Immune complexes in acute and chronic liver disease

Abstract

Anti-complementary (AC) activity and C1q-binding are increased in acute type A and B hepatitis, alcohol-induced hepatitis, HB surface antigen-positive and -negative chronic active hepatitis and primary biliary cirrhosis.

In acute type A hepatitis, a large increase in C1q-binding was demonstrated during the period of elevated transaminases. In type B hepatitis, the initial peak was small, but was followed by a further peak during the period of falling serum HB surface (HBs) antigen titre. In both diseases the C1q-binding was associated with >20S particles. In paracetamol-induced necrosis, C1q-binding remained normal. In type A and B hepatitis and in paracetamol-induced necrosis, C4, C3 and factor B concentrations were depressed in the early phase of the disease. This change may reflect either diminished synthesis or increased catabolism.

In chronic active hepatitis (HBs-positive and -negative) and in alcohol-induced disease there is a significant correlation between C1q-binding and the severity of hepatitis. C1q-binding and AC activity were also increased in primary biliary cirrhosis. Density gradient studies indicate that the C1q-binding activity in these subjects lies in the 8–14S and >19S particle-containing fractions.

These findings suggest the presence of immune complexes in patients with acute and chronic liver disease. In some cases the complexes may contained hepatitis viral antigens, but in alcohol-induced and autoimmune disease other types of complex formation must exist. The accumulation of large and small complexes in subjects with liver disease may be a reflection of an impaired function of the mononuclear phagocytes in these diseases. The potential of these complexes to activate complement will determine their pathological importance, and in this respect those found in primary biliary cirrhosis may have special significance.