Wednesday, April 25, 2012

Co-morbidities

Obesity and its histological correlate, steatosis, are common
determinants of liver disease progression in HCV infection. We
must keep in mind that “not all hepatic fat is alike” and that the
etiology of steatosis makes an important difference in the
progression of hepatic fibrosis, the development of HCC,
extrahepatic manifestations, and prognosis.
Patients with BMI>30 kg/m2 are more likely to be insulinresistant,
to have more advanced hepatic steatosis or fibrosis
20 | Hepatitis C Treatment
and to experience a reduced response to combination therapy
(Khattab 2010).
Insulin resistance (IR) is one of the strongest negative
predictors of response to HCV therapy. Improved insulin
sensitivity may be associated with better treatment response and
even with HCV clearance. It is important to control diabetes
before starting PegIFN/RBV therapy, because IFN induces a
decrease in glucose uptake by peripheral tissue and the liver.
New HCV protease inhibitors can restore insulin sensitivity in
patients chronically infected with G1 HCV. HCV G3 has a direct
steatogenic effect independent of IR.
Co-infections. Patients with human immunodeficiency virus-
HIV-HCV coinfection have been shown to respond less
favorably to antiviral therapy than patients infected with HCV
alone. Moreover, serious AEs were far more frequent (35%) than
have been reported among HIV-seronegative patients (10-15%).
However, co-infected patients have a rapid fibrosis progression
rate and experience complications of portal hypertension and
PegIFN/RBV should be initiated, if treatment response outweigh
the risks of complications from the AEs of therapy (see chapter 3
for details).
Dual infections of HCV and hepatitis B virus (HBV) occur in
up to 5% of the general population in HCV-endemic areas and
lead to more severe liver disease. Recently, a large, open-label,
comparative multicenter study confirmed the efficacy of
PegIFN/RBV for patients with chronic HCV-HBV dual infection
in Taiwan (Jamma 2010).

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