J HARIDY, C JAYASEKERA AND AJ NICOLL Department of Gastroenterology and Hepatology, The Royal Melbourne Hospital, Melbourne Australia Background: Primary Biliary Cirrhosis (PBC) is a progressive cholestatic disease

associated with the development of cirrhosis and liver failure. Ursodeoxycholic acid (UDCA) is the only medication currently approved for therapy. The biochemical response to UDCA correlates with long-term prognosis of PBC, with evidence of increased risk of mortality and liver transplantation in non-responders.1 Multiple agents are in development as second-line treatments for non-responders to UDCA. Aim: To determine the proportion of patients with known PBC who have responded adequately to initiation of UDCA. Method: A retrospective review of PBC patients located from the Liver database was conducted. Patients were excluded if they had not completed 12 months Quizartinib of UDCA or incomplete information to allow analysis. Diagnosis of PBC was confirmed when 2/3 of cholestatic biochemistry, anti-mitochondrial antibody testing

and histopathological correlates were positive. Prior history of UDCA dosage regimen was located from medical records and pharmacy dispensing systems. Compliance with UDCA was confirmed through a phone interview. Biochemical Selleckchem Sotrastaurin response was defined as an AST and ALP < 1.5 times the upper limit of normal range, with normal range bilirubin after 12 months of therapy with UDCA (Paris II Criteria).2 Results: 8 patients with confirmed PBC were identified that fit the inclusion criteria from a total

1142 patients on the liver database. Mean follow-up times were 39 +/− 13 months and median follow-up 28 (range 12 – 121) months. The mean age of patients at initiation of UDCA was 59 years and 7/8 (88%) were female. MCE 3/8 patients (38%) had an incomplete biochemical response to UDCA and may be suitable for a trial of alternative treatment. Responders tended to be younger than non-responders (mean 55 vs 63 years old). The single male case was a non-responder. 2 patients died during the followup period, 1 was a non-responder (time from initiation of UDCA 121 months) and the other a responder (time from initiation of UDCA to death 101 months). 2/8 patients (25%) had evidence of portal hypertension, both of which were non-responders. One patient had evidence overlap features with autoimmune hepatitis, and was a responder. Conclusion: In a busy tertiary centre liver clinic, PBC comprises a small number of patients seen. UDCA appears to have had a successful biochemical outcome in 5/8 patients treated. Responders tended to be younger at the time of UDCA initiation, and less likely to develop portal hypertension during followup. Alternative treatment will need to be considered in the 3/8 non-responders. 1 Kuiper EM, Hansen BE, de Vries RA, den Ouden-Muller JW, van Ditzhuijsen TJ, Haagsma EB, et al.