Past research has indicated that
hepatitis C-related liver fibrosis tends to progress more rapidly in HIV-HCV
coinfected individuals compared to those with HCV
alone. However, data have been mixed, and some studies suggest that coinfected
people with well-controlled HIV disease and well-preserved immune function may
fare as well as HIV negative people.
In
the first study (abstract 1055), Spanish researchers evaluated observed fibrosis
progression rates in HIV-HCV coinfected patients and risk factors associated with
accelerated progression.
As background, they noted that in a prior study
of observed fibrosis progression in coinfected patients, approximately half progressed
by at least 1 stage and one-quarter were very fast progressors, with liver fibrosis
increasing by 2 or more stages between liver biopsies.
The present retrospective
analysis included 83 coinfected patients who underwent 2 serial liver biopsies,
separated at least by 1 year, who did not have other possible causes of liver
disease other than hepatitis C. The median time between biopsies was 40 months.
Fibrosis was staged according to the Scheuer scale, ranging from F0 to F4. Patients
with pre-existing cirrhosis (stage F4) on the first biopsy were excluded.
Results
•
During follow-up, 81% of patients received
HAART, of whom 76% had undetectable
HIV RNA.
•
Changes in fibrosis stage between the 2 biopsies
were as follows:
•
Regression by 1 stage or more: 13 patients
(16%); •
No change: 36 patients (43%); •
Progression by 1 stage or more: 34 patients
(41%).
•
In a multivariate analysis, factors associated
with progression of 1 stage or more were moderate-to-severe lobular inflammation
and end-of-treatment or sustained virological response to treatment.
"Fibrosis
progression is frequently observed in HIV-HCV
coinfected patients under HAART
over a period of 3 years," the investigators concluded.
However,
they added, "Response to anti-HCV treatment can prevent progression."
Risk
Factors for Fibrosis Progression
In
the second study (abstract 1056), another Spanish research team assessed predictors
of liver disease severity and factors influencing fibrosis progression rate (FPR).
Between
January 1998 and May 2007, 323 consecutive HIV-HCV coinfected patients underwent
liver biopsy. All were hepatitis B surface antigen negative and had not received
hepatitis C treatment. Participants had been infected with HCV for a median of
20 years and most (80%) had genotype 1. Most (75%) were men, the average age was
40 years, and 87% had a history of injection drug use. Half had received both
protease inhibitors (PIs) and NNRTIs; about a third had a prior AIDS-defining
condition.
Resultes
•
At baseline, distribution of fibrosis was
as follows:
•
Advanced fibrosis/cirrhosis was not associated
with:
•
Time of HCV infection; •
HCV genotype; •
HCV RNA level; •
Exposure to or duration of PI use; •
Exposure to or duration of NNRTI use.
•
In a multivariate analysis, F3-F4 fibrosis/cirrhosis
was associated with:
•
Older age (P = 0.005); •
History of injection drug use (P = 0.04); •
GGT > 100 U/L (P = 0.006); •
Lower CD4 count (P = 0.004).
•
The estimated median fibrosis progression
rate was 0.09 units per year.
•
About 40% of patients progressed by more than
0.1 units per year.
•
In a univariate analysis, FPR > 0.1 was
associated with:
•
Exposure to PIs (P = 0.032); •
GGT > 100 U/I (P = 0.02); •
Lower CD4 count at time of biopsy (P = 0.03).
•
Factors not associated with FPR > 0.1 were:
•
History of injection drug use; •
Exposure to or duration of NNRTI use; •
Duration of PI use; •
Being HAART-naive.
•
In a multivariate analysis, predictors of
FPR > 0.1 were:
•
Exposure to PIs (OR 1.861; P = 0.039); •
GGT ? 100 U/l (OR 1.743; P = 0.026).
The
researchers concluded that, "Neither exposure to [or] time on PI/NNRTI significantly
affected histological severity, but PI exposure and GGT > 100 U/l at
liver biopsy were associated [with] a higher FPR."
They added that,
"In patients with PI exposure, there was a significantly higher frequency
of factors predicting histological severity: older age, severe immunosuppression,
and AIDS."
2/15/08
References
J
Macias, J Berenguer, A Arizcorreta, and others. Increased Rates of Fibrosis Progression
between Sequential Liver Biopsies in HIV/HCV-co-infected Patients. 15th Conference
on Retroviruses and Opportunistic Infections. Boston, MA. February 3-6, 2008.
Abstract 1055.
A
Moreno, S Diz, L Moreno, and others. Histological Findings, Predictors of Severe
Fibrosis, and Assessment of Factors with Effect on the Fibrosis Progression Rate
in HIV-infected Patients with Chronic Hepatitis C in the Era of HAART. 15th Conference
on Retroviruses and Opportunistic Infections. Boston, MA. February 3-6, 2008.
Abstract 1056.
Rates
and Risk Factors for Liver Fibrosis Progression in HIV-HCV Coinfected Individuals
Results
