The Following is Supplied by Dawn from
Hope4Hepatitis.
Hepatitis C's Movement for Awareness
announced plans today for the Spring Campaign,
the "National HCV March on
DC" held annually in Washington, DC.
Events are scheduled
to begin Thursday, May 22, 2003
with a pre-march rally at the Holiday Inn Downtown.
Dinner and a silent auction will be held to benefit awareness.
This will be followed by the National March to
Freedom Plaza the next day, Friday the
23rd.
The March begins at 10AM with a rally
across from the Capitol on the National Mall, located
at 3rd street.
We will arrive at Freedom Plaza with guest speakers scheduled
from 1 to 4pm. A wide variety of topics focused
on the devastation of HCV to families across America will
be presented. Doctors, Advocates, Veterans Groups
and people living with this disease will discuss the huge
hurdles in HCV awareness, prevention and education. A
dinner and raffle is scheduled that evening for all marchers
and guest speakers.
The activities continue Saturday, May 24th
with participation in veterans ceremonies honoring our
military. Things will wind down with a candle light
vigil that night taking place at Thomas Circle National
Park, located at Massachusetts and Vermont Ave. Participants
will light candles and read names in remembrance of all
those that passed from this devastating disease.
The International Quilts will be on display all three
days. Be sure to bring your square to add to a future
quilt.
Day trip transportation for just the
National March, May 23rd has been organized. Same
day return trips, at very affordable prices, are scheduled
from NY/NJ and Connecticut. Please visit our website
for more information.
HMA members believe we can take charge of our future in
the war on HCV.
Join us, together we can stop the spread of this disease.
Contact
Tricia Lupole
110 Glover Circle
Staunton VA 24401
540 248 4994
Artificial Liver Undergoes
Trial Tests
PITTSBURGH (AP)
- An experimental artificial liver system that uses human
cells to filter blood plasma is undergoing trials in the
hope that it will serve as a successful bridge for patients
awaiting a transplant following sudden acute liver failure.
The Extracorporeal Liver Assist Device is being studied
to evaluate its safety and efficiency at a dozen medical
centers across America, including the University of Pittsburgh
Medical Center.
At any given time, approximately 5 percent of the 17,000
people needing liver transplants in the United States
are people in acute liver failure who are not expected
to live more than a week without a transplant, according
to the medical center.
By using a line of human liver cells cultivated from
a hepatoblastoma, a kind of liver tumor, the ELAD appears
to be able to perform some of the liver function that
has been lost, including the manufacture of certain proteins
and the filtering of some toxins in the blood, said Dr.
Peter Linden, a principal investigator for the study at
UPMC.
``Even given the best standard of care, there is no answer
for a liver that
is dying and can't repair itself,'' he said. The
ELAD, which was developed by VitaGen Inc. of La Jolla,
Calif., and has not yet received approval from the U.S.
Food and Drug Administration, is one of a handful of devices
researchers hope can either be used to give patients'
livers time to heal themselves or keep people alive until
a transplant can be performed.
One such device, developed by Excorp Medical Inc. of
Oakdale, Minn., and also tested in Pittsburgh, uses pig
liver cells to perform a similar service, although Excorp
president and CEO Dan Miller says the intent with that
system is to give patients' own livers time to heal.
``It's definitely an exciting area. It's early in the
game. Until recently, there haven't been very many promising
technologies,'' Miller said.
Eventually, VitaGen wants to enroll 30 patients in its
Phase II study, which could lead to more widespread testing
depending on the results.
Since early last year, two UPMC patients in acute liver
failure were placed on the machine and received successful
transplants. In one case, the patient suffered an unusual
blood-clotting problem and required a five-organ transplant,
including the liver, small bowel, stomach, pancreas and
duodenum.
One of the patients was on the machine for a day and
a half; the other, about 48 hours. Both left the hospital.
Even though patients in these sorts of sudden liver
failures are typically placed on a list for a liver transplant,
that doesn't always mean one is available. The ELAD
may be able to help bridge the gap, Linden said.
About the size of a washing machine, the ELAD works in
a manner similar to kidney dialysis, in which waste products
are removed from the blood. In this case, a pump
pushes the patient's blood through a catheter into a large
filter in the machine, which separates blood cells from
plasma.
Then, the plasma is pushed through cartridges containing
the human liver cells for cleaning. Unlike some other
machines - such as one developed by HemoCleanse Inc. of
Lafayette, Ind., that uses charcoal and other materials
to clean the blood - the ELAD may also be able to create
certain proteins, as does a real liver. The blood
is recombined and pumped back into the patient.
Among the 12 medical centers involved in the ELAD study
are those at the University of Miami, the University of
Chicago, Massachusetts General and Columbia University.
Linden said when a patient is randomly selected to go
on the ELAD, the cartridges are ordered from Southern
California, where the cells are kept in an incubator.
Once they arrive - typically within a day - the
patient is placed on the machine while he or she waits
for a transplant. In some cases, it is hoped that
the patient's own liver will regenerate itself.
They undergo standard therapy - which may include mechanical
ventilation, dialysis and blood medications - in addition
to using the ELAD. Some patients do not go on the ELAD,
serving as a control group for the study.
HemoCleanse's president, Robert Truitt, said the cell-based
liver assist systems tend to be very expensive but that
the research is exciting since it may provide the best
alternative when end-stage liver failure is imminent.
Linden said the biggest downside may be that the ELAD
requires almost constant monitoring to make sure it is
operating properly.
``Development of an artificial liver is a daunting challenge
because of the many complex functions that the liver performs,''
said Dr. George Mazariegos, assistant professor of surgery
at the University of Pittsburgh's transplantation institute.
``But the need is urgent, as more than 2,000 patients
needing liver transplants die on the national waiting
list each year.''
Space City Failing Victims
of "Silent Killer"
COUNCIL MEMBER EDWARDS URGES HOUSTON
TO ACT ON HEPATITIS C VIRUS
BY ED WENDT
EDITOR, Hep C Intelligence Report
The city of Houston is home of the Texas Medical Center,
the Johnson Space Center, and several prominent universities.
Houston was the first word spoken on the moon and is the
energy capital of the world. Yet the city of Houston,
unlike most major U.S. cities, has failed to implement
a program to help combat one of the nation's leading killers
-- Hepatitis C.
City Council Member Ada Edwards, chair of the City Council
State of Emergency HIV/AIDS Task Force, is seeking permission
from the Houston health director Mary des Vinges- Kendrick
to create a city Hepatitis C Panel.
Hepatitis C, the most common blood born infection in
the United States, is now four times more prevalent than
HIV/ADS. About 5 million Americans are affected
with the virus.
Houston is one of the only remaining major U.S. cities
without a Hepatitis C Task Force. Mayor Lee Brown
was asked to act on the virus as early as 2000.
Edwards, who became chair of the HIV/AIDS Task Force
this year, has asked the health director for permission
to establish a Hepatitis C "subcommittee" as
an alternative to a full fledged task force.
Leading Hepatitis C activists supported Brown for reelection
in 2001 hoping
he would create a full fledged task force. They have been
disappointed by
his inaction.
The health department has come under criticism from activists
"for failing to act on the Hepatitis C crisis."
Criticism has come from both victims and their doctors.
Edwards is asking Kendrick to provide her with all information
related to
Hepatitis C and the city of Houston's response. "I
would like an update from the Health and Human Services
Department on all programs and activities, including any
grants it may have received, on Hepatitis C," Edwards
asked in a March 10 letter. "Additionally, please
document the department's testing program for the current
and last fiscal years, including groups responsible for
the testing."
About 70 percent of the persons with chronicle Hepatitis
C infection develop liver disease, which can progress
to cirrhosis (scarring) liver failure, and/or cancer of
the liver. Severe liver disease from Hepatitis C
infection accounts for most of the liver transplants in
the U.S.
The Center for Disease Control and Prevention (CDC) estimates
that 8,000 to 10,000 people in the U.S. dies each year
from chronic Hepatitis C. It is estimated that well
over $600 million are spent nationally each year on medical
care and lost wages related to Hepatitis C.
A recent study published by the American Journal of Public
Health projected 165,900 deaths from chronic liver disease
attributable to Hepatitis C, 27,200 deaths from hepatocellular
carcinoma (liver cancer), and 10.7 billion dollars in
directed medical costs for this disease over the next
10 years.
The Houston health department was asked to "do more
than conduct" studies on Hepatitis C by activists
who appeared before City Council as late as 2000. The
health department has provided no progress report on the
virus since that time.
Edwards, at last week's City Council meeting, informed
Mayor Lee Brown that she wants to create the Hepatitis
C subcommittee. She informed Brown that she is concerned
"about the rise of Hepatitis C in our community.
"I've sent an official memo to Dr. Kendrick
asking if we can tie in testing for Hep C with the HCV
testing," she told the Mayor. "The is
a very strong correlation that I have seen.' "I
would appreciate the administration's assistance and you
starting the dialogue so maybe we could help more people
at the same time," said the popular District D council
member.
Hepatitis C activists have criticized the health department
for "doing too many studies and too little testing
on Hepatitis C." Blacks are the largest infected
ethnic group with the killer virus in the United States.
There is no active Hepatitis C support group that
targets African-Americans in Houston or Harris County.
The Hep C Hope Foundation, the city's only grass roots-run
Hep C Support Group, shut down last August when funding
dried up due to the poor economy. The Texas Liver Coalition,
closely associated with St. Luke's Episcopal Hospital,
hosts support groups throughout the city, but does not
target the Black community.
The virus is found in the blood and is spread by direct
contact with blood and blood products. People can be infected
with the virus when they use needles, toothbrushes and
nail files that contain blood from an infected person.
People who have acupuncture, body piercing, or tattooing
done are at risk if the equipment used is not sterile
and was used on persons infected with Hepatitis C.
The highest risk of getting infected with Hepatitis C
comes from injecting illegal drugs. People who received
drug transfusions before 1992 are also at risk.
Hepatitis C is not spread by sneezing, kissing,
hugging, coughing, food or water, sharing eating utensils
or drinking glasses, or casual contact such as shaking
hands.
People with multiple sex partners are also at risk for
Hepatitis C. Hepatitis C activists want the city
to "develop and publicize" a testing program
for Hepatitis C. Many people who are at risk for
Hepatitis C are uninsured and must turn to public health
facilities for testing.
The Importance of Water
Source: By Donald S. Roberson,
MD, M. Sc.
Water suppresses the appetite naturally and helps the
body metabolize stored fat. Studies have shown that a
decrease in water intake will cause fat deposits to increase,
while an increase in water intake can actually reduce
fat deposits.
Here's why: The kidneys can't function properly without
enough water. When they don't work to capacity, some of
their load is dumped onto the liver.
One of the liver's primary functions is to metabolize
stored fat into usable energy for the body. But, if the
liver has to do some of the kidney's work, it can't operate
at full throttle. As a result, it metabolizes less fat,
more fat remains stored in the body and weight loss stops.
Drinking enough water is the best treatment for fluid
retention. When the body gets less water, it perceives
this as a threat to survival and begins to hold on to
every drop. Water is stored in extracellular spaces (outside
the cells). This shows up as swollen feet, legs and hands.
[Called edema] Diuretics offer a temporary solution at
best. They force out stored water along with some essential
nutrients. Again, the body perceives a threat
and will replace the lost water at the first opportunity.
Thus, the condition quickly returns.
The best way to overcome the problems of water retention
is to give your body what it needs - plenty of water.
Only then will stored water be released.
If you have a constant problem with water retention,
excess salt may be to blame. Your body will tolerate sodium
only in a certain concentration.
The more salt you eat, the more water your system retains
to dilute it. But getting rid of unneeded salt is easy
- just drink more water. As it's forced through the kidneys,
it takes away excess sodium.
The overweight person needs more water than the thin
one. Larger people have larger metabolic loads. Since
we know that water is the key to fat metabolism, it follows
that the overweight person needs more water.
Water helps to maintain proper muscle tone by giving muscles
their natural ability to contract and by preventing dehydration.
It also helps to prevent the sagging skin that usually
follows weight loss - shrinking cells are buoyed by water,
which plumps the skin and leaves it clear, healthy and
resilient.
Water helps rid the body of waste. During weight loss,
the body has
a lot more waste to get rid of - all that metabolized
fat must be shed.
Again, adequate water helps flush out the waste.
Water, can help relieve constipation. When the body gets
too little water, it siphons what it needs from internal
sources. The colon is one primary source. Result? Constipation.
But, when a person drinks enough water, normal bowel function
usually returns.
So far, we've discovered some remarkable truths about
water and weight loss:
* The body
will not function properly without enough water and can't
metabolize stored fat efficiently.
* Retained
water shows up as excess weight.
* To get
rid of excess water you must drink more water.
* Drinking
water is essential to weight loss.
How much water is enough? On the average, an adult should
drink eight 8-ounce glasses every day. That's about 2
quarts. However, the overweight person needs one additional
glass for every 25 pounds of excess weight. The amount
you drink also should be increased if you exercise briskly
or if the weather is hot and dry.
Water should preferably be cold - it's absorbed into
the system more quickly than warm water. And some evidence
suggests that drinking cold water can actually help burn
calories.
When the body gets the water it needs to function optimally,
its
fluids are perfectly balanced. When this happens you have
reached the "breakthrough point." What does
this mean?
* Endocrine-gland
function improves.
* Fluid
retention is alleviated - stored water is lost.
* More fat
is used as fuel because the liver is free to metabolize
stored fat.
* Natural
thirst returns.
* There
is a loss of hunger almost overnight.
If you stop drinking enough water, your body fluids will
be thrown out of balance again, and you may experience
fluid retention, unexplained weight gain and loss of thirst.
To remedy the situation you'll have to go back and force
another "breakthrough."
Complications Commom among
Living adult partial living donors
By Will Boggs,
MD NEW YORK (Reuters Health)
Feb 27 - Although mortality among adult liver donors
is low, complications are relatively common, according
to a report in the February 27th issue of The New England
Journal of Medicine.
The shortage of cadaveric livers for adult transplantation
has prompted the use of living donors for adult liver
transplant recipients, the authors explain. The larger
right lobe can be safely removed from the donor, and living
donation now accounts for approximately 5% of liver transplantations
performed in adults. However, information about the morbidity
and mortality of donors and recipients is lacking.
Dr. Robert S. Brown, Jr. from Columbia University College
of Physicians and Surgeons in New York and colleagues
surveyed US programs registered with the United Network
for Organ Sharing (UNOS) that perform adult-to-adult liver
transplantation from living donors.
The 84 responding centers performed 449 adult-to-adult
liver transplants from living donors between 1997 and
2000, the results indicate, with the number of such transplants
rising from 1 in 1997 to 266 in 2000.
In only half of the programs did potential donors see
a physician who was not a part of the transplant team,
the authors report, and only 17% of programs had potential
donors evaluated by an ethicist.
Most living donors (74.4%) were genetically related to
the recipient, the report indicates, the rest being friends
(13.4%), spouses (10.9%), or "good samaritans."
Although only one death had been reported at the time
of the survey (for a 0.2% death rate), 65 of the 449 donors
(14.5%) experienced one or more complications of donation,
the investigators note, including bile leak (in 27 donors),
the need for blood transfusion, and the need for reoperation.
Partial liver donation was associated with a median length
of stay for donors of 0.25 days in the intensive care
unit and 6 days in the hospital, the results indicate.
"Living donor procedures are growing in frequency
and are safe, with low mortality but significant morbidity,"
Dr. Brown told Reuters Health. "There is a need for
a registry and outcomes study to define the long-term
outcomes and risks of the procedure, as currently there
is no standardization."
Living donation "is here to stay and saves lives,"
Dr. Brown concluded. "More effort is needed to improve
cadaveric donor rates and to prevent liver disease, [thereby
diminishing] the need for living donor surgeries."
N Engl J Med 2003;348:818-825.
Hepatitis C: Pathogenesis,
Virology, and Immunology
Adrian M. Di Bisceglie, MD, FACP
Introduction : Several themes emerged during this year's
meeting of the American Association for the Study of Liver
Diseases that related to the pathology, virology, and
immunology of hepatitis C. This report explores these
prominent topics and places them in relevant clinical
context.
The Association Between Steatosis and Hepatitis C
It has been recognized for some time that hepatic steatosis
is frequently present in patients with chronic hepatitis
C, perhaps more so than in other forms of hepatitis. The
reasons for the latter are not clear. Certainly, infection
with hepatitis C virus (HCV) genotype 3 has been suggested
as a risk factor for hepatic steatosis, but this finding
occurs even in patients infected with other genotypes.
Patton and colleagues[1] conducted a comprehensive assessment
of the role of host and viral factors in the development
of steatosis with HCV in a large patient population. All
patients (n = 576) with chronic hepatitis C who were enrolled
in a single-center database in the United States were
included and were naive to treatment at the time of their
biopsy. These investigators found that 16% of this patient
population had grade 2 or 3 steatosis based on results
of liver biopsy. According to stepwise logistic regression
analysis, the only host factor associated with steatosis
was body mass index, whereas viral factors included HCV
genotype 3 and viral load.[1] It appears that hepatic
steatosis is associated with more severe hepatic fibrosis,[2]
linked to increased serum levels of c-peptide and insulin
as markers of hyperinsulinism. Hyperinsulinism has been
closely linked with the development of nonalcoholic fatty
liver disease.
Sustained virologic response to antiviral therapy was
found to result in a decrease in hepatic steatosis, independent
of weight loss; however, there was controversy as to whether
the latter occurred to a greater extent in patients infected
with HCV genotype 3. Infection with HCV genotype 3 appears
to cause hepatic steatosis to a greater extent than with
other genotypes.[3,4]
Other Factors Effecting the Natural History of Hepatitis
C
Role of Alcohol Consumption The outcome of chronic HCV
infection is quite variable, with some individuals having
rapidly progressive liver disease and others seemingly
having nonprogressive hepatitis. Alcohol consumption is
well known to exacerbate the chronic liver injury associated
with HCV infection, although the mechanisms by which this
occurs are not known. The quantities of alcohol typically
reported are not sufficient to result in liver injury
alone.
Sartori and colleagues[5] found that moderate alcohol
intake was associated with increased oxidative stress
in patients with chronic hepatitis C. They measured the
products of lipid peroxidation in serum of patients with
chronic hepatitis C who consumed varying degrees of alcohol
and compared them with those in normal controls. Levels
of these products were increased even in patients who
consumed moderate amounts of alcohol (up to 50 g per day).
Another interesting effect of alcohol consumption was
highlighted by a study among US Veterans with chronic
hepatitis C.[6] The study authors found that the proportion
of patients at their institution who were seropositive
for anti-HCV but negative for HCV RNA (implying that these
individuals had cleared HCV infection) was lower among
those with heavy alcohol consumption compared with those
with minimal or moderate consumption. These findings suggest
that alcohol may impair the immune response to HCV infection,
thereby increasing the rate of chronicity. The investigators
did not address the issue of how ongoing alcohol consumption
might lead to more severe hepatic fibrosis in those with
chronic HCV infection.
Chemokine and Chemokine Receptor Polymorphisms An important
study of chemokine and chemokine receptor polymorphisms
in patients with hepatitis C failed to confirm a previously
reported association between the CCR5-delta 32 mutation,
HCV infection, and increased viral loads. This mutation
has been very convincingly linked with susceptibility
to HIV infection and, in a preliminary report,[7] had
been found to be linked with susceptibility to HCV infection
as well.
Promrat and coworkers[8] from the National Institutes
of Health evaluated a series of 5 polymorphisms in chemokines
and chemokine receptors, including the CCR5-delta 32 mutation,
in a cohort of 339 patients with chronic HCV infection
and more than 2000 healthy blood donor controls. The frequency
of mutations was the same among patients with chronic
HCV infection and controls. It was interesting to note
that a mutation in the RANTES promoter (which can activate
several chemokine receptors) correlated with a less severe
degree of hepatic inflammation, a finding that needs to
be validated in further studies.
HIV Coinfection It has been suggested that HIV infection
may result in more severe liver disease among patients
with HCV infection. This concept has been called into
question by Bonacini and colleagues,[9] who followed a
cohort of 474 patients with HIV infection. Of these patients,
233 were seropositive for HCV RNA and 73 were positive
for hepatitis B surface antigen. In fact, patients with
HIV infection and no viral hepatitis had the highest all-cause
mortality rates. When this analysis was corrected for
CD4 cell count, survival curves of the HIV alone, HIV/HCV,
and HIV/hepatitis B virus (HBV) groups were superimposable.
However, the rate of liver-related death was higher in
patients with either HIV/HCV coinfection or HIV/HBV coinfection.
Thus, the picture with HIV/HCV coinfection remains unclear.
Certainly, these 2 infectious entities are often found
together. The frequency of liver mortality appears to
be greater in individuals with coinfection than in those
with HIV infection alone, but the mechanism by which this
occurs is the subject of much speculation. The role of
antiviral therapy directed against HIV-induced liver damage
requires further study.
Hepatitis C and the Brain
There is growing interest in the effect of HCV infection
on the brain. It appears that patients with hepatitis
C suffer from mild, cognitive impairment and an excess
of psychiatric problems such as depression. The causes
for the latter are not known, but possible explanations
include the effects of substance abuse (frequently associated
with HCV infection), presence of a premorbid condition
that may lead to an increased rate of substance abuse
and hence to HCV infection, or, possibly, the direct effects
of HCV infection.. In patients with advanced liver disease,
the development of hepatic encephalopathy may complicate
the picture even more.
To examine the hypothesis that HCV infects the brain,
Laskus and colleagues[10] studied cerebrospinal fluid
from a small series of patients with HCV infection. Many
of these individuals were coinfected with HIV and had
spinal tap done for various clinical indications such
as aseptic meningitis. They studied both the fluid itself
and cells found in that fluid, searching for the negative
strand of HCV (viral replicative intermediate) and for
HCV quasispecies variability. Findings from these samples
were compared with those of the peripheral blood. These
investigators found an association with HCV-RNA positivity
in the cerebrospinal fluid of HCV-infected persons, particularly
in association with the cellular compartment. The presence
of the negative strand of HCV suggested active HCV replication
rather than contamination from the peripheral blood. In
patients harboring different strains of HCV in serum and
peripheral blood mononuclear cells (PBMCs), as determined
by phylogenetic analysis, cerebrospinal fluid-derived
strains were more closely related to those found in PBMCs
than in serum. The study authors proposed that PBMCs could
carry the virus into the central nervous system and provide
a mechanism for HCV neuroinvasion.
Forton and colleagues[11] were able to identify brain-specific
variants of HCV from brain tissue of HCV-infected individuals
collected at autopsy. These variants had discrete genomic
mutations in the internal-ribosomal entry site (IRES)
region of the genome, suggesting that the IRES may be
important in promoting replication of the virus in cells
other than hepatocytes.
Newer Diagnostic Tests for
HCV Infection
The performance of several newer diagnostic tests for
HCV infection was discussed during these meeting proceedings.
A newly developed qualitative assay for the detection
of HCV RNA has a lower limit of detection of 5.3 IU/mL
of serum and appeared to have excellent performance characteristics
when evaluated by Schiff and coinvestigators.[12] Thus,
this assay may have a role in clinical practice for detecting
low levels of viremia, such as those that occur during
antiviral therapy or when other assays are negative.
A new assay is now available to detect HCV core antigen
in serum of infected individuals. This test has the advantages
over PCR-based assays of simplicity, short turnaround
time, and low false-positivity rates, but does not quite
have the sensitivity of the PCR-based studies.[13] This
novel assay may have a role in monitoring the effect of
antiviral therapy.[14]
In the setting of well-established diagnostic assays with
good sensitivity and specificity, the role of these new
assays needs to be further defined.
Predictors of Cirrhosis
Progression of liver disease due to hepatitis C is marked
by progression of hepatic fibrosis. The degree of fibrosis
is best assessed by liver biopsy. However, the search
for a noninvasive means of assessing hepatic fibrosis
has been a "holy grail" of hepatology for years.
Based on data from the HALT-C (Hepatitis C Antiviral
Long-term Treatment Against Cirrhosis) trial, Lok and
colleagues[15] developed a clinical model to predict cirrhosis
in patients with chronic hepatitis C. They found that
the use of routine laboratory tests such as platelet count,
aspartate aminotransferase/alanine aminotransferase ratio,
alkaline phosphatase level, and prothrombin time give
a very good idea of the presence of cirrhosis, but are
not yet accurate enough to replace the role of liver biopsy.
Myers and colleagues, in collaboration with Poynard,[16]
evaluated the value of a panel of serum fibrosis markers
to predict the presence of cirrhosis.. This panel included
alpha-2-macroglobulin, apolipoprotein A1, haptoglobin,
gamma glutamyl transferase, and total serum bilirubin.
Evaluation of this test was conducted using proprietary
methods and the calculated score increased with worsening
fibrosis and could predict cirrhosis with 87% sensitivity
and a negative predictive value of 98%. It is clinically
important to determine the presence of cirrhosis, not
only because these patients are at greater risk of liver
disease progression and therefore require aggressive antiviral
therapy, but also because these individuals are targets
for screening for esophageal varices and hepatocellular
carcinoma
