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Pharmacologic Approaches to Preventing Primary Sclerosing Cholangitis Recurrence After Liver Transplantation

Pharmacologic Approaches to Preventing Primary Sclerosing Cholangitis Recurrence After Liver Transplantation

Recruiting
18-75 years
All
Phase 2

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Overview

This study aims to determine the efficacy of 36 months once-daily fenofibrate in preventing clinically-detectable recurrence of primary sclerosing cholangitis after liver transplantation, compared with a historical control cohort that was not treated with

Description

Primary sclerosing cholangitis (PSC), an immune-mediated, progressive cholestatic disease with no well-established pharmacologic treatment, has an annual incidence of 2.0 per 100,000 and is responsible for 5% of liver transplants (LT) performed in the United States. Recurrent PSC (rPSC) after LT occurs in 8-27% at 5 years and is associated with an over 40% risk of graft loss.

Because PSC patients undergo LT at a younger age than non-PSC patients (median 40-50 years vs 60 years for most other LT indications), rPSC poses significant lifetime morbidity and mortality risk, and development of its early signs of biliary injury, particularly the development cholestasis (elevated alkaline phosphatase), is routinely monitored in the post-transplant setting.

There is no established pharmacologic treatment for rPSC, and the disease is usually characterized by progressive cholestasis to biliary stricturing, cholangitis, allograft fibrosis and ultimately liver failure. Trials of ursodeoxycholic acid and oral vancomycin have been inconclusive. Since most transplants for PSC are performed with Roux-en-Y biliary reconstructions that make re-transplantation challenging, any pharmacologic intervention to reduce the risk of rPSC would represent a breakthrough in disease management.

Cholestasis appears to be a surrogate for PSC disease progression since improvement in alkaline phosphatase levels is associated with slower disease progression, lower rates of cholangiocarcinoma, and improved survival in the pre-transplant setting. Peroxisome proliferator-activated receptor (PPAR) agonists (e.g. fenofibrate, bezafibrate, seladelpar, elafibranor) reduce bile acid-mediated biliary injury by downregulating their synthesis and activity, and promoting choleresis. PPAR agonists have demonstrated efficacy in potently improving cholestasis in PSC pre-transplant, and other cholestatic liver diseases post-transplant.

While fibrates have been shown to improve both biochemical and clinical parameters of PSC in non-transplant patients, whether they can prevent clinically detectable rPSC after transplantation has not been studied. Extrapolating the pre-transplant data to the post-transplant setting, this study hypothesizes that mitigating cholestasis with the use of fibrates in transplant recipients may impede the development of rPSC.

In this study, the primary aim is to assess the efficacy of once daily fenofibrate-a well-tolerated, generic PPAR-alpha agonist widely used for dyslipidemia-in preventing clinically detectable rPSC after 36 months of treatment, compared to an untreated control group. (rPSC diagnosis based on established criteria outlined below).

This study also investigates novel serum biomarkers of biliary inflammation may serve as early signals of disease either as an alternative or an adjunct to alkaline phosphatase, and before biliary stricturing occurs. The study will also employ quantitative biliary flow dynamics with gadoxetate-enhanced margentic resonance imaging (MRI) which can identify early biliary strictures, hepatocyte function and onset of fibrosis is being studied as a modality to assess pre-transplant PSC severity.

rPSC diagnosis: The study utilizes established criteria for diagnosis of rPSC, with additional inclusion and exclusion criteria for more stringent rule-out of other post-transplant complications of the biliary tree, as follows.1 The criteria will be applied to patients who are between 1 and 7 years from LT.

  • Explant findings consistent with PSC and
  • Absence of untreated hepatic arterial thrombosis, stenosis, or other reason for diminished hepatic arterial resistive indices after LT, and
  • Absence of ischemic cholangiopathy after LT, defined as the development of biliary strictures within the first year of LT as defined elsewhere32, and
  • Absence of untreated biliary anastomotic (post-surgical) stricture, and
  • Presence of intrahepatic and/or extrahepatic biliary stricturing characteristic of PSC by magnetic resonance cholangiography, endoscopic retrograde cholangiography, or percutaneous transhepatic cholangiography, and/or
  • Liver biopsy with fibrous cholangitis and/or fibro-obliterative lesions with or without ductopenia, consistent with PSC

Eligibility

Inclusion criteria:

  • Adults aged 18-75 irrespective of gender who have undergone LT for PSC or PSC-related liver malignancy between 1 year and 7 years (inclusive) prior to study enrollment
  • Absence of rPSC at time of study enrollment
  • At least one of the following additional features that increase risk of rPSC
    • LT performed for cholangiocarcinoma
    • Concurrent inflammatory bowel disease
    • Any episode of cytomegalovirus viremia in the post-transplant period before study enrollment
    • Any episode of acute cellular rejection in the post-transplant period before the study enrollment
  • If target enrollment of 40 patients is not achieved during the first 6 months of

    study, we will remove f(iii) inclusion criteria to expand enrollment to any patient meeting the other inclusion/exclusion criteria.

  • Due to lab requirements, we will only enrol patients who are within a 3 hour driving distance of Mayo Clinic Arizona and/or are willing to travel to Mayo Clinic Arizona at 4 month intervals during the study at own cost.

Exclusion criteria:

  • Presence of ischemic cholangiopathy which can mimic rPSC
  • LT performed for primary biliary cholangitis or autoimmune hepatitis, or PSC with overlapping primary biliary cholangitis or autoimmune hepatitis, which may recur after LT and confound assessment of cholestasis
  • Unaddressed post-LT hepatic artery compromise (e.g thrombosis, stenosis) which can mimic rPSC
  • History of total colectomy for curative treatment of ulcerative colitis which reduces risk of rPSC
  • Baseline GFR <30 ml/min which precludes administration of fenofibrate
  • Previously known intolerance or allergy to fenofibrate
  • Other clinically significant comorbid condition, including inability to provide consent and psychiatric conditions, which in the opinion of the study team, may interfere with patient treatment, safety, assessment, or compliance with the treatment
  • Female participants that are pregnant or planning to become pregnant

Study details
    Primary Sclerosing Cholangitis
    Liver Transplant
    Complications
    PSC
    Biliary Strictures

NCT06905054

Mayo Clinic

5 July 2025

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