HIV
and Hepatitis.com Coverage of the 14th
Annual Conference on Retroviruses and Opportunistic Infections (14th CROI) February
25 - 28, 2007, Los Angeles, CA
Does
Pre-existing HIV Infection Lead to Accelerated Liver Fibrosis in People with Acute
Hepatitis C?
Multiple
outbreaks of acute hepatitis C virus (HCV) infection have recently been reported
in cities in the UK and Europe among HIV positive men who have sex with men (MSM).
These outbreaks are notable because these patients were already infected with
HIV when they acquired HCV. More typically, individuals with both HIV and HCV
infection acquired HCV first, since it is easier to transmit (e.g., through shared
use of injection drug equipment).
Although
much is known about the course of liver disease in HCV-infected patients who later
acquire HIV, little is known about the course of liver damage in HIV-infected
patients who later acquire HCV.
Researchers
at Mount Sinai School of Medicine in New York City conducted a prospective study
of HIV-infected MSM with acute HCV infection, including examination of liver histology.
At the 14th Conference on Retroviruses and Opportunistic Infections last month
in Los Angeles, they reported data from the first 5 consecutively-enrolled patients.
The
patients underwent serological testing for hepatitis A virus (HAV) antibodies;
hepatitis B virus (HBV) antigens, antibodies, and HBV DNA; and HCV antibodies,
HCV RNA, and HCV genotype. They also received liver biopsies within 4 months of
the first-noted ALT elevation.
Acute
hepatitis C was defined as the first 6 months of HCV infection. Because no single
test result provides a definitive diagnosis of acute HCV infection, the researchers
considered 3 factors in combination:
•
Recent seroconversion
to HCV antibody positive status; •
Marked elevations in
serum ALT level; •
Wide fluctuations in
HCV viral load.
The
latter 2 factors are considered hallmarks of acute HCV infection and are uncommon
during chronic infection.
All
patients were MSM in their 40s who had:
•
Recent seroconversion
to anti-HCV antibody positive status; in 3 cases, this occurred within a year
after a previous negative test, defining a narrow time window in which the new
HCV infection could have occurred; •
Rapid changes in ALT
levels, with elevations greater than 10 times the upper limit of normal (ULN),
consistent with acute hepatitis; •
Wide HCV viral load
fluctuations, in 4 cases exceeding 1.5 log10 IU/mL.
Results
•
Liver biopsies showed moderate portal fibrosis (stage 2 of 4; Scheuer system)
in 4 or 5 patients, as well as acute HCV.
•
All patients denied
heavy alcohol use and 1 had never received HAART.
•
No cause of chronic
liver disease common to all patients could be identified to explain the degree
of fibrosis.
•
All had negative evaluations
for active HAV or HBV infection.
•
No evidence for other
etiologies of new hepatitis was found.
•
All patients had recent
histories of unprotected receptive anal intercourse, some with many partners;
•
3 acknowledged a single
recent episode of injection drug use, but without clear recollection of sharing
injection equipment.
•
1 shared paraphernalia for snorting drugs;
•
All denied any other known risk factors for HCV infection.
Conclusions
The
researchers concluded that 4 of 5 HIV-infected MSM had moderately advanced portal
fibrosis during the acute phase of HCV infection. No other etiologies were found
to explain the presence of moderate liver fibrosis in this population, suggesting
that pre-existing HIV infection results in accelerated fibrosis progression in
patients with acute hepatitis C.
The
investigators noted that, "These cases suggest that HIV-infected patients
presenting with acute HCV infection may already have significant liver disease,
and that liver biopsy should be considered in these patients."
They
added that further research is needed to define the prevalence and understand
the pathogenesis of rapid liver fibrosis in this population.
