Because of shared risk factors, HCV co-infection is common (10-
40%) among HIV-infected persons. HIV infection accelerates the
progression to advanced fibrosis and cirrhosis and increases the
risk for liver-related complications, including hepatocellular
carcinoma compared with HCV monoinfected patients. As a
result of the effectiveness of highly active antiretroviral
(HAART) therapy, the longevity of HIV-infected patients has
increased and HCV infection emerged as a major cause of
morbidity and mortality among this population.
A significant proportion of HIV-HCV coinfected patients (with
stable HIV infection, no AIDS, mean CD4 counts greater than
400x106/L and compensated liver disease) can be treated
successfully with PegIFN/RBV. SVR to PegIFN/RBV is lower in
HIV-HCV coinfected patients, ranging between 26% and 44%
(Torriani 2004, Carrat 2004).
56 | Hepatitis C Treatment
Several trials recommended 48 weeks of PegIFN/RBV in coinfected
patients, regardless of HCV genotype (Iorio 2010). The
SVR in HIV-HCV infected patients can be predicted by the so
called “Prometheus index” that associates HCV genotype, degree
of fibrosis, HCV VL, IL28B genotype (Medrano 2010).
Safety, tolerability and adherence to combination therapy are
important issues in the coinfected patients, with 12% to 42%
discontinuation rates. HAART can be associated with anemia,
thrombocytopenia, neutropenia and hepatotoxicity, ranging
from elevation in aminotransferases level to hepatic
decompensation and mitochondrial toxicity (i.e., acute
pancreatitis and lactic acidosis which occur especially in patients
receiving didanosine).
Autoantibody (ANA, ASMA, anti-LKM) seropositivity in the
setting of CHC is common, but does not impact on disease
progression, nor on response to antiviral therapy. It is important
to recognize an autoimmune component (high autoantibody
titer ANA>1:160 or ASMA>1:80, elevated liver enzymes (more
than 5-10 times UNL and specific features on LB) before starting
therapy, as PegIFN-based regimens may exacerbate underlying
autoimmune hepatitis. If immunosuppression for autoimmune
component is required, aminotransferases should be followed
closely during the first weeks of therapy.
Obesity and metabolic syndrome are common in patients with
CHC and associated with lower probability of achieving SVR with
antiviral therapy. Insulin resistance is one mechanism by which
response to antiviral therapy is reduced. Interventions targeting
at reducing obesity or/and IR may improve SVR rates. It is
important to stress that body weight-adjusted dosing regimens
improve rates of SVR.
40%) among HIV-infected persons. HIV infection accelerates the
progression to advanced fibrosis and cirrhosis and increases the
risk for liver-related complications, including hepatocellular
carcinoma compared with HCV monoinfected patients. As a
result of the effectiveness of highly active antiretroviral
(HAART) therapy, the longevity of HIV-infected patients has
increased and HCV infection emerged as a major cause of
morbidity and mortality among this population.
A significant proportion of HIV-HCV coinfected patients (with
stable HIV infection, no AIDS, mean CD4 counts greater than
400x106/L and compensated liver disease) can be treated
successfully with PegIFN/RBV. SVR to PegIFN/RBV is lower in
HIV-HCV coinfected patients, ranging between 26% and 44%
(Torriani 2004, Carrat 2004).
56 | Hepatitis C Treatment
Several trials recommended 48 weeks of PegIFN/RBV in coinfected
patients, regardless of HCV genotype (Iorio 2010). The
SVR in HIV-HCV infected patients can be predicted by the so
called “Prometheus index” that associates HCV genotype, degree
of fibrosis, HCV VL, IL28B genotype (Medrano 2010).
Safety, tolerability and adherence to combination therapy are
important issues in the coinfected patients, with 12% to 42%
discontinuation rates. HAART can be associated with anemia,
thrombocytopenia, neutropenia and hepatotoxicity, ranging
from elevation in aminotransferases level to hepatic
decompensation and mitochondrial toxicity (i.e., acute
pancreatitis and lactic acidosis which occur especially in patients
receiving didanosine).
Autoantibody (ANA, ASMA, anti-LKM) seropositivity in the
setting of CHC is common, but does not impact on disease
progression, nor on response to antiviral therapy. It is important
to recognize an autoimmune component (high autoantibody
titer ANA>1:160 or ASMA>1:80, elevated liver enzymes (more
than 5-10 times UNL and specific features on LB) before starting
therapy, as PegIFN-based regimens may exacerbate underlying
autoimmune hepatitis. If immunosuppression for autoimmune
component is required, aminotransferases should be followed
closely during the first weeks of therapy.
Obesity and metabolic syndrome are common in patients with
CHC and associated with lower probability of achieving SVR with
antiviral therapy. Insulin resistance is one mechanism by which
response to antiviral therapy is reduced. Interventions targeting
at reducing obesity or/and IR may improve SVR rates. It is
important to stress that body weight-adjusted dosing regimens
improve rates of SVR.
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