from:  http://www.medscape.com/viewarticle/540698

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                 Steatosis in Chronic Hepatitis C: Relationship to the
Virus and Host Risk Factors
                 Posted 07/25/2006

                 Carla AL Matos; Renata M Perez; Mauricio S Pacheco;
Claudio G Figueiredo-Mendes; Edmundo Lopes-Neto; Evandro B Oliveira Jr;
Valeria P Lanzoni; Antonio EB Silva; Maria LG Ferraz

           Abstract and Introduction
           Abstract
           Background: Steatosis occurs frequently in hepatitis C. However,
the mechanisms leading to this lesion are still unknown, and the role of
steatosis in the progression of the disease remains controversial. The aim
of the present paper was to determine the prevalence of steatosis in
hepatitis C and its association with hepatitis C virus (HCV) genotype, viral
load and the presence of risk factors for steatosis, and to analyze the
association between steatosis and the intensity of liver disease.
           Methods: Patients infected with HCV who underwent liver biopsy
were included. Patients coinfected with hepatitis B virus and/or human
immunodeficiency virus and those previously treated for hepatitis C were
excluded. The following risk factors for steatosis were investigated:
obesity (body mass index [BMI] > 25 kg/m2), diabetes mellitus,
hyperlipidemia, alcoholism, and use of potential steatosis-inducing drugs.
Histological analysis evaluated the presence of steatosis, the degree of
periportal activity and staging. Patients with and without steatosis were
compared regarding demographic, epidemiological, laboratory and histological
characteristics. Logistic regression analysis was applied to identify
variables that were independently associated with the presence of steatosis.
           Results: Ninety patients (55 men, 35 women) with a mean age of
45 ± 13 years were included. The prevalence of steatosis was 67%. Variables
that remained independently associated with steatosis were age, female
gender, obesity and genotype 3.
           Conclusions: The prevalence of steatosis in hepatitis C was
high. Risk factors usually related to steatosis such as age, female gender
and obesity, as well as genotype 3, were independently associated with the
presence of steatosis. Steatosis was not independently associated with the
intensity of histological liver disease.

           Introduction
           Hepatitis C virus (HCV) is one of the main causes of chronic
hepatitis worldwide.[1-2] The overall prevalence of chronic HCV infection is
estimated to be 3%, with approximately 150 million individuals infected.[2]
The annual incidence of new symptomatic infections has been estimated to be
1-3 cases/100 000 individuals.[2] Obviously, this incidence is much higher
considering that most infections are asymptomatic.

           Various techniques for the laboratory diagnosis of HCV infection
are currently available, including serological and molecular methods.
However, none of these techniques is able to evaluate the intensity of liver
disease. Only microscopic analysis of fragments obtained from a liver biopsy
permits the determination of the intensity of liver damage.[3]

           Some histological findings are frequently observed in patients
with chronic hepatitis C, thus representing etiological markers of the
infection. These findings include the presence of lymphoid aggregates and/or
follicles, bile duct injury and steatosis.[4-5] Steatosis is one of the most
frequent histological findings in chronic HCV infection.[5] However, the
pathogenic mechanisms leading to this lesion are still unknown, and it has
been questioned as to whether steatosis results from a direct cytopathic
effect of HCV or whether it is associated with other factors unrelated to
the presence of the virus. Likewise, the effect of the presence of steatosis
on the progression of the disease has not been established.

           The objectives of the present study were to determine the
prevalence of steatosis in patients with chronic HCV infection, correlating
it with the presence of other known risk factors for steatosis, to evaluate
the association between the presence of steatosis and HCV genotype and viral
load, and to determine the relationship between steatosis and
necroinflammatory activity, and between steatosis and fibrosis.

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