autoimmune pancreatitis: multidetector-row computed tomography (mdct) and magnetic resonance (mr)...
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ABDOMINAL RADIOLOGY
Autoimmune pancreatitis: multidetector-row computedtomography (MDCT) and magnetic resonance (MR) findingsin the Italian experience
Rossella Graziani • Simona Mautone • Maria Chiara Ambrosetti •
Riccardo Manfredi • Thomas J. Re • Lucia Calculli •
Luca Frulloni • Roberto Pozzi Mucelli
Received: 9 August 2012 / Accepted: 30 July 2013
� Italian Society of Medical Radiology 2014
Abstract Multidetector-row computed tomography
(MDCT) and magnetic resonance (MR) imaging are cur-
rently the most frequently performed imaging modalities
for the study of pancreatic disease. In cases of suspected
autoimmune pancreatitis (AIP), a dynamic quadriphasic
(precontrast, contrast-enhanced pancreatic, venous and late
phases) study is recommended in both techniques. In the
diffuse form of autoimmune pancreatitis (DAIP), the pan-
creatic parenchyma shows diffuse enlargement and
appears, during the MDCT and MR contrast-enhanced
pancreatic phase, diffusely hypodense and hypointense,
respectively, compared to the spleen because of lympho-
plasmacytic infiltration and pancreatic fibrosis. During the
venous phase of MDCT and MR imaging, the parenchyma
appears hyperdense and hyperintense, respectively, in
comparison to the pancreatic phase. In the delayed phase of
both imaging modalities, it shows retention of contrast
media. A ‘‘capsule-like rim’’ may be recognised as a
peripancreatic MDCT hyperdense and MR hypointense
halo in the T2-weighted images, compared to the paren-
chyma. DAIP must be differentiated from non-necrotizing
acute pancreatitis (NNAP) and lymphoma since both dis-
eases show diffuse enlargement of the pancreatic
parenchyma. The differential diagnosis is clinically diffi-
cult, and dynamic contrast-enhanced MDCT has an
important role. In the focal form of autoimmune pancrea-
titis (FAIP), the parenchyma shows segmental enlargement
involving the head, the body-tail or the tail, with the same
contrast pattern as the diffuse form on both modalities.
FAIP needs to be differentiated from pancreatic adeno-
carcinoma to avoid unnecessary surgical procedures, since
both diseases have similar clinical and imaging presenta-
tion. The differential diagnosis is clinically difficult, and
dynamic contrast-enhanced MDCT and MR imaging both
have an important role. MR cholangiopancreatography
helps in the differential diagnosis. Furthermore, MDCT and
MR imaging can identify the extrapancreatic manifesta-
tions of AIP, most commonly biliary, renal and retroperi-
toneal. Finally, in all cases of uncertain diagnosis, MDCT
and/or MR follow-up after short-term treatment
(2–3 weeks) with high-dose steroids can identify a signif-
icant reduction in size of the pancreatic parenchyma and, in
FAIP, normalisation of the calibre of the upstream main
pancreatic duct.
Keywords Chronic pancreatitis � Autoimmune
pancreatitis � Acute pancreatitis � Computed tomography �Magnetic resonance � Steroid treatment
Autoimmune pancreatitis (AIP): definition
and classification
Autoimmune pancreatitis (AIP) is a form of chronic pan-
creatitis associated with autoimmune processes. Distinct
histological and clinical profiles reveal two subtypes of
AIP, indistinguishable on the basis of imaging alone: type
1, or lymphoplasmacytic sclerosing pancreatitis (LPSP),
R. Graziani (&) � S. Mautone � M. C. Ambrosetti �R. Manfredi � T. J. Re � R. P. Mucelli
Department of Radiology, ‘‘G.B. Rossi’’ Hospital, University
of Verona, P.le L.A. Scuro 11, 37134 Verona, Italy
e-mail: [email protected]
L. Calculli
Department of Radiology, Sant’Orsola-Malpighi Hospital,
University of Bologna, 9 Via Massarenti, Bologna, Italy
L. Frulloni
Department of Medicine, ‘‘G.B. Rossi’’ Hospital,
University of Verona, P.le L.A. Scuro 10, Verona, Italy
123
Radiol med
DOI 10.1007/s11547-013-0373-9
and type 2, or idiopathic duct-centric pancreatitis (IDCP)
[1]. Type 1, LPSP, or AIP without granulocyte epithelial
lesions, seems to be an IgG4-related multiorgan disease,
characterised by elevated serum IgG4 levels, multiple ex-
trapancreatic organ involvement and IgG4-rich lympho-
plasmacytic infiltrate on histology in all the affected organs
[2, 3]. This form characteristically responds to steroid
treatment, though relapse in the pancreas or other affected
organs is common. In type 2 AIP, IDCP or AIP with
granulocyte epithelial lesions, there is no extrapancreatic
organ involvement or IgG4-rich infiltrate on histology, and
serum IgG4 elevation is unlikely. This form appears to be a
pancreas-specific disorder and is histologically character-
ised by the presence of neutrophils with typical granulocyte
epithelial lesions.
The diagnosis of AIP is challenging even at expert
centres and many different diagnostic criteria have been
developed. Recently, the International Consensus Diag-
nostic Criteria (ICDC) have unified these diagnostic crite-
ria accommodating regional differences in practice. The
comprehensive criteria that must be fulfilled for the diag-
nosis include pancreatic imaging of the parenchyma and
ductal system, serological and histopathological findings,
other organ involvement and response to steroid treatment
[1].
The clinical presentation overlaps with other forms of
acute and chronic pancreatitis, but without a history of
alcohol or tobacco abuse or biliary stone disease. AIP may
vary in its clinical presentation depending on the pancreatic
distribution of disease (focal or diffuse) and on the specific
site involved (head, body or tail of the pancreas) [4–21]. In
the case of focal distribution in the pancreatic head,
patients frequently present painless jaundice. In diffuse
forms or in focal distribution in the pancreatic body-tail,
patients may present pancreatic abdominal pain in the
epigastric region, irradiating to the back with or without
jaundice [8–21]. Therefore, the clinical presentation of AIP
may mimic pancreatic adenocarcinoma in the focal forms
and pancreatic lymphoma or non-necrotizing acute pan-
creatitis (NNAP) in the diffuse forms [22–26].
In evaluating patients with suspected pancreatic disease,
acute or chronic pancreatitis or pancreatic neoplasms,
multidetector-row computed tomography (MDCT) and
magnetic resonance (MR) are the imaging modalities of
choice [15–17, 27–33]. In the specific case of suspected
AIP, a dynamic quadriphasic study (precontrast, contrast-
enhanced arterial, pancreatic, venous and late phases) is
recommended for both techniques.
Technically, in MDCT of the pancreas, contrast medium
administration typically involves the use of bolus tracking
software with a region of interest (ROI) placed over the aorta
and a predetermined attenuation threshold of 100 HU.
Pancreatic arterial and portal venous phase images are
acquired 20–30 and 60–70 s after bolus tracking, respec-
tively, and the delayed phase images 180 s after the begin-
ning of the injection. A collimation value between a
maximum of 2.5 mm and a minimum of 0.625 mm is rec-
ommended. The standard reconstruction thickness used
during the pancreatic and portal venous phase is 1 mm, with
an interval of 0.5 mm, whereas during the late phase it is
2–1 mm, with a range of 1–0.5 mm. Postprocessed coronal
and curved MDCT multiplanar reconstruction (MPR) ima-
ges are recommended in cases of suspected AIP.
Pancreatic MR and MR cholangiopancreatography
(MRCP) imaging must be performed on a 1.5 T scanner
using a surface phased-array body coil. Patients are asked to
fast for 4–6 h before the MR examination. To eliminate
overlapping fluid-containing organs on T2-weighted MRCP
images, 50–150 ml of superparamagnetic iron oxide parti-
cles is administered 10–20 min before the MR examination.
Pancreatic MR imaging includes the following sequences:
axial T1-weighted gradient echo, axial T1-weighted fat-
saturated, axial T2-weighted fat-saturated rapid acquisition
with relaxation enhancement (RARE), T2-weighted half-
Fourier RARE, coronal true fast imaging in the steady-state
precession (true-FISP), axial and coronal, coronal oblique
2D half-Fourier RARE cholangiopancreatography, axial
fat-saturated 3D volumetric gradient echo. The dynamic
study, during gadolinium-chelate injection, is obtained by
means of a 3D volumetric gradient-echo pulse sequence
using parallel imaging. A quadriphasic dynamic study is
performed during injection of 0.1 mmol/kg body weight of
gadolinium chelates by means of a power injector at
2–2.5 ml/s, by acquiring the precontrast-phase, late arterial/
pancreatic phase (35–45 s), portal venous phase (75–80 s),
and delayed phase ([180 s). For diffusion-weighted imag-
ing (DWI), a spin-echo echoplanar sequence is performed
with a b value of 0, 50, 600 s/mm2. An apparent diffusion
coefficient (ADC) map is automatically calculated for each
section by the system’s software.
AIP: MDCT findings
Diffuse forms (DAIP)
The pancreatic parenchyma shows [15, 34–36] diffuse
enlargement (Fig. 1) and appears isodense compared to the
spleen on precontrast MDCT images (Fig. 1a); pancreatic
ductal stones are almost always absent at onset but they
may be present in advanced stages [37, 38].
Dynamic contrast-enhanced MDCT study is helpful in
the diagnosis: during the pancreatic phase, the parenchyma
is diffusely hypodense compared to the spleen because of
the lymphoplasmacytic infiltration and pancreatic fibrosis
(Fig. 1b, e). During the venous phase, the parenchyma
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Fig. 1 Diffuse autoimmune pancreatitis (DAIP) before and after
short-term high-dose steroid treatment. Multidetector computed
tomography (MDCT) imaging. Precontrast (a), contrast-enhanced
pancreatic (b, e), venous (c, f) and late (d) phases. Axial (a–d) and
multiplanar curved reconstructions (e, f) MDCT images. Diffuse
pancreatic enlargement is present (a–e). The pancreatic parenchyma
is homogeneously isodense compared to the spleen on the precontrast
MDCT image (a); pancreatic stones are absent. The pancreatic
parenchyma appears hypodense compared to the spleen during
contrast-enhanced MDCT pancreatic phase (b, e). During the portal
venous phase, it becomes more dense, appearing hyperdense
compared to the previous pancreatic phase (c). During the late phase
(d), the pancreatic parenchyma shows retention of contrast medium: it
is hyperdense compared to the previous venous phase. In the delayed
phase (d), a peripancreatic hyperdense halo is visible (‘‘capsule-like
rim’’: arrow). The intrapancreatic segment of the common bile duct is
slightly dilated (arrow head); the intrahepatic bile ducts are normal.
In the left kidney, a solid cortical lesion is present which later proved
to be chronic autoimmune pyelonephritis on biopsy (black arrows);
the right kidney shows a cystic lesion. Retroperitoneal fluid film,
peripancreatic stranding and enlarged lymphonodes are absent. Three
weeks after high-dose steroid treatment (f), the pancreatic paren-
chyma shows normal thickness and parenchymal vascularisation has
become normal during the contrast-enhanced pancreatic phase
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123
appears hyperdense in comparison to the previous pan-
creatic phase (Fig. 1c) and it shows retention of contrast
media during the delayed phase, becoming more hyper-
dense compared to the previous venous phase (Fig. 1d)
[37–43].
The pancreatic margins are smooth and well defined in
all phases of the dynamic contrast-enhanced MDCT study
(Fig. 1), probably due to peripancreatic tissue inflammation
[12, 13]. A capsule-like rim, appearing as a peripancreatic
hyperdense halo compared to the parenchyma, may be
present in the delayed phase (Fig. 1d). According to some
authors, this peripheral rim of delayed contrast enhance-
ment is due to the presence of a chronic inflammatory
process and fibrous tissue involving the peripancreatic fat
[15, 20, 21, 44]. The periductal inflammatory cell infiltra-
tion and fibrous tissue centred around the pancreatic ducts
[12, 13, 44–49] produce diffuse narrowing of the main
pancreatic duct (MPD). The MPD is frequently not visible
within a DAIP lesion in axial and MPR MDCT images
(Fig. 1a–e). If local MPD stenosis is present, the upstream
duct is dilated. Patients with AIP often demonstrate
enhancement of the MPD wall on CT imaging (the
‘‘enhanced duct sign’’) [42, 43] and this could reflect
periductal inflammatory changes. The enhanced duct sign
is strongly associated with the abnormal enhancement area
of the pancreas in AIP and, although relatively uncommon,
this finding may be useful for the diagnosis of AIP.
Both the enhanced duct sign and the inability to visu-
alise the MPD lumen within a DAIP lesion can aid in the
diagnosis of AIP. Furthermore, the side branches are not
visible in axial and MPR images. The intrapancreatic
segment of the common bile duct (CBD) may be normal or
stenotic in DAIP. Retroperitoneal fluid film, recorded at
MDCT images as thickening of the anterior pararenal
fascial plane, is never present in DAIP. Also peripancreatic
stranding, represented by inflammatory changes of peri-
pancreatic fat in mild acute non-necrotizing pancreatitis,
recorded as a hypodense peripancreatic halo in all phases
of CT examination [32, 37] is absent in DAIP [50].
DAIP must be differentiated from NNAP and lymphoma
since both these pathological conditions show diffuse
enlargement of the pancreatic parenchyma [19, 25, 51, 52].
In both DAIP and NNAP, pancreatic abdominal pain
with epigastric location irradiating to the back, increase of
serum amylase and lipase and diffuse pancreatic enlarge-
ment are frequently present [28–31]. The clinical differ-
entiation of DAIP from NNAP at onset is useful since only
DAIP responds to steroid treatment because of its auto-
immune pathogenesis [32–38, 45] (Fig. 2). Dynamic con-
trast-enhanced MDCT is helpful in differentiating DAIP
from NNAP because the parenchymal vascularisation is
significantly different in the two diseases [50, 53]. During
the pancreatic phase, the glandular parenchyma is
hypodense in DAIP (Fig. 1b, e) due to lymphoplasmacytic
infiltrates and pancreatic fibrosis, and isodense compared to
the spleen in NNAP, due to interstitial oedema without
areas of necrosis (Fig. 2b, d). During the portal venous
phase, DAIP appears hyperdense compared to the previous
pancreatic phase (Fig. 1c), while in NNAP the parenchyma
most frequently becomes hypodense during the portal
venous phase (Fig. 2c). DAIP shows retention of the con-
trast medium in the delayed phase (Fig. 1d) while NNAP
shows parenchymal wash-out. Recently, this vascularisa-
tion pattern of DAIP has been assessed using the rate of
relative variation in enhancement from the previous phase
or Relative Enhancement Rate across all phases of the
MDCT study [50]. Evaluation of the Relative Enhancement
Rate confirmed the particular vascularisation pattern of
DAIP, different from that of NNAP. The presence of a
peripheral rim of contrast enhancement in the delayed
MDCT phase, due to chronic inflammatory processes and
fibrosis involving the fatty peripancreatic tissue, is highly
suggestive of AIP (Fig. 1d) and absent in NNAP. A ret-
roperitoneal fluid film, a typical finding in NNAP (Fig. 2a–
d) due to retroperitoneal inflammation with peripancreatic
oedema, is absent in DAIP. Peripancreatic stranding,
appearing as a hypodense peripancreatic halo in all phases
of the MDCT examination, is due to mild inflammatory
changes of the fat surrounding the pancreas and is fre-
quently present in NNAP (Fig. 2a–d), whereas it is absent
in DAIP. A statistically significant difference in the two
groups of patients (DAIP and NNAP) regarding the pre-
sentation of peripancreatic stranding and retroperitoneal
fluid has been demonstrated [50]. In conclusion, the pattern
of MDCT contrast enhancement of DAIP and NNAP,
particularly considering the Relative Enhancement Rate
parameters [50], provides qualitative and quantitative clues
for differentiating the diseases. The retroperitoneal findings
of peripancreatic stranding and retroperitoneal fluid film,
characteristic of NNAP, and the late-phase peripheral rim
enhancement, characteristic of DAIP, can also assist in the
differential diagnoses.
Both in DAIP and in pancreatic lymphoma (Fig. 2e, f),
glandular enlargement and reduced parenchymal enhance-
ment in the pancreatic phase are present. In DAIP, the pan-
creatic parenchyma becomes more dense in the venous and
delayed phases, while in lymphoma it remains hypodense in
all MDCT phases. A late enhancing capsule-like rim is
suggestive of DAIP, whereas the presence of peripancreatic
and periaortic lymphadenopathy and/or focal solid splenic
lesions suggests the presence of lymphoma [54–56].
Focal forms (FAIP)
Focal parenchymal enlargement may be present exclu-
sively in the pancreatic head (Fig. 3a–d), in the body and
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Fig. 2 Diffuse autoimmune pancreatitis (DAIP): differential diagno-
sis with non-necrotizing acute pancreatitis (NNAP) and pancreatic
lymphoma. MDCT imaging. Precontrast (a), contrast-enhanced
pancreatic (b, d), venous (c, e, f) phases. Axial (a–c, e, f) and
multiplanar curved reconstructions (d) MDCT images. NNAP (a–d).
Diffuse pancreatic enlargement is present. Pancreatic parenchyma is
homogeneously isodense compared to the spleen on the precontrast
MDCT image (a); pancreatic stones are absent. The pancreatic
parenchyma appears isodense compared to the spleen during the
contrast-enhanced pancreatic phase (b, d). Areas of pancreatic
necrosis are not recognisable because of the mild inflammatory
pancreatic process and oedema. During the portal venous phase, the
pancreatic parenchyma becomes hypodense compared to the previous
pancreatic phase (c). A retroperitoneal fluid film is present in the
pararenal anterior space (arrow). The pancreatic gland is surrounded
by a hypodense halo in all MDCT phases (peripancreatic stranding:
arrow head) due to mild inflammatory changes of peripancreatic fat.
Pancreatic lymphoma (e, f). The pancreatic parenchyma appears
enlarged (especially in the pancreatic head) and hypodense during the
portal venous phase compared to the spleen. Diffuse intra- and extra-
hepatic bile duct dilatation (black arrow) is present. Pancreatic core
biopsies confirmed the diagnosis of non-Hodgkin lymphoma
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tail (Fig. 3e, f), or only in the pancreatic tail. Enlarged
glandular portions of the pancreas appear isodense com-
pared to the spleen on precontrast MDCT images (Fig. 3a).
Pancreatic ductal stones are always absent.
During the contrast-enhanced pancreatic phase of
MDCT, the enlarged parenchyma appears hypodense
(Fig. 3b, e) compared to the spleen and the unaffected
adjacent parenchyma, due to inflammatory cell infiltration
and glandular fibrosis [50]. During the venous phase
(Fig. 3c), the parenchyma in FAIP becomes more dense,
and appears hyperdense compared to its attenuation during
the previous pancreatic phase. During the delayed phase,
FAIP shows retention of contrast medium: the parenchyma
becomes more hyperdense compared to its attenuation in
the previous venous phase and to the adjacent unaffected
glandular portions.
As in DAIP, the pancreatic margins are smooth and well
defined in all phases of dynamic contrast-enhanced MDCT
(Fig. 3), probably due to the peripancreatic tissue inflam-
matory process. A capsule-like-rim appearing as a hyper-
dense halo compared to the parenchyma surrounding the
areas involved by FAIP may be present in the delayed
phase. This is probably due to chronic inflammatory and
fibrotic processes of the peripancreatic fat. When this
peripheral rim is present, it is highly suggestive of AIP [15,
40, 57].
The MPD is not visible within FAIP or it may present a
focal short stenosis with a short segment of upstream
dilatation in the axial and MPR MDCT images, reflecting
inflammatory cell infiltrates and fibrosis centred around the
pancreatic ducts (Fig. 3). The upstream MPD may be
dilated (Fig. 3), as it is in patients with adenocarcinoma, or
may be normal. Patients with FAIP also often demonstrate
enhancement of the MPD walls on MDCT imaging [42,
43]. This ductal enhancement may reflect periductal
inflammatory changes and, although relatively uncommon,
this finding may be useful for the diagnosis of AIP (Fig. 3e,
f). The enhanced duct sign is strongly associated with the
abnormal enhancement area of the pancreas in AIP. The
side branches are also not visible in the axial and MPR
MDCT images. The intrapancreatic segment of the CBD
may be normal or stenotic (Fig. 3) in FAIP of the pan-
creatic head. If CBD stenosis is present, suprapancreatic
CBD has an enlarged calibre.
FAIP needs to be differentiated from pancreatic ade-
nocarcinoma (Fig. 4) since both these diseases show focal
enlargement, frequently in the pancreatic head, bile duct
dilation and a similar clinical presentation at onset [58–61].
Differentiating FAIP from adenocarcinoma is important to
avoid unnecessary surgical procedures. In both diseases,
the affected parenchyma appears hypovascular, hypodense
in the pancreatic phase (Figs. 3, 4) of the dynamic contrast-
enhanced MDCT study. The upstream MPD is frequently
dilated in adenocarcinoma. In FAIP, the upstream MPD
may be dilated, as in adenocarcinoma, but it may also be
normal. The latter finding is uncommon in patients with
adenocarcinoma. Therefore, in patients with enlarged
pancreatic head and normal size of upstream MPD, FAIP
should be considered in the differential diagnosis. In FAIP,
however, the hypodensity of the affected parenchyma
decreases in the venous and late phases (Fig. 3), unlike in
the case of adenocarcinoma (Fig. 4). The margins in FAIP
are more sharply defined than in adenocarcinoma, without
any extrapancreatic extension. The peripancreatic vessels
are normal. The presence of a capsule-like rim excludes
adenocarcinoma. Sometimes, the final diagnosis can only
be confirmed by a fine-needle aspiration biopsy [62].
AIP: MR and MRCP findings
MR imaging, especially completed by MRCP, with or
without secretin stimulation, is recommended for the
identification and characterisation of parenchymal and
ductal change in AIP.
At MR imaging, the pancreatic parenchyma shows dif-
fuse (Fig. 5) or focal (Fig. 6) enlargement with sharp
borders. It presents an abnormal signal intensity, usually
hypointense on T1-weighted images (Fig. 6a) and hyper-
intense on T2-weighted images, compared to the liver [63,
64]. On T2-weighted images, an hypointense capsule-like
rim may be present.
During the pancreatic phase of the dynamic study, the
parenchyma affected by AIP appears hypointense compared
to the spleen in diffuse forms (Fig. 5a, d) and to the unaf-
fected parenchyma in focal forms (Fig. 6b) [63]. In both
diffuse and focal forms of AIP, the affected parenchyma
usually appears hyperintense during the portal venous phase
(Figs. 5b, 6c) compared with the previous pancreatic phase
and it appears hyperintense in the delayed phase (Figs. 5c,
6d) compared with the venous phase, due to the contrast
medium retention, as in the MDCT study [63].
MRCP best depicts the pancreatic and biliary ductal
systems and it has a good correlation with the endoscopic
retrograde cholangiopancreatography (ERCP). The MPD is
typically not dilated and generally not visible within the
affected pancreatic parenchyma because of extrinsic com-
pression by the periductal cell infiltrate (Figs. 5, 6e). In the
focal forms, the MPD may present an upstream dilation
(Fig. 6e). MRCP after secretin stimulation can be useful to
better visualise the MPD. It is particularly important in the
focal forms, when a short ductal stricture can mimic a
malignant process. Secretin is a polypeptide hormone that
induces pancreatic bicarbonate-rich fluid secretion into the
duodenum and increases the tone of the sphincter of Oddi
with a temporary distension of the pancreatic ducts. If the
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123
Fig. 3 Focal autoimmune pancreatitis (FAIP). MDCT imaging.
Precontrast (a), contrast-enhanced pancreatic (b, d, e), venous (c,
f) phases. Axial (a–c, e) and multiplanar curved reconstruction (d,
f) MDCT images. Two cases (a–d, e, f). In the first case (a–d), the
MDCT images show focal enlargement of the pancreatic head. The
pancreatic parenchyma of the enlarged glandular portion (short
arrow) is homogeneously isodense to the spleen on precontrast
MDCT image (a). Pancreatic stones are absent. The pancreatic
parenchyma appears hypodense compared to the spleen and unaf-
fected adjacent parenchyma of the body-tail during the contrast-
enhanced MDCT pancreatic phase (b, d). During the portal venous
phase, the pancreatic parenchyma becomes more dense appearing
hyperdense compared to the attenuation of the previous pancreatic
phase (c). The intrahepatic bile ducts are dilated. The main pancreatic
duct is not visible within FAIP. Stenting of the upstream main
pancreatic duct was performed (arrows) to treat duct stenosis. A
nasogastric tube is present (arrow head). In the second case (e, f), the
MDCT images show focal enlargement of the pancreatic body and
tail. The parenchyma appears hypodense during the contrast-
enhanced MDCT pancreatic phase (e). The main pancreatic duct is
partially invisible because of focal ductal stenosis due to lympho-
plasmacytic infiltration and areas of fibrosis in the pancreatic body
and head, with upstream main duct dilatation. Enhancement of the
main duct walls is present (the enhanced duct sign: arrows). The
intrapancreatic segment of the common bile duct is slightly dilated
(arrow head)
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123
MPD stricture resolves after secretin stimulation, this rules
out a malignancy and is suggestive of AIP (the so-called
‘‘duct penetrating sign’’) [61]. Finally, MRCP is important
for evaluating the involvement of the biliary ducts, which
is frequently associated because the periductal infiltration
can extend to the intrapancreatic CBD and even to its su-
prapancreatic segment.
Recently, some authors [65–68] have reported that the
affected pancreatic parenchyma in both diffuse and focal
forms of AIP appears slightly hyperintense in the axial MR
DW images with b value = 600 s/mm2 and the baseline
ADC value is lower than the normal pancreatic paren-
chyma of patients without chronic pancreatitis (Fig. 5e, f).
It is possible that replacement of normal pancreatic
parenchyma with a severe inflammatory cellular infiltration
of lymphocytes, plasma cells and granulocytes, fibrous
tissue and/or reduced exocrine pancreatic function may
reduce diffusible tissue water and result in decreased
measured ADCs. Thus, in diffuse forms there is a diffusion
restriction at DWI and the ADC is low. In most instances,
diffusion restriction is not discernible because the entire
pancreatic gland is involved. When only a focal region is
involved this finding is more indicative. On the other hand,
DWI and ADC values are variable in pancreatic cancer,
allowing for this modality to differentiate between mass-
forming focal AIP and pancreatic carcinoma.
The final differential diagnosis between focal DAIP and
pancreatic cancer can only be confirmed by a fine-needle
aspiration biopsy [62, 69, 70].
Extrapancreatic AIP: MDCT and MR findings
CT and MR can identify some of the many extrapancreatic
manifestations of AIP, most commonly biliary, renal and
retroperitoneal [17, 71].
Biliary involvement, present in up to 80 % of AIP
patients, is the most common extrapancreatic involvement.
Both intrahepatic and extrahepatic bile ducts can be
involved, showing multifocal stenosis and wall thickening
Fig. 4 Focal autoimmune pancreatitis (FAIP): differential diagnosis
with pancreatic adenocarcinoma. MDCT imaging. Precontrast (a),
contrast-enhanced pancreatic (b), venous (c) and late (d) phases.
Axial MDCT images. MDCT images show focal enlargement of the
pancreatic head. The pancreatic head parenchyma is hypodense
compared to the spleen on precontrast MDCT images (a). The
pancreatic head lesion (short arrow) appears more hypodense
compared to the spleen and to the body-tail during pancreatic (b),
venous (c) and late (d) phases. The main pancreatic duct of the body-
tail (arrow) is dilated. The mesenteric vein lumen (arrow head) near
the solid lesion in the pancreatic head has a reduced diameter
(vascular infiltration)
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123
resembling primary sclerosing cholangitis. [72]. MDCT
shows only focal or diffuse thickening and enhancement of
bile duct wall. If the gallbladder is involved, it shows
diffuse wall thickening.
Biliary involvement by AIP is, therefore, best evaluated
by MRCP. This is an important technique to evaluate
involvement of the biliary ducts, which is frequently
associated because the periductal infiltration can extend to
the intrapancreatic CBD and even to its suprapancreatic
segment. This causes thickening and enhancement of the
CBD walls, a pattern similar to primary sclerosing cho-
langitis [73].
Renal involvement (Figs. 1, 6) is more rare than biliary
involvement (35 %). Renal lesions in AIP patients are
often multiple, bilateral cortex solid nodular lesions fre-
quently well circumscribed and well shaped. At MDCT
(Fig. 1) and MR imaging (Fig. 6), they appear as cortical
solid lesions, which are hypovascular during the pancreatic
Fig. 5 Diffuse autoimmune pancreatitis (DAIP). MR imaging. Axial
3D volumetric T1-weighted fat-suppressed gradient-echo images after
intravenous contrast medium administration during pancreatic (a),
venous (b) and delayed phase (c). Coronal true fast imaging in the
steady-state precession (true-FIST) (d). Diffusion-weighted MR
imaging (DWI): axial spin-echo echoplanar DW image with
b value = 600 s/mm2 (e); axial apparent diffusion coefficient
(ADC) map calculated from baseline images obtained with b value
of 0, 50, 600 (f). The overall pancreatic gland is enlarged with sharp
borders (a–d) and presents decreased enhancement in the arterial
pancreatic phase (a, d) compared to the spleen, with an increased
progressive contrast uptake during the venous (b) and the delayed
(c) phases. The affected pancreatic parenchyma appears slightly
hyperintense in the DW images (e) with lower ADC value (f) than
patients without pancreatitis due to a severe inflammatory cellular
infiltration (lymphocytes, plasma cells and granulocytes)
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phase of both modalities (Fig. 1b), with enhancement in
the venous (Fig. 1c) and delayed phases (Figs. 1d, 6f).
These lesions respond to steroid treatment with a reduction
in size.
Retroperitoneal involvement in AIP is represented by
retroperitoneal fibrosis. MDCT and MR identify a soft
tissue mass surrounding peripancreatic (Fig. 7a, b) and
retroperitoneal (Fig. 7d) vessels.
Fig. 6 Focal autoimmune pancreatitis (FAIP). MR imaging. Axial
3D volumetric T1-weighted fat-suppressed gradient-echo images
before (a) and after intravenous contrast medium administration
during the pancreatic (b), venous (c) and delayed phases (d, f). MR
cholangio-pancreatography (e). The parenchyma of the pancreatic
body-tail shows focal enlargement (arrows) with sharp borders and
abnormal signal intensity: it appears hypointense in the T1-weighted
images (a) compared to the unaffected parenchyma. In the dynamic
study, the AIP-affected parenchyma shows decreased enhancement
during the pancreatic phase (b), with a homogeneous and progressive
contrast uptake during the venous (c) and delayed phases (d). The
main pancreatic duct is not visible within the FAIP (e: arrowhead),
compressed by the crowded cellularity all around, with an upstream
dilation (e). This patient also presents renal involvement (f) with
multiple, bilateral, cortical solid lesions (black arrows: autoimmune
pyelonephritis)
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123
Post-treatment focal and diffuse AIP: MDCT and MR
findings
After a short-term treatment (2–3 weeks) with high-dose
steroid (Figs. 1f, 7e, f), MDCT and MR imaging can identify
a significant reduction in size of the pancreatic parenchyma
both in the diffuse and focal forms, as well as normalisation
of the calibre of the upstream MPD in the pancreatic head or
body of focal AIP [71]. Pancreatic enhancement during
MDCT and MR dynamic studies also becomes normal in
AIP. Both in diffuse and focal AIP, the pancreatic paren-
chyma appears isovascular to the spleen in the enhanced
Fig. 7 Extrapancreatic AIP findings. MDCT imaging. Contrast-
enhanced pancreatic (a–c, e), venous (d, f) phases. Axial (a, c–
f) and multiplanar coronal reconstruction (b). Two cases (a, b, c–f). In
both cases (a, b, c–f), diffuse pancreatic enlargement and hypodense
pancreatic parenchyma are present during the pancreatic phase.
MDCT also shows a retroperitoneal soft tissue mass surrounding
peripancreatic vessels (a, b: arrows) and right side pelvic vessels (d:
arrow). Histological analysis of pancreatic, retroperitoneal and pelvic
soft tissue mass showed lymphoplasmacytic infiltrate and fibrosis. In
the second case, the pancreatic parenchyma (e) and pelvic soft tissue
mass (f: arrow) are reduced in size at follow-up CT 3 weeks after
high-dose steroid treatment
Radiol med
123
pancreatic phase and hypovascular in the venous phase, with
wash-out in the delayed phase. Finally, MDCT and MR
imaging can easily identify normalisation of the calibre of
the intra- and suprapancreatic common bile duct [19, 20, 37].
The Japan Pancreas Society has proposed diagnostic cri-
teria for the diagnosis of AIP [74–78]. These criteria include:
the finding of typical pancreatic imaging results (enlargement
of the pancreatic parenchyma and MPD narrowing), positive
laboratory tests (autoantibodies and elevated serum levels of
immunoglobulin G4) and positive histopathologic al findings
(lymphoplasmacytic infiltrate and pancreatic fibrosis). When
all three diagnostic criteria proposed by the Japan Pancreas
Society are present, AIP diagnosis is easy. However, there are
clinical conditions in which AIP diagnosis and the differential
diagnosis with other pancreatic diseases may be difficult. The
differential diagnosis of AIP is difficult when a patient with
typical clinical findings has other associated autoimmune
disorders with only non-specific imaging and/or histopathol-
ogical findings. In all the cases in which AIP is strongly sus-
pected but the diagnosis is uncertain, MDCT and MR are
useful imaging modalities to suggest the correct diagnosis.
Repeated MDCT and/or MR examinations after short-term
treatment (2–3 weeks) with high-dose steroids can identify a
significant reduction in the size of pancreatic parenchyma, and
the normalisation of the calibre of the MPD and bile ducts. The
results of this short-term follow-up are obviously present in
AIP and absent in the case of pancreatic adenocarcinoma. The
response at short-term imaging follow-up after steroid treat-
ment was recently considered a diagnostic criterion of AIP [1].
Conflict of interest RGraziani, S. Mautone, M.C. Ambrosetti, R.
Manfredi, T.J. Re, L. Calculli, L. Frulloni, R. Pozzi Mucelli declare
no conflict of interest.
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