Autoimmune Liver Disease (PBC, PSC & AIH)

Meet the patient

A 52-year-old woman comes to clinic with six months of fatigue she blames on "the change", and pruritus that has her scratching her palms and soles at 3am. Her LFTs show an isolated ALP of 320 with a normal bilirubin and ALT. The registrar writes "fatty liver, recheck in six months".[1]

The two questions that decide her next year are the two that decide every autoimmune liver case: is the ALP or the ALT leading? (cholestatic versus hepatitic) and whose autoimmune signature is this? Hold those two and the three diseases sort themselves out — and the wrong drug never gets reached for.[1]

Three diseases on one grid — the grid that sorts them

Read these three diseases as a grid of target (bile ducts versus hepatocytes) and duct size (small versus large), and you will never confuse them.[1]

• PBC is an autoimmune epithelitis of the small intrahepatic ducts — AMA-positive, cholestatic; about half of patients are completely asymptomatic at diagnosis these days.[1][2]
• PSC is a progressive fibroinflammatory disease of intra- and extra-hepatic ducts — multifocal strictures on MRCP, recurrent cholangitis, and a markedly increased lifetime risk of cholangiocarcinoma.[6][17]
• AIH hits hepatocytes, not ducts — diagnosed by convergent autoantibodies, high IgG, histology and exclusion of viral hepatitis. Hepatitic, not cholestatic.[10][12]

All three share a final common pathway — chronic inflammation, fibrosis, cirrhosis — and they can co-exist as overlap syndromes: PSC with AIH overlap accounts for roughly 5% of PSC. The IgG4-sclerosing cholangitis mimic sits beside PSC on the grid but, unlike PSC, is steroid-responsive.[6][8]

[2] [6] [10] [12]

The headline numbers every stem turns on:[2][6][7]

[2] [6]

PBC — the middle-aged woman with AMA and a raised ALP

PBC is an autoimmune epithelitis of the small intrahepatic bile ducts that affects predominantly women, and when untreated will culminate in end-stage biliary cirrhosis. Diagnosis is usually based on liver tests indicative of a cholestatic hepatitis in association with circulating antimitochondrial antibodies — and about half of patients are nowadays completely asymptomatic at diagnosis, picked up on a routine raised ALP, exactly like the patient you met at the top of this topic.[1][2]

The presence of antimitochondrial antibodies is a key diagnostic marker, and PBC-specific antinuclear antibodies — anti-gp210 and anti-sp100 — also bear diagnostic and prognostic significance, which is how AMA-negative disease is confirmed serologically.[2]

Clinically PBC declares itself with pruritus, fatigue, hyperpigmentation, dry-gland (sicca) syndrome and xanthelasmas, and concurrent extrahepatic autoimmune diseases are frequent. Risk stratification at diagnosis uses demographic factors, clinical and biochemical findings, liver autoimmune serology and fibrosis stage.[2]

The classic trap: a middle-aged woman with fatigue and pruritus is labelled "menopause" or "fatty liver" while her cholestatic ALP sits unexplained. An unexplained cholestatic ALP with a positive AMA is PBC — start therapy, do not "recheck in six months".[1][2]

PSC — the cholestatic ALP with IBD and a beaded MRCP

PSC is a chronic, progressive cholestatic disease of unknown aetiology characterized by inflammation and fibrosis of the intra- and extra-hepatic bile ducts, producing multifocal strictures and eventual biliary cirrhosis. A strong association exists with inflammatory bowel disease, particularly ulcerative colitis, which occurs in 60% to 80% of PSC cases. In the other direction, a 2026 meta-analysis pooled PSC prevalence in IBD at about 15 per 1000 patients — roughly 2% — and twice as high in ulcerative colitis (20.6 per 1000) as in Crohn's disease (10.2 per 1000). Large-duct (classic) PSC makes up about 90% of cases, small-duct PSC about 5%, and PSC-AIH overlap about 5%.[6][7]

MRCP is now the preferred non-invasive imaging modality for the cholangiographic diagnosis that historically required ERCP; ERCP has moved to a therapeutic and diagnostic role for complications and cancer evaluation.[6][17]

Clinically PSC is a cholestatic picture complicated by recurrent bacterial cholangitis and the need to evaluate dominant strictures, because PSC carries a markedly increased lifetime risk of cholangiocarcinoma (CCA). Concurrent PSC and ulcerative colitis markedly increase colorectal cancer risk, warranting surveillance colonoscopy every 1 to 2 years.[6][17]

The classic trap: the UC patient with a raised ALP written off as "fatty liver" or "drug effect". A cholestatic ALP in IBD is PSC until MRCP says otherwise — and the same patient needs colonoscopy for the IBD itself and lifelong cancer vigilance.[6]

AIH — the raised transaminases, high IgG and characteristic histology

AIH is a chronic liver disease of unknown aetiology which may affect any patient irrespective of age, sex, or ethnicity. At baseline, the clinical spectrum varies largely from asymptomatic cases to acute liver failure with massive hepatocyte necrosis — the single widest spectrum of the three diseases, and the reason a jaundiced coagulopathic patient can still be "autoimmune".[12]

Diagnosis rests on convergence, not on one test: the simplified diagnostic criteria (Hennes 2008) score autoantibodies, immunoglobulin G, histology, and exclusion of viral hepatitis — sex and age were candidate criteria that fell away. A cut-off of at least 6 points gives probable AIH (88% sensitivity, 97% specificity) and at least 7 points definite AIH (81% sensitivity, 99% specificity).[10]

Histology matters: "compatible with AIH" scores less than "typical of AIH", and immunosuppression is life-saving — which is why early diagnosis is the game.[10]

Etymology for viva gold: "interface hepatitis" — inflammation breaching the limiting plate between portal tracts and parenchyma — is the classic histological pattern the pathologist is asked to grade as compatible with, or typical of, AIH.[10]

How the immune attack does its damage — and why all three end in cirrhosis

All three arise from loss of immune self-tolerance, but the antigenic target decides the biochemistry and the biopsy. In PBC the small duct is the target (autoimmune epithelitis); in PSC the duct wall is fibrosed (multifocal strictures on MRCP); in AIH the hepatocyte is attacked (hepatitic pattern). Untreated PBC culminates in end-stage biliary cirrhosis; PSC progresses to biliary cirrhosis and cancer risk; AIH-associated cirrhosis requires surveillance for portal hypertension and hepatocellular carcinoma, and decompensated AIH cirrhosis is a transplant disease.[1][2][12]

[2] [6] [10] [12]

The natural history is distinct for each: untreated PBC progresses to end-stage biliary cirrhosis; PSC progresses despite therapy with the ever-present threat of cholangiocarcinoma; and acute severe AIH carries a real risk of needing liver transplantation when corticosteroids fail.[1][13]

The traps — mimics before immunosuppression, IgG4 before you call it PSC

The discriminator in autoimmune liver disease is rarely a single test — it is the convergence of serology, immunoglobulins, imaging and histology. Two named traps fail candidates every year, and both are about applying the wrong label too early.[1][10]

The classic trap — other hepatitis before steroids. The simplified AIH criteria make exclusion of viral hepatitis a scoring domain precisely because a hepatitic picture with autoantibodies is not automatically AIH — exclude the mimics before committing to long-term immunosuppression.[10]

Everyone forgets — IgG4-sclerosing cholangitis. This is the steroid-responsive mimic of PSC: a fibroinflammatory condition found more commonly in older men, strongly associated with autoimmune pancreatitis, that can closely mimic PSC, secondary sclerosing cholangitis and even cholangiocarcinoma. First-line therapy is corticosteroids, and it has an excellent prognosis when promptly diagnosed and treated with steroids — classic PSC, by contrast, does not respond to steroids.[8][9]

[6] [8] [9]

Investigations — pattern, antibodies, imaging, histology

Work these patients up in a fixed order: pattern first, then the antibody and immunoglobulin panel, then imaging, then histology where the picture is not diagnostic or an overlap is suspected. Jumping straight to a biopsy before you have the antibodies wastes a needle.[1]

The autoimmune panel is the centrepiece:[1]

[2] [8] [10]

Imaging. MRCP is now the preferred non-invasive imaging modality for PSC, showing the characteristic multifocal strictures of intra- and extra-hepatic ducts; ERCP is reserved for the evaluation and management of dominant strictures and their complications, including the work-up of suspected cholangiocarcinoma.[6][17]

Liver biopsy contributes to diagnosis where the picture is not diagnostic — in the simplified AIH score, histology "typical of AIH" scores higher than "compatible with".[10]

Surveillance. In PSC with ulcerative colitis, surveillance colonoscopy every 1 to 2 years is warranted because concurrent disease markedly increases colorectal cancer risk. In AIH-associated cirrhosis, guidelines direct surveillance for portal hypertension and hepatocellular carcinoma, and liver transplantation in decompensated cirrhosis.[6][12]

The simplified AIH score — turn the work-up into a number

The simplified diagnostic criteria for AIH (Hennes 2008) turn a messy work-up into a score you can defend in a viva. The final score retained only four domains — autoantibodies, IgG, histology, and absence of viral hepatitis — validated across international cohorts:[10]

[10]

A score of at least 6 points = probable AIH (88% sensitivity, 97% specificity) and at least 7 points = definite AIH (81% sensitivity, 99% specificity). The score rewards the convergence of antibodies, IgG, histology and a negative viral screen — never one feature in isolation.[10]

Management — the right drug for the right disease

The single most important principle in autoimmune liver disease: the therapy is disease-specific, and the wrong therapy is at best useless and at worst harmful. Steroids are not licensed therapy for PBC; high-dose UDCA harmed PSC patients in a randomised trial; immunosuppression is the answer for AIH. Pick the pattern, then pick the drug.[1][5]

PBC — UDCA first-line

First-line: ursodeoxycholic acid (UDCA) 13 to 15 mg/kg/day — the standard first-line therapy for PBC at every risk stratum. Up to one-third of patients show an unsatisfactory response to UDCA, which is exactly why a structured second look is built into care.[2][3]

After 6 to 12 months of UDCA, perform a new risk-stratification based on the assessment of biochemical response using a continuous scoring system — either the GLOBE or UK-PBC score. In non-responders, add a second-line agent: the FXR agonist obeticholic acid is an approved second-line treatment (used at 5 to 10 mg in trials), and fibrates remain an off-label option; the Hellenic consensus now also recommends the PPAR agonists elafibranor and seladelpar as add-on therapy.[2][3][4]

Everyone forgets — OCA in advanced disease. Obeticholic acid is approved, but carries adverse effects including pruritus and the potential risk of hepatic decompensation in patients with advanced disease. In a decompensated PBC patient, reach for transplant assessment, not OCA.[3]

Symptom control follows a stepwise ladder for cholestatic pruritus recommended by AASLD and EASL: cholestyramine first-line, followed by rifampicin, then naltrexone, then sertraline; refractory itch may need experimental therapies. Pruritus, fatigue and cognitive dysfunction should be promptly recognised and managed because they damage quality of life — and PBC care is meant to be structured, life-long and individualised.[2][14]

PSC — no therapy proven to modify progression

No medical therapy has demonstrated the ability to modify disease progression. UDCA is frequently used empirically and may improve alkaline phosphatase levels, but long-term benefit is unproven — and high-dose UDCA (28 to 30 mg/kg/day versus placebo, Lindor 2009) must be avoided: it did not improve survival, carried 2.3 times the risk of reaching a primary endpoint (cirrhosis, varices, cholangiocarcinoma, transplant or death), 2.1 times the risk of death, transplantation or minimal listing criteria, and serious adverse events were more common (63% versus 37%).[5][6]

Dominant strictures are evaluated and managed at ERCP — brush cytology, fluorescence in situ hybridization and biopsies are the traditional techniques to evaluate a dominant stricture and exclude cholangiocarcinoma, acknowledging their limited sensitivity.[17]

Liver transplantation provides the only curative treatment for advanced disease, yet PSC recurs in up to one-third of transplant recipients.[6]

AIH — corticosteroids to induce, azathioprine to maintain

Induce remission with a corticosteroid plus azathioprine 1 to 2 mg/kg/day. The classic regimen from the landmark controlled trial was prednisone 40 mg/day tapered to 10 mg/day, with azathioprine 1 to 2 mg/kg/day — and budesonide 3 mg three times daily (9 mg/day) induced complete biochemical remission more effectively than prednisone, in non-cirrhotic AIH only (patients with cirrhosis were excluded), with fewer steroid side effects.[11]

Maintain remission with continued immunosuppression — the trial programme continued azathioprine-based maintenance after induction, and EASL guidance frames AIH as a chronic disease requiring sustained, guideline-directed management, with surveillance for portal hypertension and hepatocellular carcinoma once cirrhotic, and liver transplantation for decompensated cirrhosis.[11][12]

Overlap syndromes are part of the map: PSC with AIH overlap is about 5% of PSC and combines the imaging of PSC with the serology of AIH.[6]

Acute emergencies — three time-critical bundles

Most autoimmune liver disease is chronic, but three scenarios will not wait for a clinic slot. Acute severe AIH is one: it is defined as acute presentation with INR 1.5 or above, without cirrhosis or hepatic encephalopathy, and every patient receives high-dose corticosteroid therapy. Earlier is better — delayed initiation (after versus before 5 days from presentation) independently predicted non-response and worse transplant-free survival, and baseline INR predicts outcome; non-responders need liver transplantation.[13]

Acute bacterial cholangitis in PSC is managed by the Tokyo Guidelines 2018 flowchart: initial resuscitation with antibiotics; in mild disease antibiotics alone are usually sufficient and most patients do not require drainage; in moderate disease early endoscopic or percutaneous biliary drainage is indicated; in severe disease organ support comes first and biliary drainage should be performed as soon as possible once the patient stabilises.[15]

Severe intractable pruritus is treated up the stepwise ladder — cholestyramine first-line, then rifampicin, then naltrexone, then sertraline — with experimental therapies for refractory itch. A variceal bleed in cirrhotic-stage disease has a standard bundle: vasoactive drug started as soon as bleeding is suspected (terlipressin preferred where available — the only agent with proven mortality benefit), prophylactic antibiotics such as ceftriaxone, and endoscopic therapy within the first 12 hours once stable, with variceal band ligation the recommended endoscopic treatment.[14][16]

[13] [15] [16]

Complications and the surveillance that catches them

Complications fall into three groups: cirrhotic (shared), disease-specific (the discriminator), and treatment-related (the reason you monitor). The cirrhotic complications of portal-hypertensive and decompensated disease are shared and are the reason guidelines mandate surveillance once cirrhosis is established in AIH.[12]

[2] [6] [12]

Treatment complications drive monitoring. Obeticholic acid can cause pruritus and carries the potential risk of hepatic decompensation in patients with advanced disease — the reason a decompensated patient should not be started on it.[3]

The recurring pitfalls are wrong-therapy and missed-mimic errors:[5]

[3] [5] [6] [8] [10] [12] [17]

Prognosis — who does well, who does not

Treated PBC is built for risk-stratified care: response to UDCA 13 to 15 mg/kg/day assessed at 6 to 12 months with the GLOBE or UK-PBC continuous scores determines who needs second-line add-on therapy — the deep-response target being normalised ALP with bilirubin under 0.6 times the upper limit of normal.[2]

PSC carries the hardest outlook of the three: no therapy modifies progression, there is a markedly increased lifetime risk of cholangiocarcinoma, and although transplant is the only curative treatment, PSC recurs in up to one-third of recipients.[6][17]

AIH spans the widest range — from asymptomatic to acute liver failure — and in acute severe disease, corticosteroid non-responders follow a transplant pathway; decompensated AIH cirrhosis is likewise a transplant disease.[12][13]

Special populations

Paediatric autoimmune liver disease is explicitly covered by EASL guidance, which manages AIH in both adults and children, including variants and specific forms.[12]

PSC with IBD is a distinct high-risk population: surveillance colonoscopy every 1 to 2 years, because concurrent PSC and ulcerative colitis markedly increase colorectal cancer risk.[6]

Post-liver-transplant patients need surveillance for recurrence of the native disease — PSC recurs in up to one-third of transplant recipients.[6]

The trials that set practice

Modern PBC practice is shaped by EASL (2017) and the Hellenic consensus (2026): UDCA 13 to 15 mg/kg/day first-line, biochemical response assessed at 6 to 12 months with GLOBE or UK-PBC, and second-line add-on therapy (FXR agonists, PPAR agonists) for inadequate responders. PSC practice is defined by the Lindor 2009 trial (high-dose UDCA harmful) and the absence of any therapy proven to modify progression. AIH practice rests on the budesonide-versus-prednisone trial (Manns 2010) and the simplified diagnostic score (Hennes 2008), now updated by EASL (2025).[1][2][5][10][11][12]

The landmark evidence every examiner expects you to name:[5]

[5] [4] [11] [10]

The role of PPAR agonists (elafibranor, seladelpar) as second-line add-ons is now embedded in consensus statements, and NOX inhibitors and ileal bile acid transporter inhibitors are emerging for symptom relief in PBC.[2][3]

The mantra, and the FLAIR mnemonic

The mantra — repeat it under the 3am LFT printout: ALP cholestatic, transaminases hepatitic — pick the right disease before you reach for the drug.[1]

The high-yield one-liners to carry into the exam:[2]

• PBC = predominantly women, AMA, raised ALP, small-duct disease, UDCA 13 to 15 mg/kg/day; AMA-negative disease is confirmed with anti-gp210 / anti-sp100.[2]
• PSC = IBD (especially UC) in 60 to 80%, multifocal strictures on MRCP, cholangiocarcinoma risk, NO therapy proven to modify progression; high-dose UDCA is harmful.[5][6]
• AIH = raised transaminases, high IgG, autoantibodies, histology and viral exclusion — scored; corticosteroids plus azathioprine.[10][11]
• PBC and PSC are cholestatic (ALP); AIH is hepatitic (transaminases). PSC-AIH overlap exists (about 5% of PSC).[6]
• Pruritus ladder = cholestyramine first, then rifampicin, then naltrexone, then sertraline.[14]
• IgG4-sclerosing cholangitis is the steroid-responsive mimic of PSC (older men, autoimmune pancreatitis).[8][9]
• PSC plus UC = surveillance colonoscopy every 1 to 2 years (markedly elevated colorectal cancer risk).[6]
• Obeticholic acid risks hepatic decompensation in advanced disease — transplant assessment, not OCA, in the decompensated patient.[3]
• Score AIH before you treat it — at least 6 points = probable, at least 7 = definite.[10]
• Acute severe AIH (INR 1.5 or above) — corticosteroids early; non-responders go to transplant assessment.[13]

Ward-round test — four stems, thirty seconds each

Stem 1 — the 52-year-old woman from the top of the topic (answer)

The woman you met in Meet the patient: fatigue, pruritus at 3am, isolated ALP 320, normal bilirubin and ALT. What is the diagnosis, the confirmatory test, and the first drug with its dose? Model: This is primary biliary cholangitis — the demography (predominantly a disease of women), the cholestatic isolated ALP, and the pruritus point straight there. Confirm with antimitochondrial antibody (AMA); if AMA-negative, anti-gp210 and anti-sp100 carry the diagnosis (they also carry prognostic weight). About half of PBC patients today are completely asymptomatic at diagnosis — she is textbook. Start ursodeoxycholic acid 13 to 15 mg/kg/day, and reassess the biochemical response at 6 to 12 months with GLOBE or UK-PBC before considering a second-line add-on. The "fatty liver, recheck in six months" note was the trap.[1][2]

Stem 2 — the young UC patient with a raised ALP (answer)

A 28-year-old man with ulcerative colitis, well otherwise, has an ALP of 280 picked up on IBD surveillance bloods. Bilirubin and ALT normal. The registrar calls it "fatty liver". What do you do? Model: This is PSC until proven otherwise — a cholestatic ALP in a patient with IBD, in a disease where ulcerative colitis accompanies 60 to 80% of cases. Order MRCP — now the preferred non-invasive imaging modality: multifocal strictures of the intra- and extra-hepatic ducts confirm PSC. Then surveillance colonoscopy every 1 to 2 years (concurrent PSC and UC markedly raise colorectal cancer risk), lifelong vigilance for cholangiocarcinoma, and honesty that no medical therapy modifies progression — high-dose UDCA is actively harmful. ERCP is for dominant strictures and cancer evaluation.[5][6][17]

Stem 3 — the older man with a stricture, a big pancreas and a high IgG4 (answer)

A 68-year-old man presents with painless jaundice, weight loss, a long irregular common-bile-duct stricture on MRCP, and a diffusely enlarged pancreas. Serum IgG4 is markedly raised. Is this PSC, and what is the treatment? Model: This is NOT classic PSC — it is IgG4-related sclerosing cholangitis, the steroid-responsive mimic. The clues that flip it: an older man (IgG4-SC is more common in older men), the strong association with autoimmune pancreatitis, a stricture that can mimic PSC, secondary sclerosing cholangitis or even cholangiocarcinoma, and the raised serum IgG4. Treat with corticosteroids — first-line therapy — and expect an excellent prognosis when it is promptly diagnosed and treated; classic PSC does not respond to steroids, which is the single most important distinction before labelling a patient "PSC" and withholding the therapy that works.[8][9]

Stem 4 — the decompensated cirrhotic offered obeticholic acid (answer)

A PBC patient with ascites, jaundice and an INR of 1.8 has an inadequate UDCA response. The registrar adds obeticholic acid 5 mg daily. What is wrong with this plan? Model: Obeticholic acid is an approved second-line agent — but it carries the potential risk of hepatic decompensation in patients with advanced disease, alongside pruritus. This patient is already decompensated (ascites, jaundice, raised INR). The right move is to stop the OCA and refer for liver transplant assessment — OCA is for the compensated PBC patient with an inadequate UDCA response after structured response assessment at 6 to 12 months; in decompensation the answer is transplant, not OCA.[2][3]

References

1. [1]European Association for the Study of the Liver. EASL Clinical Practice Guidelines: The diagnosis and management of patients with primary biliary cholangitis J Hepatol, 2017.PMID 28427765
2. [2]Dalekos GN, Gatselis N, Androutsakos T, et al. Consensus statements of the Hellenic Autoimmune Liver Diseases Study Group on the diagnosis and current management of primary biliary cholangitis Ann Gastroenterol, 2026.PMID 41868880
3. [3]Cho EJ. Emerging Therapeutics for Primary Biliary Cholangitis Korean J Gastroenterol, 2025.PMID 40709422
4. [4]Kowdley KV, Hirschfield GM, Coombs C, et al. COBALT: A Confirmatory Trial of Obeticholic Acid in Primary Biliary Cholangitis With Placebo and External Controls Am J Gastroenterol, 2025.PMID 39140490
5. [5]Lindor KD, Kowdley KV, Luketic VA, et al. High-dose ursodeoxycholic acid for the treatment of primary sclerosing cholangitis Hepatology, 2009.PMID 19585548
6. [6]Malik S, Dbouk N, Grant LM, Samant H. Primary Sclerosing Cholangitis StatPearls, 2026.PMID 30725866
7. [7]Ho GJK, Selvakumar A, Yeo LYY, et al. Epidemiology of primary sclerosing cholangitis in general and IBD populations: a systematic review and meta-analysis Hepatol Int, 2026.PMID 42435161
8. [8]Khoury NC, Birk JW. A Review of IgG4-related Sclerosing Cholangitis (IgG4-SC) J Clin Gastroenterol, 2024.PMID 38385591
9. [9]Khalaf K, Calo NC. Immunoglobulin G4-Related Sclerosing Cholangitis: A Review Clin Liver Dis, 2026.PMID 42486600
10. [10]Hennes EM, Zeniya M, Czaja AJ, et al. Simplified criteria for the diagnosis of autoimmune hepatitis Hepatology, 2008.PMID 18537184
11. [11]Manns MP, Woynarowski M, Kreisel W, et al. Budesonide induces remission more effectively than prednisone in a controlled trial of patients with autoimmune hepatitis Gastroenterology, 2010.PMID 20600032
12. [12]European Association for the Study of the Liver. EASL Clinical Practice Guidelines on the management of autoimmune hepatitis J Hepatol, 2025.PMID 40348684
13. [13]Eshraghian A, Taghavi A, Nikeghbalian S. Outcomes of patients with acute severe autoimmune hepatitis: Predictors of non-response to corticosteroids and need for liver transplantation United European Gastroenterol J, 2024.PMID 38733314
14. [14]Trivella J, Levy C. Safety considerations for the management of cholestatic itch Expert Opin Drug Saf, 2021.PMID 33836644
15. [15]Miura F, Okamoto K, Takada T, et al. Tokyo Guidelines 2018: initial management of acute biliary infection and flowchart for acute cholangitis J Hepatobiliary Pancreat Sci, 2018.PMID 28941329
16. [16]García-Pagán JC, Reverter E, Abraldes JG, Bosch J. Acute variceal bleeding Semin Respir Crit Care Med, 2012.PMID 22447260
17. [17]Xia JY, Sawhney M, Hussain HK, Machicado JD. Endoscopic management of biliary stricture in primary sclerosing cholangitis Liver Transpl, 2026.PMID 41879306