Sclerosing diseases of the biliary tree
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- Corey Bell
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1 Sclerosing diseases of the biliary tree Reiner Wiest M.D. BC 2017 R.Wiest 1
2 PSC Histomorphology concentric ductal fibrosis onion skinning involving bile ducts within portal tract areas BC 2017 R.Wiest 2 2
3 BC 2017 R.Wiest 3
4 What can cause sclerosing of biliary tree? BC 2017 R.Wiest 4
5 What can cause sclerosing of biliary tree? Sclerosing cholangitis of unknown origin PSC: Primary sclerosing cholangitis IgG4-SC: IgG4-related sclerosing cholangitis Secondary sclerosing cholangitis Infection: bacterial/parasitic/pyogenic cholangitis Immunodeficiency: e.g. congenital, AIDS patients Mechanical/toxic: stone, surgical, trauma, CTx, drug Cholangiocarcinoma, diffuse metastasis Ischemic: vascular trauma, arterial insuff., PNH Pancreatobiliary disease: CF, CP, ABCB4-CP Systemic inflammatory disease: Sarcoidosis, GvHD, Eosinophilic Others: Portal-hypertensive Biliopathy, Mastozytosis, Caroli,... BC 2017 R.Wiest 5
6 BC 2017 R.Wiest 6
7 Pathogenesis of Primary Sclerosing Cholangitis? PSC BC 2017 R.Wiest 7
8 Pathogenesis of Primary Sclerosing Cholangitis? PSC BC 2017 R.Wiest 8
9 5 BC 2017 R.Wiest 9
10 Most difficult questions in the bible class history! PSC Which genes are shared between UC and PSC?d Medizin Inselspital, Bern. 5 BC 2017 R.Wiest 10
11 Most difficult questions in the bible class history! PSC Which genes are shared between UC and PSC?d Medizin Inselspital, Bern. IL2, CARD 9 and REL Hanse et al. Hepatology BC 2017 R.Wiest 11
12 Most difficult questions in the bible class history! PSC Which genes are shared between UC and PSC?d Medizin Inselspital, Bern. IL2, CARD 9 and REL Hanse et al. Hepatology 2011 Which cell-type is responsible for PSC development after colectomy? 5 BC 2017 R.Wiest 12
13 Most difficult questions in the bible class history! PSC Which genes are shared between UC and PSC?d Medizin Inselspital, Bern. IL2, CARD 9 and REL Hanse et al. Hepatology 2011 Which cell-type is responsible for PSC development after colectomy? Memory a4b7-ccr9+cd8+t-cells primed by retinoic dependent idc Eksteen B et al. Gastroenterology BC 2017 R.Wiest 13
14 BC 2017 R.Wiest 14 6
15 Factors modulating risk for PSC? selspital, Bern. PSC BC 2017 R.Wiest 15 6
16 Factors modulating risk for PSC? selspital, Bern. PSC IBD, mostly UC - 2-4% (max 8%) of IBD patients, in their lifetime - up to 88% of PSC-patients suffer IBD male predominance Sometimes family history of disease smoking protectes against PSC BC 2017 R.Wiest 16 6
17 BC 2017 R.Wiest 17
18 Symptoms in PSC? Prognosis in patient with and without symptoms? PSC BC 2017 R.Wiest 18
19 Symptoms in PSC? Prognosis in patient with and without symptoms? PSC - often asymptomatic (about 50%) - right upper quadrant pain, abdominal discomfort, - fatigue, pruritus, fever/chills and weight loss. (very variable) - If symptoms: time till death or transplantation reduced 9 years vs years BC 2017 R.Wiest 19
20 BC 2017 R.Wiest 20
21 Mayo Risk Score for PSC? PSC BC 2017 R.Wiest 21
22 Mayo Risk Score for PSC? PSC R= ( * (age in years)) + ( * LN(total bilirubin in mg/dl)) - ( * (serum albumin in g/dl)) + ( * LN(AST in IU/L) + ( * (points for variceal bleeding)) Points for variceal bleeding: 0 if none, 1 if present. Each unit increase in the Mayo Risk Score (R) is associated with a 2.5-fold increase in the risk of death. The score shows very slight upward slope over time in stable patients, but during the terminal phase it shows an acceleration in progression ( R < 0 = low" risk R= 0-2 = "intermediate" risk R > 2 = "high" risk Kim et al. Mayo Proc 2000 BC 2017 R.Wiest 22
23 Mayo Risk Score for PSC? PSC R= ( * (age in years)) + ( * LN(total bilirubin in mg/dl)) - ( * (serum albumin in g/dl)) + ( * LN(AST in IU/L) + ( * (points for variceal bleeding)) Points for variceal bleeding: 0 if none, 1 if present. Each unit increase in the Mayo Risk Score (R) is associated with a 2.5-fold increase in the risk of death. The score shows very slight upward slope over time in stable patients, but during the terminal phase it shows an acceleration in progression ( R < 0 = low" risk R= 0-2 = "intermediate" risk R > 2 = "high" risk Kim et al. Mayo Proc 2000 BC 2017 R.Wiest 23
24 Mayo Risk Score for PSC? PSC R= ( * (age in years)) + ( * LN(total bilirubin in mg/dl)) - ( * (serum albumin in g/dl)) + ( * LN(AST in IU/L) + ( * (points for variceal bleeding)) Points for variceal bleeding: 0 if none, 1 if present. Each unit increase in the Mayo Risk Score (R) is associated with a 2.5-fold increase in the risk of death. The score shows very slight upward slope over time in stable patients, but during the terminal phase it shows an acceleration in progression ( R < 0 = low" risk R= 0-2 = "intermediate" risk R > 2 = "high" risk Kim et al. Mayo Proc 2000 BC 2017 R.Wiest 24
25 Lab tests of Primary Sclerosing Cholangitis? 9 BC 2017 R.Wiest 25
26 Lab tests of Primary Sclerosing Cholangitis? - cholestatic ( GGT, AP, bilirubin ) + high transaminases ( 2-3x normal value ) in a majority of patients 9 BC 2017 R.Wiest 26
27 Lab tests of Primary Sclerosing Cholangitis? - cholestatic ( GGT, AP, bilirubin ) + high transaminases ( 2-3x normal value ) in a majority of patients Other lab tests? 9 BC 2017 R.Wiest 27
28 Lab tests of Primary Sclerosing Cholangitis? - cholestatic ( GGT, AP, bilirubin ) PSC + high transaminases ( 2-3x normal value ) in a majority of patients Other lab tests? -Serology : Antibodies 9 BC 2017 R.Wiest 28
29 Diagnosis of Primary Sclerosing Cholangitis? PSC BC 2017 R.Wiest 29
30 Diagnosis of Primary Sclerosing Cholangitis? PSC -Lab: CHOLESTASIS (not other wise explained ) BC 2017 R.Wiest 30
31 Diagnosis of Primary Sclerosing Cholangitis? PSC -Lab: CHOLESTASIS (not other wise explained ) - MRC (P) Method of choice - ERC(P) BC 2017 R.Wiest 31
32 Diagnosis of Primary Sclerosing Cholangitis? PSC -Lab: CHOLESTASIS (not other wise explained ) - MRC (P) Method of choice - ERC(P) abnormal cholangiogram (strictures / dilatations) BC 2017 R.Wiest 32
33 Diagnosis of Primary Sclerosing Cholangitis? PSC -Lab: CHOLESTASIS (not other wise explained ) - MRC (P) Method of choice - ERC(P) abnormal cholangiogram (strictures / dilatations) BC 2017 R.Wiest 33
34 BC 2017 R.Wiest 34 11
35 What is small duct PSC? PSC BC 2017 R.Wiest 35 11
36 What is small duct PSC? PSC Disease variant which is characterized by typical cholestatic and histological features of PSC but normal bile ducts on cholangiography Survival is longer Lower risk for CCA 20% develop large duct disases over 7-10 years BC 2017 R.Wiest 36 11
37 What is small duct PSC? PSC Disease variant which is characterized by typical cholestatic and histological features of PSC but normal bile ducts on cholangiography Survival is longer Lower risk for CCA 20% develop large duct disases over 7-10 years Normal cholangiogram but high suspicion perform? BC 2017 R.Wiest 37 11
38 What is small duct PSC? PSC Disease variant which is characterized by typical cholestatic and histological features of PSC but normal bile ducts on cholangiography Survival is longer Lower risk for CCA 20% develop large duct disases over 7-10 years Normal cholangiogram but high suspicion perform? Liver Biopsies (small duct PSC and/or Overlap-Syndrom with AIH) BC 2017 R.Wiest 38 11
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41 Nakanuma-Histo-Score with strongest predictive value BC 2017 R.Wiest 41
42 Nakanuma-Histo-Score with strongest predictive value BC 2017 R.Wiest 42
43 BC 2017 R.Wiest 43 13
44 Most common complications of PSC? PSC BC 2017 R.Wiest 44 13
45 Most common complications of PSC? PSC Cholangiocarcinoma (5-10% of PSC patients) Biliary (secondary) Cirrhosis portal hypertension/ liver failure hepatocellular carcinoma (about 2% per year) Colorectal Carcinoma 5-10 fold increase BC 2017 R.Wiest 45 13
46 Most common complications of PSC? PSC Cholangiocarcinoma (5-10% of PSC patients) Biliary (secondary) Cirrhosis portal hypertension/ liver failure hepatocellular carcinoma (about 2% per year) Colorectal Carcinoma 5-10 fold increase BC 2017 R.Wiest 46 13
47 BC 2017 R.Wiest 47
48 Colon and PSC: When colonoscopy in PSC? PSC BC 2017 R.Wiest 48
49 Colon and PSC: When colonoscopy in PSC? PSC Every PSC patient at least once, at ED even asymptomatic patients Plus Biopsy even if macroscopically intact (4 quadrant in each colon segment+ileum) Every (3-)5 year after PSC diagnosis or when symptoms develop to seek IBD IBD: annual surveillance colonoscopy with chromoendoscopy (also after LTx) BC 2017 R.Wiest 49
50 BC 2017 R.Wiest 50
51 When to go for ERCP? PSC BC 2017 R.Wiest 51
52 When to go for ERCP? PSC Established PSC: i) therapeutic indication or ii) risk of CCA -clinically relevant or worsening symptoms jaundice, cholangitis, pruritus, weight loss -rapid increase ofap and/or bilirubin -new or progression of known dominant stricture (MR) persistent PSC suscpicion despite normal high-quality MR/MRCP and normal liver biopsy In advanced stage/cirrhosis: benefit maybe limited BC 2017 R.Wiest 52
53 BC 2017 R.Wiest 53
54 ERCP-findings: Amsterdam-classification PSC BC 2017 R.Wiest 54
55 ERCP-findings: Amsterdam-classification PSC BC 2017 R.Wiest 55
56 ERCP-findings: Amsterdam-classification PSC Full occlusion cholangiogramm mandatory: Type I (intra- and extrahepatic) BC 2017 R.Wiest 56
57 ERCP-findings: Amsterdam-classification PSC Full occlusion cholangiogramm mandatory: Type I (intra- and extrahepatic) BC 2017 R.Wiest 57
58 ERCP-findings: Amsterdam-classification PSC Full occlusion cholangiogramm mandatory: Type I (intra- and extrahepatic) BC 2017 R.Wiest 58
59 ERCP-findings: Amsterdam-classification PSC Full occlusion cholangiogramm mandatory: Type I (intra- and extrahepatic) Type II intra- Type III extrahepatic BC 2017 R.Wiest 59
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61 ERCP-findings: Amsterdam-classification BC 2017 R.Wiest 61
62 ERCP-findings: Amsterdam-classification BC 2017 R.Wiest 62
63 ERCP-findings: Amsterdam-classification BC 2017 R.Wiest 63
64 ERCP-findings: Amsterdam-classification BC 2017 R.Wiest 64
65 BC 2017 R.Wiest 65 18
66 Dominant stricture? - definition, frequency, risks PSC BC 2017 R.Wiest 66 18
67 Dominant stricture? - definition, frequency, risks PSC Definition: stenosis with a diameter of <1.5 mm in the CBD < 1 mm in the right or left hepatic duct Mostly associated with increased cholestasis and pruritus Frequency: 45% to 58% of PSC patients during follow up. Risks: CCA, cholangitis BC 2017 R.Wiest 67 18
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69 ERCP: management of dominant stricture? PSC BC 2017 R.Wiest 69
70 ERCP: management of dominant stricture? PSC Always use peri-interventional antibiotics! Sphincterotomy not routinely - only small if at all done when difficult access and/or therapeutic interventions Before any endoscopic therapy: brush cytology and/or biopsy Dilatation preferred method because majority of studies only dilated significant improvement in LTx-free survival only shown for dilatation scheme: repeat every 1-4 weeks, CBD 8mm, DHR/L 6 mm till success Stenting: Perforation rate higher and hence, only in selected cases and only short-term (1-2 weeks) BC 2017 R.Wiest 70
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72 PSC and CCA: epidemiology, risk, prognosis PSC BC 2017 R.Wiest 72
73 PSC and CCA: epidemiology, risk, prognosis Life-time risk up to 15-20% (=400-fold increased) 10-year cumulative risk: 6-9% Up to 50% discovered at initial diagnosis of PSC (or < 1 year FU) Prognosis dismal: < 2 years median overall survival PSC Risk factors for CCA: Presence and duration of IBD (but not PSC) UC with colorectal cancer/ dysplasia Elevated serum bilirubin, variceal bleeding NKG2D gene polymorphism. BC 2017 R.Wiest 73
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75 Stricture diagnostics Brush + FISH + Cholangioscopy? BC 2017 R.Wiest 75
76 Stricture diagnostics Brush + FISH + Cholangioscopy? Brush-cytology: Sensitivity 43%; Specificty 97%, NPV 87% Chance of CCA in dominant stricture: ca. 5% > 90% CBD or perihilar in location Lack of dominant stricture does not rule out CCA-> always do Brushing! FISH/chromosomal assessment: - Polysomy prognostic as relevant as proven CCA - Dominant stricture: polysomy: 88% specificity for CCA - Persistent polysomy-> 69% develop CCA 3 9p Normale Zelle Je 2 Signale der 4 eingesetzten Homozygote Proben 9p21 Deletion Cholangioscopy with SpyBite-Biopsy - Improves diagnostic yield - Triple (Brush+Biopsy+FISH): increased sensitivity to 82% (NPV 87%) Trisomie 7 und Homozygote 9p21 Deletion Polysomie aller 4 Proben BC 2017 R.Wiest 76
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78 PSC and Gallbladder: Polyps and Cancer PSC BC 2017 R.Wiest 78
79 PSC and Gallbladder: Polyps and Cancer 286 PSC patients: 18 (6%) GB mass lesion (21+9 mm) 10 cases (56%) GB cancer PSC Said K et al. J. Hepatol PSC patients undergoing cholecystectomy 8 GB adenocarcinoma Buckles AJG PSC patients (66 removed at LTx) > 50% abnormal histology of GB: Dysplasia in 37% and adenocarcinoma 14% Lewis JT Am J Surg Pathol 2007 BC 2017 R.Wiest 79
80 PSC and Gallbladder: Polyps and Cancer 286 PSC patients: 18 (6%) GB mass lesion (21+9 mm) 10 cases (56%) GB cancer PSC Said K et al. J. Hepatol PSC patients undergoing cholecystectomy Annual ultrasound recommended 8 GB adenocarcinoma 72 PSC patients (66 removed at LTx) > 50% abnormal histology of GB: Dysplasia in 37% and adenocarcinoma 14% Buckles AJG 2002 Any mass lesion (> 10 mm): cholecystectomy Lewis JT Am J Surg Pathol 2007 BC 2017 R.Wiest 80
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82 PSC Surveillance How? BC 2017 R.Wiest 82
83 PSC Surveillance How? Aim: Detection of early lesions No studies on optimal screening/surveillance strategies Yearly MR/MRCP most experts recommend BC 2017 R.Wiest 83
84 PSC Surveillance How? Aim: Detection of early lesions No studies on optimal screening/surveillance strategies Yearly MR/MRCP most experts recommend No dominant stricture in MRCP - Liver tests every 6 months - annual CA 19-9 (cut-off-level?) - MRCP if increasing AP/bilirubin Dominant stricture in MRCP - CA ERCP + Cytologie/ Biopsy - MRT Any doubts /suspect malignancy - Cholangioscopy/Biopsy - EUS/FNA BC 2017 R.Wiest 84
85 PSC Surveillance How? Aim: Detection of early lesions No studies on optimal screening/surveillance strategies Yearly MR/MRCP most experts recommend No dominant stricture in MRCP - Liver tests every 6 months - annual CA 19-9 (cut-off-level?) - MRCP if increasing AP/bilirubin Dominant stricture in MRCP - CA ERCP + Cytologie/ Biopsy - MRT Any doubts /suspect malignancy - Cholangioscopy/Biopsy - EUS/FNA BC 2017 R.Wiest 85
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87 Medical Treatment of PSC? UDCA others? PSC BC 2017 R.Wiest 87 24
88 Medical Treatment of PSC? UDCA others? still no evidence that UDCA is beneficial in improving symptoms or transplant-free survival. PSC BC 2017 R.Wiest 88 24
89 Medical Treatment of PSC? UDCA others? still no evidence that UDCA is beneficial in improving symptoms or transplant-free survival. PSC High-dosage: > 25 mg/kg: even poorer clinical outcome (CRC, cirrhosis, varices, need for liver transplantation or death) BC 2017 R.Wiest 89 24
90 Medical Treatment of PSC? UDCA others? still no evidence that UDCA is beneficial in improving symptoms or transplant-free survival. PSC High-dosage: > 25 mg/kg: even poorer clinical outcome (CRC, cirrhosis, varices, need for liver transplantation or death) UDCA is also not recommended as chemopreventive agent (CRC) BC 2017 R.Wiest 90 24
91 Medical Treatment of PSC? UDCA others? still no evidence that UDCA is beneficial in improving symptoms or transplant-free survival. PSC High-dosage: > 25 mg/kg: even poorer clinical outcome (CRC, cirrhosis, varices, need for liver transplantation or death) UDCA is also not recommended as chemopreventive agent (CRC) Corticosteroids, Immunosuppresants for AIH (overlap-patients) BC 2017 R.Wiest 91 24
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93 Potential future Medical Treatment of PSC? PSC BC 2017 R.Wiest 93 25
94 Potential future Medical Treatment of PSC? PSC New form of UDCA: 24-norUrsodeoxycholic acid (norudca) is the C23 homologue of the 3a,7b-dihydroxy C24 bile acid UDCA hydrophilic, anti-fibrotic,-inflammatory, -proliferative FxR-agonists: e.g. Obeticholic acid, INT-767 also choloretic, cholangiocyte modulator, gut-barriere etc. Vedolizumab : α4 β7 inhibitors / anti-integrin (Trial ongoing) aberrant gut-homing lymphocyte hypothesis focuses on the relationship between PSC and IBD. Traumer M et al. Dig Dis Sci 2016 BC 2017 R.Wiest 94 25
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96 Liver Transplantation in PSC: when, how... PSC BC 2017 R.Wiest 96
97 Liver Transplantation in PSC: when, how... PSC One of the best indications per se: 5y survival > 80% Listed due to complications of cirrhosis, portal hypertension Specific of PSC (rarely): Recurrent/ refractory cholangitis, intractable pruritus BC 2017 R.Wiest 97
98 Liver Transplantation in PSC: when, how... PSC One of the best indications per se: 5y survival > 80% Listed due to complications of cirrhosis, portal hypertension Specific of PSC (rarely): Recurrent/ refractory cholangitis, intractable pruritus CCA: perihilar and < 3 cm Mayo-Protocol: neoadjuvant radiation, radiation-sensitization chemotherapy, oral capecitabine, laparoscopy before LTx Re-PSC of graft: 20-25% in 5-10 years UC: Colectomy seems to protect from recurrence of PSC (controversial, not recommended) BC 2017 R.Wiest 98 26
99 Liver Transplantation in PSC: when, how... PSC One of the best indications per se: 5y survival > 80% Listed due to complications of cirrhosis, portal hypertension Specific of PSC (rarely): Recurrent/ refractory cholangitis, intractable pruritus CCA: perihilar and < 3 cm Mayo-Protocol: neoadjuvant radiation, radiation-sensitization chemotherapy, oral capecitabine, laparoscopy before LTx Re-PSC of graft: 20-25% in 5-10 years UC: Colectomy seems to protect from recurrence of PSC (controversial, not recommended) BC 2017 R.Wiest 99 26
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101 IgG4-hepatobiliary disease - definition IgG4 BC 2017 R.Wiest 101
102 IgG4-hepatobiliary disease - definition IgG4 BC 2017 R.Wiest 102
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104 Microscopic characteristics in IgG4-hepatobiliary disease IgG4 BC 2017 R.Wiest 104
105 Microscopic characteristics in IgG4-hepatobiliary disease IgG4 lymphoplasmacytic infiltration storiform pattern of fibrosis obliterative phlebitis with a variable presence of eosinophils >10 IgG4+ plasma cells per HPF in a biopsy specimen >50 IgG4+ plasma cells per HPF in a resection specimen Plus an IgG4+:IgG+ plasma cell ratio of >40% BC 2017 R.Wiest 105
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107 IgG4-sclerosing cholangitis: classification IgG4 BC 2017 R.Wiest 107
108 IgG4-sclerosing cholangitis: classification IgG4 Distal CBD Most frequent Often with AIP A: with Pre-stenotic dilatation B: without Pre-stenotic dilatation Hilar + CBD Hilar alone DD: pancreatic Ca, Distal CCC, CP DD: PSC, SSC DD: Hilar CCA Okazaki et al. J.Hepatol 2014 BC 2017 R.Wiest 108
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110 IgG4-hepatobiliary disease epidemiology, risk factors IgG4 BC 2017 R.Wiest 110
111 IgG4-hepatobiliary disease epidemiology, risk factors IgG4 Most frequent extra-pancreatic manifestation of IgG4-related diseases BC 2017 R.Wiest 111
112 IgG4-hepatobiliary disease epidemiology, risk factors IgG4 Most frequent extra-pancreatic manifestation of IgG4-related diseases In AIP: ca. 10% IgG4-SC and 23% IgG4-Hepatopathy BC 2017 R.Wiest 112
113 IgG4-hepatobiliary disease epidemiology, risk factors IgG4 Most frequent extra-pancreatic manifestation of IgG4-related diseases In AIP: ca. 10% IgG4-SC and 23% IgG4-Hepatopathy Rarely (1-8%) hepatic involvement without AIP BC 2017 R.Wiest 113
114 IgG4-hepatobiliary disease epidemiology, risk factors IgG4 Most frequent extra-pancreatic manifestation of IgG4-related diseases In AIP: ca. 10% IgG4-SC and 23% IgG4-Hepatopathy Rarely (1-8%) hepatic involvement without AIP Male (7:1!), > 60 year of age, BC 2017 R.Wiest 114
115 IgG4-hepatobiliary disease epidemiology, risk factors IgG4 Most frequent extra-pancreatic manifestation of IgG4-related diseases In AIP: ca. 10% IgG4-SC and 23% IgG4-Hepatopathy Rarely (1-8%) hepatic involvement without AIP Male (7:1!), > 60 year of age, Risk factors: chemicals/toxins (blue-collar-worker), allergy/atopy/eosinophlia, other autoimmune disease (thyroid, coeliac..) BC 2017 R.Wiest 115
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117 Pathogenesis of IgG4-sclerosing cholangitis IgG4 BC 2017 R.Wiest 117
118 Pathogenesis of IgG4-sclerosing cholangitis IgG4 Kamisawa et al. Lancet 2015 BC 2017 R.Wiest 118
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120 IgG4-serum levels- how useful? Differentiate PSC IgG4 BC 2017 R.Wiest 120
121 IgG4-serum levels- how useful? Differentiate PSC > 1.4g/l: 65-80% of IgG4-SC (but 20% normal levels) IgG4 > 2.5 g/l: IgG4-SC vs. PSC: sensitivity 70-89%, specificity 95% g/l: ratio IgG1:IgG4 > 0.24: sensitivity 86%, specificity 95%, NPV 90% > 5.6 g/l: specificity and PPV 100% (?) vs. PSC (+ CCA) BC 2017 R.Wiest 121
122 IgG4-serum levels- how useful? Differentiate PSC > 1.4g/l: 65-80% of IgG4-SC (but 20% normal levels) IgG4 > 2.5 g/l: IgG4-SC vs. PSC: sensitivity 70-89%, specificity 95% g/l: ratio IgG1:IgG4 > 0.24: sensitivity 86%, specificity 95%, NPV 90% > 5.6 g/l: specificity and PPV 100% (?) vs. PSC (+ CCA) PSC per se: > 20% liver explants present with IgG4+cell infiltrate > 10% present with increased serum IgG4 (> 1.4 g/l) both conditions associate with worse prognosis/= seek CCC + associates with: reduced HLA-B*08, increased B*07, DR-B1*15 frequency BC 2017 R.Wiest 122
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124 Typical ERCP-features in IgG4-sclerosing cholangitis? IgG4 BC 2017 R.Wiest 124
125 Typical ERCP-features in IgG4-sclerosing cholangitis? Strictures in cholangiogramm: IgG4 BC 2017 R.Wiest 125
126 Typical ERCP-features in IgG4-sclerosing cholangitis? Strictures in cholangiogramm: IgG4 Long + multifocal BC 2017 R.Wiest 126
127 Typical ERCP-features in IgG4-sclerosing cholangitis? Strictures in cholangiogramm: IgG4 Long + multifocal mild dilatations upstream BC 2017 R.Wiest 127
128 Typical ERCP-features in IgG4-sclerosing cholangitis? Strictures in cholangiogramm: IgG4 Long + multifocal mild dilatations upstream thin diffusely narrowed pancreatic duct BC 2017 R.Wiest 128
129 Typical ERCP-features in IgG4-sclerosing cholangitis? Strictures in cholangiogramm: IgG4 Long + multifocal mild dilatations upstream thin diffusely narrowed pancreatic duct How helpful for differential diagnostic purpose? BC 2017 R.Wiest 129
130 Typical ERCP-features in IgG4-sclerosing cholangitis? Strictures in cholangiogramm: IgG4 Long + multifocal mild dilatations upstream thin diffusely narrowed pancreatic duct How helpful for differential diagnostic purpose? BC 2017 R.Wiest 130
131 Typical ERCP-features in IgG4-sclerosing cholangitis? Strictures in cholangiogramm: IgG4 Long + multifocal mild dilatations upstream thin diffusely narrowed pancreatic duct How helpful for differential diagnostic purpose? Sensitivity 45% = forget it! BC 2017 R.Wiest 131
132 Typical ERCP-features in IgG4-sclerosing cholangitis? Strictures in cholangiogramm: IgG4 Long + multifocal mild dilatations upstream thin diffusely narrowed pancreatic duct Malignancy must be excluded How helpful for differential diagnostic purpose? Sensitivity 45% = forget it! BC 2017 R.Wiest 132
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134 Diagnostic endoscopic optimized work-up? IgG4 BC 2017 R.Wiest 134
135 Diagnostic endoscopic optimized work-up? IgG4 All you can do: ERCP (plus cholangioscopy) Brush-cytology, biopsy Bile fluid EUS (plus FNA) Ampullary biopsy Liver biopsy Caveats/problems: patchy disease insufficient tissue/cells reduced numbers IgG4-cells E.g. in fibrotic stages IgG4-cells in other diseases e.g. malignancy, inflammation BC 2017 R.Wiest 135
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137 How to differentiate PSC/CCA from IgG4-SC? BC 2017 R.Wiest 137
138 How to differentiate PSC/CCA from IgG4-SC? NGS-> qpcr for expanded B-Cell-Clone and IgG4+-RNA Sensitivity 94%, Specificity 99% Breuers et al. Curr Opin Gastroenterol 2017 BC 2017 R.Wiest 138
139 How to differentiate PSC/CCA from IgG4-SC? NGS-> qpcr for expanded B-Cell-Clone and IgG4+-RNA Circulating Plasmablast-number can help differentiate IgG4-RD from other diseases =Biomarker for IgG4-RD (even when normal serum IgG4) Breton-Zeron et al. BestPractGastro 2017 Sensitivity 94%, Specificity 99% Breuers et al. Curr Opin Gastroenterol 2017 BC 2017 R.Wiest 139
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141 Treatment for IgG4-sclerosing cholangitis? IgG4 BC 2017 R.Wiest 141
142 Treatment for IgG4-sclerosing cholangitis? IgG4 Corticosteroid 0.6 (-1) mg/kg KG (30-40mg/Tag) for 4 weeks Tapering: 5mg/week, ending at week 12 Maintenance therapy ( mg/d) for 3 years reduces relapse rate compared to stop at 26 weeks (23% vs. 57%) BC 2017 R.Wiest 142
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144 Treatment-success for IgG4-sclerosing cholangitis? IgG4 BC 2017 R.Wiest 144
145 Treatment-success for IgG4-sclerosing cholangitis? IgG4 Re-assess after 4-6 weeks Serum IgG4: only minority will normalize Complete resolution of strictures and liver tests = response Achieved in about 2/3 of IgG4-SC BC 2017 R.Wiest 145
146 Recurrence/Refractory IgG4-sclerosing cholangitis Risk? Treatment-Options? Ca. 50% will show some recurrence (majority < 6 months after EOT) Risk-factors: high IgG4, multi-organ-involvement, prior recurrence Typ 2-4 (hilar and intrahepatic disease manifestation) Immunmodulators: best evaluated azathioprine Rescue: Rituximab (Anti-CD20-> killing expanded B-cell-clone) BC 2017 R.Wiest 146
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148 IgG4-SC differs from PSC in... BC 2017 R.Wiest 148
149 IgG4-SC differs from PSC in... Rare disease Usually multi-organ-disease Histology needed to confirm diagnosis More benign disease less malignant development (2-fold*), infrequent end-stage cirrhosis Good response to steroids *: presumably only if chronically active disease BC 2017 R.Wiest 149
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151 Danke für die Aufmerksamkeit Danke BC 2017 R.Wiest 151
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