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Abstract
Chronic hepatitis C is one of the most important health problems. End-stage liver disease
due to hepatitis C is the leading indication for liver transplantation. Hepatic fibrosis, the common
final manifestation of several chronic liver diseases, is the result of a prominent accumulation of
extracellular matrix (ECM) materials and ultimately can lead to cirrhosis. HSCs have a crucial role
in determining the pathogenesis and clinical course of liver fibrosis and cirrhosis. The alpha
isotype of actin (α-SMA) expressed by hepatic stellate cells reflects their activation to
myofibroblast-like cell and has been directly related to experimental liver fibrogenesis, and
indirectly to human fibrosis in chronic liver disease. The role of GFAP expression in HSCs is
currently unknown. Previous studies in rodents showed that, when rodent HSCs were activated,
the expression of GFAP decreased. The decreased GFAP expression in an advanced stage of
fibrosis suggested that GFAP could be a marker for quiescent cells in rodents.
This study was conducted on 69 chronic HCV patients, presented to the Department of
Gastroenterology and Hepatology, Theodor Bilharz Research Institute, Egypt, in the period
between 2004-2007. Amongst whom, there were 11 patients having mixed chronic HCV and
schistosomal infections (served as pathological controls). In addition to 10 liver disease-free
individuals serving as normal controls.
Clinical characteristics of the studied patients revealed the presence of fatigue as a
common symptom among them, occurring in 87%. Rt hypochondrial dull aching pain was
reported in 65.2%. None of the studied patients had clinically palpable spleen or ascites.