Serum from 23 of 26 patients with fulminant hepatic failure and grade IV encephalopathy had defective opsonisation of E. coli and yeast (S. cerevisiae). No toxic serum factors acting on the polymorphonuclear leucocytes or inactivators of the normal serum opsonisation factors were found. Complement deficiency was shown to be the most likely cause of the defect in opsonisation. The addition of a heat-labile fraction of normal serum at low concentration corrected the defect and factors of both the classical and the alternative pathways of complement were reduced to below 40% of the activity of the control serum. During the early stages of clinical recovery serum opsonisation and complement activity returned to normal with statistically significant correlations between tests of opsonisation and total haemolytic complement CH50, C3 and total alternative pathway activity. Defective serum opsonisation and complement deficiency represent major defects in the body's defences against infection.
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