; 5Hosp Univ Virgen de la Victoria, Malaga, Spain; 6Hosp Juan Ramon Jimenez, Huelva, Spain; and 7Hosp Univ Virgen de la Macarena, Seville, Spain
Background: Compensated
hepatitis C virus (HCV) -related cirrhosis is a common finding in HIV-infected
populations in areas where HCV/HIV co-infection is prevalent. Information is
scarce on the clinical outcome of this condition. The aim of this study was to
provide information about the incidence of hepatic decompensations and the
mortality and the predictors thereof in HIV-infected patients with compensated
HCV-related cirrhosis.
Methods: In
this retrospective study, 154 HIV/HCV-co-infected patients in whom a new
diagnosis of compensated, Child-Pugh-Turcotte (CPT) class A cirrhosis was made in
the infectious diseases units of 7 hospitals, from January 1996 to September
2006, were included. The time from diagnosis to the first hepatic
decompensation and the survival were evaluated.
Results: The median (Q1-Q3)
follow-up of the population studied was 29.1 (14.9 to 51.3) months: 36 (23.4%) patients developed a liver
decompensation. The density of incidence of hepatic decompensations was 8.88
per 100 person-years. The probability of decompensation at 3 and 5 years was 27
and 33%, respectively. Ascites was the most common first decompensation of
cirrhosis, followed by hepatic encephalopathy and portal hypertensive
gastrointestinal bleeding (50%, 17%, and 17%, respectively). The factors
independently associated (HR; 95%CI) with the emergence of liver decompensation
were no HCV therapy during the follow-up (3.71; 1.25 to 10.99), a baseline CD4 cell counts lower than
300/mm3 (2.12; 1.06 to 4.25), a Child-Pugh-Turcotte
(CPT) score of 6 vs 5 (4.38; 2.03 to 9.43),
and a diagnosis of cirrhosis based on clinical findings (3.81; 1.8 to 8.05); 15 (9.7%) patients died during the follow-up of
whom 11 (73%) died due to liver disease. Of those 11 deaths, 9 (81%) resulted
from hepatic encephalopathy. The mortality rate due to liver failure was 2.44
deaths per 100 person-years. The 3- and 5-year survival estimates were 91 and 82%,
respectively. Hepatic encephalopathy as the
first liver decompensation (29.75; 6.25 to 141.51) and
a higher baseline CPT (5.59; 1.28 to 24.42) score were independently
associated with liver-related mortality.
Conclusions: Clinical liver events are more common in
HIV/HCV-co-infected patients with compensated CPT class A cirrhosis than
previously reported in HCV-mono-infected patients. Liver disease is the
main cause of death in this population. Lower baseline CD4
cell count, lack of therapy against HCV, and higher CPT score are the factors related
to the occurrence of clinical liver events.
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