Thyroxine-bindig globulin (TBG) is the major thyroid hormone carrier protein. The molecule contains approximately 10 sialic acid residues which play a key role in the peripheral metabolism of TBG. Since the serum of patients with liver disease often contains large amounts of several desialylated glycoproteins, the aim of the present studies was to characterize circulating TBG and to examine the possible presence of desialylated TBG (dTBG) in 24 patients with a variety of hepatobiliary diseases and selected on the basis of elevated serum levels of desialylated glycoproteins. Using 4 immunochemical techniques applied for the measurement of TBG, for the detection of dTBG and for the characterization of TBG microheterogeneity, the results indicated: a) a wide scatter of serum TBG levels between 4 and 23 mg/l; b) the absence of detectable amounts of dTBG in any of the sera tested; and c) a close similarity between the microheterogeneity of TBG in patients with liver disease with that of control sera or of purified TBG. In conclusion, in patients with acute and chronic liver disease, TBG, although quantitatively modified, remains qualitatively unaltered, suggesting that diseased liver produces fully sialylated TBG and that its catabolism is not impaired.

Absence of circulating desialylated thyroxine-binding globulin in patients wiht hepatobiliary disease

Costante G.;
1985-01-01

Abstract

Thyroxine-bindig globulin (TBG) is the major thyroid hormone carrier protein. The molecule contains approximately 10 sialic acid residues which play a key role in the peripheral metabolism of TBG. Since the serum of patients with liver disease often contains large amounts of several desialylated glycoproteins, the aim of the present studies was to characterize circulating TBG and to examine the possible presence of desialylated TBG (dTBG) in 24 patients with a variety of hepatobiliary diseases and selected on the basis of elevated serum levels of desialylated glycoproteins. Using 4 immunochemical techniques applied for the measurement of TBG, for the detection of dTBG and for the characterization of TBG microheterogeneity, the results indicated: a) a wide scatter of serum TBG levels between 4 and 23 mg/l; b) the absence of detectable amounts of dTBG in any of the sera tested; and c) a close similarity between the microheterogeneity of TBG in patients with liver disease with that of control sera or of purified TBG. In conclusion, in patients with acute and chronic liver disease, TBG, although quantitatively modified, remains qualitatively unaltered, suggesting that diseased liver produces fully sialylated TBG and that its catabolism is not impaired.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12317/63802
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