Interactions between metabolic disorders [diabetes, gallstones, and dyslipidaemia] and the progression of chronic hepatitis C virus infection to cirrhosis and hepatocellular carcinoma. A cross-sectional multicentre survey
L. Cimino et al., Interactions between metabolic disorders [diabetes, gallstones, and dyslipidaemia] and the progression of chronic hepatitis C virus infection to cirrhosis and hepatocellular carcinoma. A cross-sectional multicentre survey, DIG LIVER D, 33(3), 2001, pp. 240-246
Background. Diabetes, gallstones and dyslipidaemia are widespread, metaboli
cally related, disorders that can affect the liver: often in a clinically s
ilent fashion.
Aim. To investigate whether the presence of these disorders may worsen chro
nic viral disease by inducing additional liver damage, revealed by variatio
ns in serum increases of aminotransferase, alkaline phosphatase and gamma-g
lutamyl-transpeptidase activities.
Patients and methods. This retrospective, cross-sectional study involved 11
95 patients with chronic hepatitis C virus infection: 47.2% chronic hepatit
is, 45.2% cirrhosis, and 7.6% hepatocellular carcinoma. 14.9% of patients h
ad enzymatic cholestasis, defined as combined increase of alkaline phosphat
ase and gamma-glutamyl-transpeptidase. A Log-linear statistical model was a
pplied to the following variables: stages of liver disease, diabetes, chole
lithiasis, hypertriglyceridaemia, hypercholesterolaemia, and enzymatic chol
estasis.
Results. Log-linear analysis, applied to categorical variables, revealed, f
or the first time, a three-way interaction between the stages of chronic li
ver disease, diabetes, and enzymatic cholestasis. Two-way interactions demo
nstrated that liver disease stages correlated directly to the prevalence of
cholelithiasis and inversely to hypercholesterolaemia. Irrespective of the
liver disease stage, hypertriglyceridaemia correlated to hypercholesterola
emia.
Conclusions. This study discloses a synergistic liver damaging effect of di
abetes and hepatitis C virus. The three-way interaction obtained by our ana
lysis suggests that diabetes is a risk factor for the progression of viral
liver disease and that it contributes to disease evolution, at least in par
t, by induction of cholestasis.