Diagnositic value of serum bile acid estimations in liver disease.

Abstract

Bile acid concentrations were estimated enzymatically in fasting and postprandial (two-hour) serum samples from 18 normal subjects and 30 patients with histologically proven hepatobiliary disease. The serum bile acid concentration was less than 15 mumol/1 in normal subjects and did not increase postprandially. The fasting serum bile acid concentration was raised in 27 of the patients with hepatobiliary disease, and following a meal was outside the normal range in all 30 patients. Other liver function tests were abnormal less frequently. These results suggest that the estimation of serum bile acids in the postprandial state is a sensitive screening test of hepatobiliary disease. They should be of particular value in patients in whom liver disease is suspected but not proven, and in those recovering from liver disease, especially following therapy.

A Simplified Procedure for the Isolation of Bile Acids from Serum Based on a Batch Extraction with the Non-Ionic Resin—Amberlite XAD-7

“…The mean value (± standard deviation) in normal subjects for fasting samples was 13.2 ± 2.9 fLmolfl and two hours postprandially 12.6 ± 4.9 fLmol/1. These values are higher than we previously reported (Barnes et al, 1975) using ethanol precipitation of serum, although the upper limit of the normal range went up by only I fLmol/l to 16 fLmolfI.…”

“…'Liver function' tests based on the measurement of the bile acids with the hydroxysteroid dehydrogenase enzymes (Barnes et al, 1975;Schwarz et al, 1975) are not affected by the lower recovery of the bile acid sulphates as these enzymes do not act on the bile acid sulphates even when the appropriate hydroxyl group is available (Haslewood and Haslewood, 1976). Thus all the bile acids measured by the enzyme method are essentially completely recovered by the XAD-7 resin.…”

The G-protein coupled bile salt receptor TGR5 is expressed in liver sinusoidal endothelial cells

“…Under pathological conditions such as chronic liver diseases, increased systemic bile salt concentrations due to defects in bile salt secretion may occur. 27,32 Expression of TGR5 by SEC provides the possibility to adapt to changing bile salt concentrations. TGR5 has been shown to signal via cAMP.…”

Serum bile acids in hepatobiliary disease.

“…In another study, total postprandial serum bile acids were increased in all 30 patients with histological evidence of liver disease. The fasting serum bile acids were normal in three patients, and normal values for bilirubin, alkaline phosphatase, and aspartate aminotransferase were found in at least seven patients (Barnes et al, 1975). It is notable, however, that the former study excluded patients with non-functioning gallbladders, and the methods employed in both studies were insufficiently sensitive to discriminate between fasting and postprandial serum bile acid values in normal subjects.…”