Impaired opsonization by serum from patients with chronic liver disease

Serum opsonization of two organisms, E. coli and yeasts (S. cerivisiae), was examined in 68 patients with chronic liver disease (CLD). Impaired opsonization for yeasts was found in seven (29%) of 24 patients with chronic active hepatitis, six (27%) of 22 with alcoholic cirrhosis and five (23%) of 22 with primary biliary cirrhosis. Opsonization for E. coli was normal in patients with primary biliary cirrhosis but impaired in seven (29%) patients with chronic active hepatitis and three (14%) of those with alcoholic cirrhosis. The defect of opsonization in chronic active hepatitis was found mainly in patients with histological evidence of active disease. A deficiency, rather than antagonism or inhibition, of normal opsonization factors was responsible, but could not be related to reduced levels of serum complement factors of either the classical or the alternative pathway present in 45% of the patients with chronic active hepatitis, 71% with alcoholic cirrhosis and 18% of those with primary biliary cirrhosis. Serum from two of 11 patients with impaired opsonization antagonised the function of normal polymorphonuclear leucocytes, and polymorphonuclear leucocytes from six of seven patients had slightly reduced phagocytosis/killing of E. coli opsonized in normal serum. Defects of serum opsonization, complement activity and polymorphonuclear leucocyte function may be causes of the increased susceptibility to bacterial infection in patients with CLD.