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Steatosis Is Less Common in HIV-HCV Coinfected Patients Than in
Similar HCV-monoinfected Patients, and Predictors of Steatosis Differ
between the Two Groups
Liver
disease in patients coinfected with HIV and hepatitis C virus
(HCV) has received increasing attention in recent years. Steatosis
is accepted as an important contributor to liver disease in patients
with HCV, but despite coinfected patients having several reasons
to have steatosis, the prevalence and significance of such changes
has received scant attention.
We
examined steatosis in an unselected cohort of coinfected patients
and compared its prevalence
and predictors with findings in monoinfected patients, where these
relationships have been established.
Results
·
92 coinfected and 372 monoinfected patients undergoing staging liver
biopsy were studied
· Baseline
characteristics of the two groups differed significantly, pointing
at different contributors to steatosis in each.
· Histological
inflammation and fibrosis
were very similar in the two groups, but steatosis was less in coinfected
patients.
· Steatosis
had a univariate association with fibrosis in both groups, but retained
a multivariate association only in monoinfected patients.
· Other
multivariate predictors of steatosis in HCV monoinfected patients
were the accepted variables of elevated body mass index, male
sex, and genotype
3a infection, as well as age.
· In
coinfected patients, however, age was the only multivariate predictor.
· Undetectable
HIV viral load was associated with steatosis in coinfected patients
in univariate analysis, but HAART or its individual components could
not be initially linked to steatosis.
The
authors conclude, “In conclusion, steatosis is less common in HIV-HCV
coinfected patients than similar HCV monoinfected patients, and
predictors of steatosis differ between the two groups.”
Commentary
Before
conducting this study, the investigators anticipated that hepatic
steatosis would be more common in coinfected than in HCV-monoinfected
patients. However, in this large cohort of patients with chronic
hepatitis C, we found that patients coinfected with HIV had somewhat
less steatosis than those with HCV infection alone.
Possible explanations
for this somewhat surprising finding include the fact that, in this
cohort, previously described steatosis risk factors (e.g., high
BMI, type 2 diabetes mellitus, and genotype 3a infection)] were
less prevalent in coinfected than in monoinfected patients.
The
authors note, “Coinfected patients may differ from monoinfected
patients in the same community in important ways, which should be
borne in mind when evaluating liver disease in these two groups.”
“Predictors
of steatosis in coinfected patients in this study also differed
from those in monoinfected patients in all models examined. Whether
interventions could be undertaken to ameliorate steatosis in coinfected
patients and whether doing so would slow liver disease progression
and/or improve response to HCV antiviral therapy will require further
investigation.”
07/18/05
Reference
H
A Monto and others. Hepatic steatosis in HIV/hepatitis C coinfection:
Prevalence and significance compared with hepatitis C monoinfection.
Hepatology 42(2): 310-316. August 2005.
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