A194 CAN NOVEL SEROLOGICAL MARKERS BE USED TO BETTER DEFINE PRIMARY BILIARY CHOLANGITIS (PBC)-AUTOIMMUNE HEPATITIS (AIH) OVERLAP SYNDROME

It is estimated that up to 18% of patients with Primary Biliary Cholangitis (PBC) can be classified as having overlap features with Autoimmune Hepatitis (AIH). Patients with PBC-AIH overlap syndrome (OS) have been reported to exhibit suboptimal responses to Ursodeoxycholic acid therapy, and are more likely to progress to cirrhosis and its’ complications. Serological markers, including anti-double stranded DNA (anti-dsDNA) and anti-P53, have been suggested to be robust markers for identifying patients with PBC-AIH OS. The identification of serological markers that can be confidently used to identify patients with PBC-AIH OS would be useful for the clinical management of PBC-AIH OS. In our well defined PBC patient cohorts, various serological markers were evaluated for their potential utility for identifying PBC-AIH OS patients. Blood samples from 214 patients from University of Calgary Liver Unit and University of Alberta biobanks were analyzed by Mitogen Diagnostic Laboratory (Calgary, AB Canada) for various classical and novel autoantibodies. Anti-dsDNA was measured by either the Crithidia luciliae immunofluorescence (CLIFT) assay (1:20 dilution) or a chemiluminescent immunoassay (CIA; Inova Diagnostics, SanDiego). Anti-P53, anti-Ro52/TRIM21, anti-YB 1, anti-MPP1, anti-GW182, anti-Ge-1, and anti-Ago 2 were measured by either an Addressable Laser Bead Immunoassay (ALBIA) or Line Immunoassay (LIA). Frequency of autoantibodies were compared between study groups using non-parametric statistical methods. The performance of patient serum biochemistry and autoantibody profiles to predict OS was determined using multivariate analysis. PBC-AIH OS was diagnosed according to the Paris criteria (Chazouilleres et al) and PBC was diagnosed as per European Association for the Study of the Liver guidelines. Of the 214 patients assessed, 16 (7.5%) had a diagnosis of OS. Compared to PBC patients, OS patients had similar age (median: 59 vs. 63, P=0.21) and female predominance (94% vs. 89%, P=1.00). Anti-dsDNA measured by CLIFT (37.5% in OS vs. 9.1% in PBC, P=<0.01), elevated serum ALT (62 IU/L in OS vs. 35 IU/L in PBC, P<0.01), and an elevated serum IgG (17.6 g/L in OS vs. 12.1 g/L in PBC, P<0.01) were associated with OS. In a multivariate model, Anti-dsDNA-by CLIFT, ALT and IgG were significant predictors of OS with area under the receiver operator curve (AUROC) value of 0.84. The combination of presence of anti-dsDNA, elevated serum ALT, and elevated serum IgG can be used to identify patients with PBC-AIH OS. Contrary to previous reports, anti-P53 was not associated with OS. In addition, other autoantibodies including anti-dsDNA (measured via CIA), anti-Ro52/TRIM21, anti-YB 1, anti-MPP1, anti-GW182, anti-Ge-1, and anti-Ago 2 were not associated with OS. CIHRCal Wenzel Family Foundation Chair in Hepatology

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