AMA-positives without PBC and healthy subjects have similar bile acid profiles but are different from PBC patients

S Zandanell; A Feldman; M Strasser; J Tevini; T Felder; U Huber-Schönauer; C Datz; E Aigner

doi:10.1055/s-0039-1691940

Zeitschrift für Gastroenterologie, Table of Contents

Z Gastroenterol 2019; 57(05): e164
DOI: 10.1055/s-0039-1691940

POSTER

Hepatologie

Georg Thieme Verlag KG Stuttgart · New York

AMA-positives without PBC and healthy subjects have similar bile acid profiles but are different from PBC patients

Authors

S Zandanell

¹First Department of Medicine, Paracelsus Medical University, Salzburg, Austria
A Feldman

¹First Department of Medicine, Paracelsus Medical University, Salzburg, Austria
M Strasser

¹First Department of Medicine, Paracelsus Medical University, Salzburg, Austria
J Tevini

²Department of Laboratory Medicine, Paracelsus Medical University, Salzburg, Austria
T Felder

²Department of Laboratory Medicine, Paracelsus Medical University, Salzburg, Austria
U Huber-Schönauer

³Department of Internal Medicine, Oberndorf Hospital, Oberndorf, Austria
C Datz

³Department of Internal Medicine, Oberndorf Hospital, Oberndorf, Austria
E Aigner

¹First Department of Medicine, Paracelsus Medical University, Salzburg, Austria

Abstract

Full Text

Background:

Antimitochondrial antibody (AMA) positivity may precede the development of primary biliary cholangitis (PBC). It is unclear whether changes in serum bile acid (BA) composition already occur in AMA-positive subjects without clinically overt PBC. We aimed to determine the serum BA profile across the spectrum of AMA-positivity including known PBC (UDCA responders and non-responders), newly diagnosed PBC, AMA-positives without PBC, AMA-negatives (negative AMA at second testing) and healthy controls to identify potential changes of BA homeostasis linked to early PBC.

Methods:

446 subjects (85 males, 361 females) tested AMA-positive over a ten-year period. All subjects were invited to an outpatient follow-up (FU) visit, and data were determined in 271 subjects after 6.8 ± 5.1 years. Serum BA profiles were available in 161 subjects. By the time of FU, 87 patients had died. BA concentrations of those 161 patients were compared to 59 age-matched healthy controls (28 males, 31 females). 20 serum bile acids were quantified using a commercially available mass spectrometry based kit.

Results:

AMA-positives without PBC showed similar concentrations of chenodeoxycholic acid (CDCA) compared to controls, but only controls were lower than UDCA responders (p = 0.042). Regarding secondary BA deoxycholic acid (DCA) and conjugated secondary BA glycodeoxycholic acid (GDCA), AMA-positives without PBC had similar concentrations compared to known PBC and were higher than controls (p < 0.05). Levels of glycoursodeoxycholic acid (GUDCA) were higher in UDCA responders compared to AMA-positives without PBC and controls (p < 0.001), while tauroursodeoxycholic acid (TUDCA) was higher in treated PBC compared to AMA-positives without PBC (p < 0.001) but not controls.

Conclusions:

AMA-positive subjects revealed a serum BA profile similar to that of healthy controls except increases of DCA and GDCA, which showed similar concentrations to PBC patients. These findings suggest that rises in DCA and GDCA may represent an early finding of altered BA homeostasis in AMA-positives without PBC.