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When the two immunological methods, radial immunodiffusion (RID) and electroimmunodiffusion (EID), were used for the determination of alpha 1-acid glycoprotein, a significant discrepancy in the results was encountered depending on the degree of sialylation. It appeared that with desialylated alpha 1-acid glycoprotein, amounts estimated by EID were much lower than those actually present as assayed by the RID method. Determination of glycoprotein samples treated with neuraminidase for varying periods of time revealed an increasing underestimation by the EID method with decreasing sialic acid content. Partial resialylation of asialo-alpha 1-acid glycoprotein by bovine colostrum beta-galactoside alpha (2 leads to 6) sialyltransferase on the other hand resulted in less underestimation. Differential determination of alpha 1-acid glycoprotein by the two immunological methods thus offers a method for the estimation of the degree of sialylation of alpha 1-acid glycoprotein and other sialoglycoproteins in serum and body fluids.

The calibration curves for evaluating the degree of desialylation of C1-inactivator (sialic acid content 12.5%) and haemopexin (sialic acid content 4%) have been plotted. No desialylation of either glycoprotein occurs in normal subjects. In the patients (liver damage) studied, C1-inactivator is often desialylated, whereas haemopexin is not. In a previous report, we had shown that alpha1-acid glycoprotein is more often desialylated than alpha1-antitrypsin. Thus, it appears that the degree of desialylation of the sialic acid-rich glycoproteins is a more sensitive index of the severity of hepatic injury than that of the sialic acid-poor glycoproteins. This could be due to a defect in the sialylation process during synthesis.

A method for evaluating the degree of desialylation of alpha 1-AGP and alpha 1-AT has been developed. It consists in their simultaneous determination by radial immunodiffusion (RID) and electroimmunodiffusion (EID). When a desialylation exists, an underestimation by EID relative to RID is found. (1) No significant desialylation of alpha 1-AGP and alpha 1-AT occurred in normal subjects. (2) No correlation between desialylation of alpha 1-AGP and alpha 1-AT and their amounts existed. (3) Desialylation was preferentially observed in patients with severe hepatic damage but also with inflammatory disorders.