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Autoimmune Pancreatitis
Giuseppe Zamboni
University of VeronaIRCS-Ospedale SC Don Calabria, Negrar
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• Increasingly better recognized
• Different clinical profiles by subtype
• Extra-pancreatic involvement
• Differential diagnosis
• Steroid treatment
• Increased risk of malignancy
AUTOIMMUNE PANCREATITIS
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Fibro-inflammatory condition, often mistaken for malignancy, that affect virtually any organs, characterized by a dense lymphoplasmacytic infiltrate, storiform fibrosis, obliterative phlebitis, frequent elevation of serum and tissutal IgG4 and initial response to glucocorticoid.
IgG4-Related DiseaseDefinition
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• Increasingly better recognized
• Different clinical profiles by subtype
• Extra-pancreatic involvement
• Differential diagnosis
• Steroid treatment
• Increased risk of malignancy
AUTOIMMUNE PANCREATITIS
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Periductal inflammation Storiform fibrosis
Venulitis
Diffuse LPC infiltration
Type 1 AIP
SMA
Obliterative phlebitis
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IgG4 IgG
414 534IgG4/IgG 78%
Type 1 AIP, IgG4-RD
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Granulocytic Epithelial Lesions (GELs)
Acinar GEL
Type 2 AIP (GELs-pos)
Serum IgG4: low
Tissue IgG4: 0 /< 5
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Type 2 AIPYounger age (mean 40), equal M/F ratio
High coincidence of UC or Crohn’s disease
Few IgG4 / GELs
Storiform fibrosis: mild
Obliterative phlebitis: unusual
Recurrence: uncommon
Type 1 AIP, IgG4-RD Older age (mean 64), M preponderance
Any organ system can be affected
Storiform fibrosis: very common
Obliterative phlebitis: very common
Many IgG4 / no GELs
Recurrence: frequent, multiple lesions
IgG4
Two Clinico-Pathologic Subtypes
GELs
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Conclusions:
Type 2 AIP in histologically confirmed AIP cases in Korea may not be as rare as originally thought, with an estimated prevalence rate of 28.8% (15/52)
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Young IBD (specially UC) patients who present with clinical acute
pancreatitis are clinically suspicious for type 2 AIP
12 (44%) with UC
(8 before, 4 simultaneously)
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Definition of AIP-NOS (ICDC):
1- the absence of conclusive criteria for AIP type 1 (probable or definitive)
2- the absence of suggestive histology (definitive) for AIP type 2 or in the
presence of concurrent IBD (probable)
8 pts (17.4%) reclassified as AIP type 2 because developed UC
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Autoimmune PancreatitisRisk of Relapse by AIP Subtype
Type 1
Type NOS
Type 2
Verona AIP database, 23.2.2018
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• Increasingly better recognized
• Different clinical profiles by subtype
• Extra-pancreatic involvement
• Differential diagnosis
• Steroid treatment
• Increased risk of malignancy
AUTOIMMUNE PANCREATITIS
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AIP: ANATOMIC DISTRIBUTION OF LESIONS
1a. PANCREATICOCENTRIC
1b. PANCREATICOBILIARYCENTRIC
2a. EXTRAPANCREATICOBILIARYCENTRIC
Type 2 AIP-Ulcerative Colitis
Type 1 AIP-IgG4-RD
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• Increasingly better recognized
• Different clinical profiles by subtype
• Extra-pancreatic involvement
• Differential diagnosis
• Steroid treatment
• Increased risk of malignancy
AUTOIMMUNE PANCREATITIS
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AUTOIMMUNE PANCREATITISDifferential Diagnosis
1.“Inflammatory” lesions
2. Pancreatic carcinoma
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• 50% of pts are asymptomatic
• Not associated with IgG4, IgG4-RDs or IBD
• Mainly affects hilar BD and pancreatic head
• The potential response to steroids remains to be explored
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Follicular Pancreatitis and Cholangitis
CD 20
Female, 58yrs, ? Head PDCA
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Follicular PancreatitisMale, 70yrs, ? PNET, uncinate process
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Follicular PancreatitisMale, 70yrs, ? PNET, uncinate process
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Follicular Pancreatitis
Differential Diagnosis
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Male, 62yrs, pancreatic head mass
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Mono-Clonal peak
Low Grade B-cell Lymphoma
Male, 62yrs, pancreatic head mass
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AUTOIMMUNE PANCREATITISDifferential Diagnosis
1. “Inflammatory” lesions
2.Pancreatic carcinoma
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Autoimmune PancreatitisSurgery over the time in Verona
AIP Database of Verona Pancreas Center, 2014
Retrospective
on surgical specimens
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AIP-FNACytology
PancreatitisCarcinoma AIP
Established criteria
sensitivity: 80-90%specificity: ~100%
Established criteria
mixed inflammationfibrosis
acinar disruptionbland ductal cells
Criteria
Low specificity
Type1-IgG4+cellular stroma
lymphocytic backgroundrare ductal cells
?IgG4-ICC
Type2-GEL+neutrophils infiltration
ductal/acinar intraepithelialneutrophils
cellular stroma
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Extremely difficult/Impossible
Important to exclude neoplasia
AIP-FNACytologic diagnosis
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A distinct entity with characteristic
The knwoledge of the full range of
morphology of AIP is crucial in the
interpretation of biopsy specimens
AUTOIMMUNE PANCREATITIS
Biopsy diagnosis
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Feature Clinically
suggestive of
AIP
Clinically
suggestive of
Non-AIP CP
Granulocytic
epithelial lesion (GEL)
48.3% (14/29) 0% (0/15)
>10 IgG4 positive
plasma cells/HPF
41.4% (12/29) 13.3% (2/15)
>10 eosinophilic
granulocytes/HPF
62.1% (18/29) 33.3% (5/15)
Cellular fibrosis with
inflammation
96.6% (28/29) 40.0% (6/15)
Lymphoplasmacytic
infiltration
93.1% (27/29) 33.3% (5/15)
Venulitis 65.5% (19/29) 26.7% (4/15)
71% of AIP recognized, if 4/6 microscopic features are
present (sensitivity of 76%, with GEL 86%)
Detlefsen-Klöppel, 2009
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Storiform fibrosis
Venulitis
1. AIP type 1: Core Biopsy
IgG4
IgG
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GEL
2. AIP type 2: Core Biopsy
Storiform Fibrosis
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IL-8 immunostaining or IL-8/CD3 double staining may become an ancillary diagnostic tools
Am J Surg Pathol 2017;41:1129
* IL-8 expression in UC suggests a pathogenetic link between the 2 conditions
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Am J Surg Pathol 2019;43:898–906
In a subset cases (n=20), 47% of
PD-L1-positive ducts were not
associated with GELs
PD-L1-positivity in 24/35 AIP-2 (69%)
PD-L1-negativity in all 14 AIP-1
*PD-L1-positivity in:
3% PDCA and other type CP
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PD-L1-positivity in 8/11 AIP-2
PD-L1-negativity in 7 AIP-1
PD-L1-negativity in 17 PDCA
Validation of PD-L1 Stain in Type 2 AIP on EUS-guided Biopsies
PD-L1 positivity may serve as an ancillary test for the
diagnosis of AIP-2
• Not in isolation, but in the larger clinical and
histologic context
Am J Surg Pathol 2019;43:898–906
* No PD-L1-positivity observed in UC
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• Increasingly better recognized
• Different clinical profiles by subtype
• Extra-pancreatic involvement
• Differential diagnosis
• Steroid treatment
• Increased risk of malignancy
AUTOIMMUNE PANCREATITIS
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Autoimmune PancreatitisResponse to Steroids and Relapse
August 2003 December 2003 (after steroids)
October 2006 December 2006 (after steroids)
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Rituximab in AIP Type 1Pancreatic Relapses, Azathioprine Intolerant
Before RXT 6 month after RXT (2 infusions)
June 2014
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• Increasingly better recognized
• Different clinical profiles by subtype
• Extra-pancreatic involvement
• Differential diagnosis
• Steroid treatment
• Increased risk of malignancy
AUTOIMMUNE PANCREATITIS
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Intern Med 2019 - Advance Publication DOI: 10.2169 / internalmedicine.2210-18
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Two proposed mechanisms
1.Inflammation/CA development:
- the risk increases with duration
2.CA induces AIP (paraneoplastic syndrome)
- the highest risk < 1 years
- clinical improvement after successfultreatment of CA
AIP-INCREASED RISK OF MALIGNANCY
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• Increasingly better recognized: worldwide
• Different clinical profiles by subtype:AIPtype1-2,NOS
• Extra-pancreatic involvement: IgG4-RD vs IBD
• Differential diagnosis: inflammatory lesions/neoplasms
• Steroid treatment:Azathioprine/Rituximab in relapse
• Increased risk of malignancy: extrapancreatic>pancreatic
AUTOIMMUNE PANCREATITIS
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Many thanks to:
VERONA PANCREATIC TEAM
Günter Klöppel
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