Conversion between FibroTest and fibrosis stages, and between ActiTest and

necroinflammatory activity grades - Panels. Conversion between FibroTest and Iibrosis

stages using METAVIR, Knodell and Ishak Iibrosis scoring systems (upper panel). Conversion
between ActiTest and activity grades using METAVIR, Knodell and Ishak necroinIlammatory
activity scoring systems (lower panel).
Poynard et al. Comparative Hepatology 2004 :8 doi:10.1186/1476-5926-3-8
Download authors' original image

The Biopsy
.
Examples Of Staging According To The Metavir Score;
What Does My METAVIR Score Mean?
The Iibrosis is graded on a 5-point scale Irom 0 to 4.
The activity, which is the amount oI inIlammation (speciIically, the intensity oI necro-
inIlammatory lesions), is graded on a 4-point scale Irom A0 to A3.
Fibrosis
Stages of fibrosis (F)
F0 no Iibrosis
F1 portal Iibrosis without septa
F2 portal Iibrosis with Iew septa
F3 numerous septa without cirrhosis
F4 cirrhosis
Activity score:
Amount of inflammation (A for activity)
A0 no activity
A1 mild activity
A2 moderate activity
A3 severe activity
Other scoring systems are available, such as the Knodell score (also called the histologic activity
index, or HAI). However, the METAVIR score is simple to use and is popular in many clinics
Scoring system for chronic hepatitis C (the Metavir Score System).
*Note F1-F4 On Figure



Conversion ; FibroTest and fibrosis stages
Conversion between FibroTest and Iibrosis stages using METAVIR, Knodell and Ishak Iibrosis
scoring systems (upper panel).

Conversion between ActiTest and activity grades using METAVIR, Knodell and Ishak
necroinIlammatory activity scoring systems (lower panel).
$ource



epatic Consequences
Individuals with CHC (Chronic Hepatitis C) are at increased risk oI liver related morbidity and
mortality.
HCV inIection was associated with 27 oI all U$ liver transplants perIormed in 2007, and U$-
based studies demonstrated that up to 5155 oI HCC patients have anti-HCV antibodies.
There is also a link between steatosis and liver Iibrosis in HCV-inIected patients, as well as a
potential association between HCV inIection and HCC or, as described more recently, oI
intrahepatic cholangiocarcinoma (ICC). In some ethnic groups such as Latinos the course oI
HCV inIection is more aggressive, with a higher risk oI cirrhosis than other ethnic groups.
Furthermore, disease progression is more rapid in patients who are coinIected with HCV and
HIV. CoinIected patients have approximately double the risk oI cirrhosis or decompensation than
those inIected with HCV alone.

Fibrosis and Cirrhosis
Progressive hepatic Iibrosis leading to cirrhosis is the major complication oI chronic HCV
inIection and accounts Ior almost all HCV-related morbidity and mortality. Early studies
suggested little, iI any, Iibrosis progression during the Iirst decade oI inIection, Iollowed by a
slow, regular progression during the next 15 years, increasing to an intermediate rate during the
subsequent decade.

In a German cohort study oI 1833 women inIected with HCV-contaminated immunoglobulin,
0.5 oI patients developed cirrhosis aIter 25 years. $imilarly, in a study oI 376 HCV-inIected
women conducted by the Irish Hepatology Research Group, 51 oI patients had Iibrosis aIter 17
years, but only 2 had probable/deIinite cirrhosis. These estimates oI cirrhosis rates are
considerably lower than those Irom the U$ multicohort study and the widely cited U$ military
study (approximately 35). Fibrosis outcomes oI 184 women Irom the same cohort were
Iollowed up Ior the subsequent 5 years; 49 showed no change in Iibrosis, 24 showed
regression, and 27 showed progression.

Recent data reinIorce the potential Ior severe liver disease to develop in some patients. Among
485 plasma donors inIected during the early 1970s, 34 had stage F3/F4 Iibrosis (bridging
Iibrosis), cirrhosis, or HCC aIter 31 years; their 35-year cumulative survival was 84 versus
9195 Ior the general population. $imilarly, a study oI 300 black and white Americans with
untreated HCV inIection Iound that 29 oI patients had stage F3/F4 Iibrosis aIter 20 years, and
4.7 had conIirmed cirrhosis. It should be noted, however, that these studies could have selected
patients with severe disease.

The nonlinear progression oI Iibrosis was recently conIirmed in a meta-analysis oI 111 HCV
studies. The mean annual stage-speciIic transition probabilities were Ior stage F0 to F1, Ior F1 to
F2, 0.120 Ior F2 to F3, and 0.116 Ior F3 to F4. Although the estimated prevalence oI cirrhosis
was 16 aIter 20 years, there was wide variation between studies, suggesting that Iibrosis is a
highly unpredictable process.
InIection duration is a major risk Iactor Ior severe Iibrosis, with the progression rate in a 50-year-
old being almost 3 times that in a 20-year-old. Age at time oI inIection is also important. In a
biopsy analysis oI 247 treatment-nave HCV patients, progression rates were 0.13, 0.14, 0.27,
and 0.36 Iibrosis units/year Ior patients aged _19, 2024, 2536, and ~36 years at inIection,
respectively. Age ~36 years (vs _36 years) at time oI inIection was independently associated
with Iaster progression. Men inIected beIore age 50 have been identiIied as comprising the
majority oI cases oI cirrhosis today (73.6), whereas men aged ~50 years when inIected have
Iaster disease progression compared with other age groups.

$everal other Iactors, including sex, baseline Iibrosis, HCV genotype, HIV/HBV coinIection,
and alcohol consumption, also inIluence Iibrosis progression . IdentiIying these Iactors can be
useIul when determining prognosis and advising patients on minimizing liver damage. Indeed, a
recent study suggested that HCV genotype 3 might pose a particularly high risk oI progressive
Iibrosis.
Insulin resistance has been linked with Iibrosis, and several studies have reported that this
relationship remains signiIicant, irrespective oI HCV genotype.

In addition, serum aminotransIerase level elevations and the degree oI hepatocellular
necrosis/inIlammation on biopsy have been Iound to predict Iibrosis progression. Genetic Iactors
might also play a role in Iibrosis progression. Recent data indicate that the cirrhosis risk score,
which is based on the association oI 7 host genes, might help to diIIerentiate HCV patients at
high versus low risk oI progressing toward cirrhosis, including those with early or mild CHC.
$teatosis has also been linked to Iibrosis progression, as has regular cannabis use. There is
evidence oI an association between cigarette smoking and hepatitis Iibrosis, but not all studies
have veriIied such an association.

The Biopsy
.
Examples Of Staging According To The Metavir Score;
What Does My METAVIR Score Mean?
The Iibrosis is graded on a 5-point scale Irom 0 to 4.
The activity, which is the amount oI inIlammation (speciIically, the intensity oI necro-
inIlammatory lesions), is graded on a 4-point scale Irom A0 to A3.
Fibrosis
Stages of fibrosis (F)
F0 no Iibrosis
F1 portal Iibrosis without septa
F2 portal Iibrosis with Iew septa
F3 numerous septa without cirrhosis
F4 cirrhosis
Activity score:
Amount of inflammation (A for activity)
A0 no activity
A1 mild activity
A2 moderate activity
A3 severe activity
Other scoring systems are available, such as the Knodell score (also called the histologic activity
index, or HAI). However, the METAVIR score is simple to use and is popular in many clinics
Scoring system for chronic hepatitis C (the Metavir Score System).
*Note F1-F4 On Figure



Conversion ; FibroTest and fibrosis stages
Conversion between FibroTest and Iibrosis stages using METAVIR, Knodell and Ishak Iibrosis
scoring systems (upper panel).

Conversion between ActiTest and activity grades using METAVIR, Knodell and Ishak
necroinIlammatory activity scoring systems (lower panel).
$ource



epatic Consequences
Individuals with CHC (Chronic Hepatitis C) are at increased risk oI liver related morbidity and
mortality.
HCV inIection was associated with 27 oI all U$ liver transplants perIormed in 2007, and U$-
based studies demonstrated that up to 5155 oI HCC patients have anti-HCV antibodies.
There is also a link between steatosis and liver Iibrosis in HCV-inIected patients, as well as a
potential association between HCV inIection and HCC or, as described more recently, oI
intrahepatic cholangiocarcinoma (ICC). In some ethnic groups such as Latinos the course oI
HCV inIection is more aggressive, with a higher risk oI cirrhosis than other ethnic groups.
Furthermore, disease progression is more rapid in patients who are coinIected with HCV and
HIV. CoinIected patients have approximately double the risk oI cirrhosis or decompensation than
those inIected with HCV alone.

Fibrosis and Cirrhosis
Progressive hepatic Iibrosis leading to cirrhosis is the major complication oI chronic HCV
inIection and accounts Ior almost all HCV-related morbidity and mortality. Early studies
suggested little, iI any, Iibrosis progression during the Iirst decade oI inIection, Iollowed by a
slow, regular progression during the next 15 years, increasing to an intermediate rate during the
subsequent decade.

In a German cohort study oI 1833 women inIected with HCV-contaminated immunoglobulin,
0.5 oI patients developed cirrhosis aIter 25 years. $imilarly, in a study oI 376 HCV-inIected
women conducted by the Irish Hepatology Research Group, 51 oI patients had Iibrosis aIter 17
years, but only 2 had probable/deIinite cirrhosis. These estimates oI cirrhosis rates are
considerably lower than those Irom the U$ multicohort study and the widely cited U$ military
study (approximately 35). Fibrosis outcomes oI 184 women Irom the same cohort were
Iollowed up Ior the subsequent 5 years; 49 showed no change in Iibrosis, 24 showed
regression, and 27 showed progression.

Recent data reinIorce the potential Ior severe liver disease to develop in some patients. Among
485 plasma donors inIected during the early 1970s, 34 had stage F3/F4 Iibrosis (bridging
Iibrosis), cirrhosis, or HCC aIter 31 years; their 35-year cumulative survival was 84 versus
9195 Ior the general population. $imilarly, a study oI 300 black and white Americans with
untreated HCV inIection Iound that 29 oI patients had stage F3/F4 Iibrosis aIter 20 years, and
4.7 had conIirmed cirrhosis. It should be noted, however, that these studies could have selected
patients with severe disease.

The nonlinear progression oI Iibrosis was recently conIirmed in a meta-analysis oI 111 HCV
studies. The mean annual stage-speciIic transition probabilities were Ior stage F0 to F1, Ior F1 to
F2, 0.120 Ior F2 to F3, and 0.116 Ior F3 to F4. Although the estimated prevalence oI cirrhosis
was 16 aIter 20 years, there was wide variation between studies, suggesting that Iibrosis is a
highly unpredictable process.
InIection duration is a major risk Iactor Ior severe Iibrosis, with the progression rate in a 50-year-
old being almost 3 times that in a 20-year-old. Age at time oI inIection is also important. In a
biopsy analysis oI 247 treatment-nave HCV patients, progression rates were 0.13, 0.14, 0.27,
and 0.36 Iibrosis units/year Ior patients aged _19, 2024, 2536, and ~36 years at inIection,
respectively. Age ~36 years (vs _36 years) at time oI inIection was independently associated
with Iaster progression. Men inIected beIore age 50 have been identiIied as comprising the
majority oI cases oI cirrhosis today (73.6), whereas men aged ~50 years when inIected have
Iaster disease progression compared with other age groups.

$everal other Iactors, including sex, baseline Iibrosis, HCV genotype, HIV/HBV coinIection,
and alcohol consumption, also inIluence Iibrosis progression . IdentiIying these Iactors can be
useIul when determining prognosis and advising patients on minimizing liver damage. Indeed, a
recent study suggested that HCV genotype 3 might pose a particularly high risk oI progressive
Iibrosis.
Insulin resistance has been linked with Iibrosis, and several studies have reported that this
relationship remains signiIicant, irrespective oI HCV genotype.

In addition, serum aminotransIerase level elevations and the degree oI hepatocellular
necrosis/inIlammation on biopsy have been Iound to predict Iibrosis progression. Genetic Iactors
might also play a role in Iibrosis progression. Recent data indicate that the cirrhosis risk score,
which is based on the association oI 7 host genes, might help to diIIerentiate HCV patients at
high versus low risk oI progressing toward cirrhosis, including those with early or mild CHC.
$teatosis has also been linked to Iibrosis progression, as has regular cannabis use. There is
evidence oI an association between cigarette smoking and hepatitis Iibrosis, but not all studies
have veriIied such an association.