Medium-term survival rates in patients co-infected with HIV
and hepatitis C who have compensated cirrhosis are good and comparable to those
seen in hepatitis C-mono-infected individuals, Spanish investigators report in
the online edition of AIDS.
Their analysis showed that 87% of patients with compensated
cirrhosis were still alive after three years. However, co-infected patients
with decompensated cirrhosis had a much poorer prognosis and their two-year
survival rate was only 50%. “Once decompensation has occurred, prognosis
rapidly worsens”, comment the authors.
HIV treatment status and baseline Child-Pugh scores (an
assessment of prognosis) were significantly associated with outcomes.
- compensated cirrhosis
The earlier stage of
cirrhosis, during which the liver is damaged but still able to perform most of
its functions. See also ‘cirrhosis’ and ‘decompensated cirrhosis’.
- decompensated cirrhosis
The later stage of
cirrhosis, during which the liver cannot perform some vital functions and
complications occur. See also ‘cirrhosis’ and ‘compensated cirrhosis’.
Cell of the liver.
Liver disease is now a major cause of serious illness and
death in patients co-infected with HIV and hepatitis C.
Spanish investigators wished to establish a better
understanding of the natural history of liver cirrhosis and factors associated
with prognosis in co-infected patients.
Between June 2004 and June 2005 the investigators enrolled
340 co-infected patients with liver cirrhosis into a prospective study. The
patients were assessed at baseline and then at six-monthly intervals.
The majority of patients (n = 248) had compensated cirrhosis
(i.e. even though severe liver damage is present, the liver is still able to compensate or cope with the damage it has
Patients with compensated cirrhosis had significantly higher
CD4 cell counts than individuals with decompensated cirrhosis (p = 0.0001). Predicted prognosis at
baseline was much better for patients with compensated cirrhosis, and 90% had a
Child Pugh score A (100% one year survival rate; 85% three year survival rate)
compared to 28% of patients with decompensated cirrhosis.
The overall mortality rate was 8.55 per 100 person years.
Two-thirds of total deaths were attributed to liver disease. The mortality rate
for patients with decompensated cirrhosis was 27 deaths per 100 person years
compared to 4 deaths per 100 person years for patients with compensated
After three years of follow-up the overall survival rate was
75%. However, 87% of patients with compensated cirrhosis were alive at this
follow-up interval compared to 43% of individuals with decompensated liver
Most (89%) patients with a baseline Child Pugh score A were
alive after three years, compared to 50% of individuals with a baseline score
B, and 16% of those whose prognosis was assessed as Child Pugh C.
In the complete cohort, factors associated with poorer
survival were permanent interruption of antiretroviral therapy (p = 0.0001),
nadir CD4 cell count (p = 0.017), and a baseline Child Pugh score B or C (p =
For patients with compensated cirrhosis at baseline, factors
associated with poorer survival were progression to decompensated disease,
permanent interruption of HIV treatment, and a poorer Child Pugh score at
Longer duration of infection with hepatitis C, stopping HIV
therapy, and a Child Pugh score B or C were all associated with a risk of
progressing to decompensated cirrhosis.
“Our study emphasises the clinical utility of the Child Pugh
score in this population,” note the investigators.
They also comment on the association between interruption of
HIV therapy and poorer prognosis, and suggest “it is possible that HAART
[highly active antiretroviral therapy] might be beneficial for co-infected
patients due to relative preservation of immune function or even by decreasing
HIV-induced progression of liver fibrosis or hepatocyte apoptosis.”
Finally, the investigators conducted an analysis involving
patients with compensated cirrhosis at baseline that received hepatitis C
therapy during follow-up. A sustained virological response to this treatment did
not improve survival.
“It is possible that the reason we have not found a survival
benefit…is lack of power and/or insufficient follow-up,” explain the
investigators. They add that the probability of patients who responded to
hepatitis C therapy dying, developing liver cancer, or needing a transplant was
“Our study shows a relatively good three year survival of
HIV-hepatitis C-co-infected patients with compensated liver disease,” conclude
the authors, adding “further follow-up is needed to confirm a possible survival
benefit for patients with cirrhosis who achieve a sustained virologic