Objectives: To describe serum Gc-globulin and the extent to which it complexes with monomeric actin in the initial phase of acetaminophen (Paracetamol) intoxication and to relate this to the severity of liver necrosis and the clinical course.
Patients and methods: Serial measurements of Gc-globulin and the proportion of Gc-globulin complexed to G-actin (complex ratio) were made on admission and every 3 h thereafter in eighteen consecutive patients with acetaminophen intoxication. Eight patients developed hepatic encephalopathy (HE) and two died.
Results: On admission, all patients had significantly reduced serum Gc-globulin levels compared with normal individuals (P < 0.0001); patients with HE had significantly lower values than patients without HE (P < 0.001). Gc-globulin levels in the two patients who died did not differ from those in patients who survived hepatic encephalopathy. Fourty-four of 52 serum samples with Gc-globulin levels below 120 mg/l were from patients with encephalopathy (all eight of these patients provided at least three samples). The complex ratio on admission did not differ significantly between patients with and those without HE and fluctuated considerably during the observation period. The peak complex ratio was, however, higher in patients with HE than in patients without HE (P < 0.01), and three of four patients with peak complex ratios above 75% had HE. In addition, the mean complex ratio was greater in the two patients who died than in those who survived HE (P < 0.05).
Conclusion: Gc-globulin levels were decreased in individuals suffering from acetaminophen intoxication; this decrease correlated with the most severe sign of liver dysfunction, HE. Serum Gc-globulin levels below 120 mg/l and peak complex ratios above 75% may be critical values. However, as a result of considerable fluctuations in the complex ratio, serial measurements are needed to evaluate the Gc-globulin complexing capacity.