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Mass forming chronic pancreatitis mimicking pancreatic cystic neoplasm: A case report

Authors:

Abstract

Mass forming chronic pancreatitis is very rare. Diagnosis could be done by the pathologic findings of focal inflammatory fibrosis without evidence of tumor in pancreas. A 34-year-old man presented with right upper abdominal pain for a few weeks and slightly elevated bilirubin level on clinical findings. Radiological findings of multidetector-row computed tomography, magnetic resonance (MR) imaging with MR cholangiopancreatography and endoscopic ultrasonography revealed focal branch pancreatic duct dilatation with surrounding delayed enhancing solid component at uncinate process and head of pancreas, suggesting branch duct type intraductal papillary mucinous neoplasm. Surgery was done and pathology revealed the focal chronic inflammation, fibrosis, and branch duct dilatation. Herein, I would like to report the first case report of mass forming chronic pancreatitis mimicking pancreatic cystic neoplasm.
World Journal of
Gastroenterology
World J Gastroenterol 2018 January 14; 24(2): 161-314
ISSN 1007-9327 (print)
ISSN 2219-2840 (online)
Published by Baishideng Publishing Group Inc
S
MINIREVIEWS
161 Drug-eluting beads transarterial chemoembolization for hepatocellular carcinoma: Current state of the art
Facciorusso A
ORIGINAL ARTICLE
Basic Study
170 AntibrogeniceffectsofvitaminDderivativesonmousepancreaticstellatecells
Wallbaum P, Rohde S, Ehlers L, Lange F, Hohn A, Bergner C, Schwarzenböck SM, Krause BJ, Jaster R
179 Metabolicandhepaticeffectsofliraglutide,obeticholicacidandelabranorindiet-inducedobesemouse
modelsofbiopsy-conrmednonalcoholicsteatohepatitis
Tølbøl KS, Kristiansen MNB, Hansen HH, Veidal SS, Rigbolt KTG, Gillum MP, Jelsing J, Vrang N, Feigh M
195 INT-767improveshistopathologicalfeaturesinadiet-induced
ob/ob
mousemodelofbiopsy-conrmednon-
alcoholic steatohepatitis
Roth JD, Feigh M, Veidal SS, Fensholdt LKD, Rigbolt KT, Hansen HH, Chen LC, Petitjean M, Friley W, Vrang N, Jelsing J,
Young M
211 Novelconceptofendoscopicdevicedeliverystationsystemforrapidandtightattachmentofpolyglycolic
acid sheet
Mori H, Kobara H, Nishiyama N, Masaki T
216 β-arrestin2attenuateslipopolysaccharide-inducedliverinjury
via
inhibition of TLR4/NF-kB signaling
pathway-mediatedinammationinmice
Jiang MP, Xu C, Guo YW, Luo QJ, Li L, Liu HL, Jiang J, Chen HX, Wei XQ
226 HepatitisCviruscoreprotein-inducedmiR-93-5pup-regulationinhibitsinterferonsignalingpathwayby
targeting IFNAR1
He CL, Liu M, Tan ZX, Hu YJ, Zhang QY, Kuang XM, Kong WL, Mao Q
237 Transplantationofbonemarrow-derivedendothelialprogenitorcellsandhepatocytestemcellsfromliver
brosisratsamelioratesliverbrosis
Lan L, Liu R, Qin LY, Cheng P, Liu BW, Zhang BY, Ding SZ, Li XL
Case Control Study
248 Geneticvariantsofinterferonregulatoryfactor5associatedwithchronichepatitisBinfection
Sy BT, Hoan NX, Tong HV, Meyer CG, Toan NL, Song LH, Bock CT, Velavan TP
Contents Weekly Volume 24 Number 2 January 14, 2018
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Contents World Journal of Gastroenterology
Volume 24 Number 2 January 14, 2018
Retrospective Study
257 Timingofsurgeryafterneoadjuvantchemotherapyforgastriccancer:Impactonoutcomes
Liu Y, Zhang KC, Huang XH, Xi HQ, Gao YH, Liang WQ, Wang XX, Chen L
266 PredictiveandprognosticvalueofserumAFPlevelanditsdynamicchangesinadvancedgastriccancer
patientswithelevatedserumAFP
Wang YK, Zhang XT, Jiao X, Shen L
SYSTEMATIC REVIEWS
274 Neoadjuvantchemotherapyforgastriccancer.Isitamustorafake?
Reddavid R, Soa S, Chiaro P, Colli F, Trapani R, Esposito L, Solej M, Degiuli M
CASE REPORT
290 Clinically diagnosed late-onset fulminant Wilson’s disease without cirrhosis: A case report
Amano T, Matsubara T, Nishida T, Shimakoshi H, Shimoda A, Sugimoto A, Takahashi K, Mukai K, Yamamoto M, Hayashi S,
Nakajima S, Fukui K, Inada M
297 Massformingchronicpancreatitismimickingpancreaticcysticneoplasm:Acasereport
Jee KN
303 Successfultreatmentofagiantossiedbenignmesentericschwannoma
Wu YS, Xu SY, Jin J, Sun K, Hu ZH, Wang WL
LETTER TO THE EDITOR
310
Candida
accommodates non-culturable
Helicobacter pylori
initsvacuole-Koch’spostulatesaren’tapplicable
Siavoshi F, Saniee P
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NAME OF JOURNAL
World Journal of Gastroenterology
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ISSN 1007-9327 (print)
ISSN 2219-2840 (online)
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Stephen C Strom, PhD, Professor, Department of
Laboratory Medicine, Division of Pathology, Karo-
linska Institutet, Stockholm 141-86, Sweden
Andrzej S Tarn awski , MD, PhD, DSc (Med),
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INDEXING/ABSTRACTING
AIMS AND SCOPE
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Mass forming chronic pancreatitis mimicking pancreatic
cystic neoplasm: A case report
Keum Nahn Jee
Keum Nahn Jee, Department of Radiology, Dankook University
Hospital, Chungcheongnam-do 330-715, South Korea
ORCID number: Keum Nahn Jee: (0000-0003-2669-4381).
Author contributions: Jee KN designed the report, collected
the patient’s clinical data, drafting the article and reviewed the
manuscript and approved the nal manuscript as submitted.
Informed consent statement: This study was reviewed and
approved the retrospective case review by Institutional Review
Board of Dankook University Hospital, Cheonan, South Korea,
with informed consent from the patient waived.
Conict-of-interest statement: There are no potential conicts
(financial, professional, or personal) of interest relevant to this
article to disclose by the author.
Open-Access: This article is an open-access article which was
selected by an in-house editor and fully peer-reviewed by external
reviewers. It is distributed in accordance with the Creative
Commons Attribution Non Commercial (CC BY-NC 4.0) license,
which permits others to distribute, remix, adapt, build upon this
work non-commercially, and license their derivative works on
different terms, provided the original work is properly cited and
the use is non-commercial. See: http://creativecommons.org/
licenses/by-nc/4.0/
Manuscript source: Unsolicited manuscript
Correspondence to: Keum Nahn Jee, MD, PhD, Professor,
Department of Radiology, Dankook University Hospital,
Mang-hyang Street 201, Anseo-dong, Dongnam-gu, Cheonan,
Chungcheongnam-do 330-715,
South Korea. jkn1303@dkuh.co.kr
Telephone: +82-41-5506921
Fax: +82-41-5529674
Received: October 19, 2017
Peer-review started: October 20, 2017
First decision: November 8, 2017
Revised: November 15, 2017
Accepted: November 22, 2017
Article in press: November 22, 2017
Published online: January 14, 2018
Abstract
Mass forming chronic pancreatitis is very rare.
Diagnosis could be done by the pathologic findings
of focal inflammatory fibrosis without evidence of
tumor in pancreas. A 34-year-old man presented
with right upper abdominal pain for a few weeks and
slightly elevated bilirubin level on clinical findings.
Radiological findings of multidetector-row computed
tomography, magnetic resonance (MR) imaging
with MR cholangiopancreatography and endoscopic
ultrasonography revealed focal branch pancreatic duct
dilatation with surrounding delayed enhancing solid
component at uncinate process and head of pancreas,
suggesting branch duct type intraductal papillary
mucinous neoplasm. Surgery was done and pathology
revealed the focal chronic inflammation, fibrosis, and
branch duct dilatation. Herein, I would like to report the
first case report of mass forming chronic pancreatitis
mimicking pancreatic cystic neoplasm.
Key words: Chronic pancreatitis; Pseudotumor; Com-
puted tomography; Magnetic resonance imaging; En-
doscopic ultrasound
© The Author(s) 2018. Published by Baishideng Publishing
Group Inc. All rights reserved.
Core tip: Extremely unusual radiological manifestation
of ma ss form ing chroni c pancreat itis mimic king
pancreatic cystic neoplasm is the rst case report in the
English-written medical literature.
Jee KN. Mass forming chronic pancreatitis mimicking pancreatic
cystic neoplasm: A case report. World J Gastroenterol 2018;
CASE REPORT
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Submit a Manuscript: http://www.f6publishing.com
DOI: 10.3748/wjg.v24.i2.297
World J Gastroenterol 2018 January 14; 24(2): 297-302
ISSN 1007-9327 (print) ISSN 2219-2840 (online)
24(2): 297-302 Available from: URL: http://www.wjgnet.
com/1007-9327/full/v24/i2/297.htm DOI: http://dx.doi.
org/10.3748/wjg.v24.i2.297
INTRODUCTION
Chronic pancreatitis represents a recurrent, prolonged
inflammatory process and progressive fibrosis of the
pancreas. These results in irreversible morphologic
change of the pancreas, clinical symptoms of abdominal
pain, and insufficiency of exocrine and endocrine
function[1-3]. On computed tomography (CT) and ma-
gnetic resonance (MR) image, dilatation of the main
pancreatic duct, parenchymal atrophy, pancreatic ca-
lcification or stone, focal pancreatic enlargement or
inflammatory pancreatic mass, bile duct dilatation,
attenuation change of peripancreatic fat and fluid colle
ction are frequent findings[4-6].
Inflammatory mass in chronic pancreatitis retain a
large degree of fibrosis like pancreatic carcinoma[7-9],
and both lesions are shown as a gradual progressive
enhancement on contrast-enhanced CT and dynamic
MR imaging, making the discrimination of the two
entities difficult[5,6,10].
In the case of mass forming chronic pancreatitis,
diagnosis of inflammatory pancreatic mass could be
almost impossible if associated radiological findings of
chronic pancreatitis is not shown.
This paper presents a very unique case of mass
forming chronic pancreatitis mimicking pancreatic
cystic neoplasm.
CASE REPORT
A 34-year-old man complained for right upper abdominal
pain for a few days. His laboratory findings including
white blood cell count, C-reactive protein, alkaline
phosphatase, liver enzyme level and tumor markers
of carbohydrate antigen 19-9 and carcinoembryonic
antigen were within normal range except slight elevation
of total bilirubin (1.3 mg/dL, normal range of 0.2-1.2),
gamma-glutamyl transferase (108 IU/L, normal range
of 8-60) and lipase (90 U/L, normal range of 30-60).
The patient had past medical history of admission due
to acute alcoholic pancreatitis 13 years ago and social
history of daily alcohol consumption for 15 years and
having smoked 20 pack years.
Unenhanced abdomen CT image showed slight low
attenuating lesion involving pancreatic uncinate process
and head (Figure 1A). Contrast-enhanced abdominal
CT images showed a delayed enhancing solid portion
surrounding a few tubular cystic attenuating lesion
sized about 2.5 cm × 2.1 cm in pancreatic uncinate
process and head, and mild dilatation of common bile
duct (CBD) and gallbladder (Figure 1B and C). MR
cholangiopancreatography showed branch pancreatic
duct dilation in head and uncinate process causing
extrinsic indentation and tapering of distal CBD, and mild
dilatation of proximal CBD and gallbladder (Figure 2A).
Fat-saturated T2-weighted MR image showed a slight
high signal intensity solid component surrounding bright
signal intensity branch duct dilatation in pancreatic
uncinate process and head, with the lesion sized about
2.6 cm × 2.2 cm (Figure 1B). Fat-suppressed T1-
weighted MR image showed a well-demarcated low
signal intensity lesion in head and uncinate process of
pancreas (Figure 2C), and delayed contrast-enhancing
solid component surrounding low signal intensity branch-
duct dilation in pancreatic uncinate process and head
was shown on fat-suppressed T1-weighted dynamic
gadolinium-enhanced MR images (Figure 2D and E).
Diffusion-weighted MR images showed higher signal
intensity on low b factor (b = 20 s/m2) image and low
signal intensity on high b factor (b = 800 s/m2) image,
suggesting no diffusion restriction on apparent diffusion
coefficient map (Figure 2H), which reflecting the large
area of cystic component of the lesion. Endoscopic
ultrasonography (EUS) showed pruning pattern,
anechoic branch duct dilatation containing a few small
hyperechoic mural nodules (Figure 3A and B).
The lesion located in uncinate process and head of
pancreas with indenting distal CBD and dilatation of
proximal CBD, without dilatation of main pancreatic duct
due to anatomic variation of pancreatic divisum which
was detected on MR image (Figure 2B). Radiological
diagnostic impression was branch duct type intraductal
papillary mucinous neoplasm (IPMN) of pancreas.
However, some worrisome features of delayed contrast-
enhancing solid component around the wall of dilated
branch duct on CT and MR images and small mural
nodules in dilated branch ducts on EUS were shown.
EUS guided fine needle aspiration (FNA) cytology was
obtained from the solid component along the wall of
dilated duct and suggested the possibility of intraductal-
growing epithelial neoplasm.
The patient underwent pylorus-preserving pan-
creaticoduodenectomy, due to considering FNA finding,
imaging findings of CT, MRI, and EUS and aggravated
right upper abdominal pain and persistent mild elevation
of bilirubin and gamma-glutamyl transferase levels
without response to conservative medical treatment for
four weeks. The gross pathology of resected specimen
showed whitish hard infiltrating lesion in pancreatic
uncinate process and head portion (Figure 4A). The
histopathologic report revealed periductal inflammation
with fibrosis and mild dilatation of branch pancreatic
ducts and intralobular fibrosis, consistent with chronic
pancreatitis (Figure 4B).
DISCUSSION
Chronic pancreatitis is defined as inflammatory and
fibrotic disease of pancreatic tissue, characterized
by irreversible functional and morphologic change.
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Jee KN. Mass forming chronic pancreatitis
Alcohol abuse is the most common (70%-80%) cause
of chronic pancreatitis in the developed countries[1,2,3,7].
In addition, smoking, gene mutations, autoimmune
syndromes, metabolic disturbances, environmental
conditions and anatomical abnormalities are suggested
as other associated factors with occurrence of the
disease[3,11,12].
The pathology of advanced alcoholic chronic pan-
creatitis revealed a firm consistency of pancreas with
an irregular contour without the normal lobulation[13].
The fibrosis may diffusely affect the entire gland, but
occasionally it is unevenly distributed, with preserved
normal lobular pattern in some areas. The severity
of the duct changes depends on the extent of the
surrounding fibrosis. Thus, the main duct may be focally
or diffusely involved with obstruction, irregular dilatation
and distortion[14,15]. Fibrosis in the pancreas head may
cause a tapering stenosis of CBD[16].
In this case, initial clinical symptom of right upper
abdominal pain was developed due to dilatation of
gallbladder by stenosis of distal CBD, and the causative
lesion of CBD obstruction was a focal mass lesion,
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A B C
Figure 1 Findings from computed tomography. A: Unenhanced computed tomography (CT) image shows a slight low attenuating lesion (arrow) in pancreatic
uncinated process and head and dilatation of gallbladder; B: Contrast-enhanced arterial phase CT image shows minimal enhancing low attenuating lesion (long arrow)
surrounding a few tubular low cystic attenuating structures (short arrow), and homogenous highly enhancing normal pancreas (arrowhead); C: Contrast-enhanced
portal venous phase CT image shows delayed enhancing lesion (long arrow) containing a few tubular cystic structures (short arrow).
Figure 2 Findings from magnetic resonance image. A: Magnetic resonance (MR) cholangiopancreatography shows localized branch pancreatic duct dilatation (short
arrow) in head of pancreas with tapering of distal common bile duct and dilatation of proximal common duct (long arrow); B: T2-weighted MR image shows slight high
signal intensity lesion (long arrow) containing bright intensity branch duct dilatation (short arrow) in head and uncinate process of pancreas, and incidental nding
of pancreatic divisum (arrowhead); C: Fat-suppressed T1-weighted MR image shows a well-demarcated low signal intensity lesion (long arrow) in uncinate process
and head of pancreas; D-E: Fat-suppressed T1-weighted gadolinium-enhanced arterial- (D) and delayed-phase (E) MR images show delayed highly enhancing solid
mass-like lesion (long arrows) containing non-enhancing dark intensity branch duct dilatation (short arrows) in pancreatic head; F: The higher signal intensity lesion
(arrow) on diffusion-weighted image obtained with b = 20 s/m2 shows as low signal intensity (arrow) on diffusion-weighted image obtained with b = 800 s/m2 and as
higher (arrow) apparent diffusion coefcient (ADC) without diffusion restriction.
EF
A B C D
b
= 20 ADC
G H
b
= 800
Jee KN. Mass forming chronic pancreatitis
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CT in spectral imaging mode, 18F fluorodeoxyglucose
positron emission tomography/CT combined with
carbohydrate antigen 19-9, and quantitative endoscopic
ultrasound elastography, but still it is very difficult to
distinguish accurately between the two[5,10,20-24]. MRI is
much better than CT for detection and characterization
of focal pancreatic lesion, but it could not differentiate
mass forming chronic pancreatitis from pancreatic
carcinoma, even using diffusion-weighted functional
MR imaging technique[5,10,25,26]. In addition, none of the
above mentioned papers included a case of a solid mass
containing cystic lesion like this in their research of
differentiation between mass forming pancreatitis and
pancreatic carcinoma.
Among the papers on relationship between main
pancreatic duct (MPD) and the mass, theduct-penetrating
sign of MPD on MR cholangiopancreatography was
reported to be helpful with relatively high sensitivity and
specificity, and the result was smoothly stenotic or normal
MPD penetrating a mass was seen more frequently
in inflammatory pancreatic mass than in pancreatic
carcinoma[27]. However, in this peculiar case, inflammatory
mass possessed dilated branch pancreatic duct without
stenosis.
In this very unique case, it could be comprehended
including branch duct dilatation with surrounding solid
component in uncinate process and head of pancreas,
detected on CT, MRI and EUS findings. The diagnostic
impression based on radiological imaging findings
was branch duct type IPMN most likely and serous
cystadenoma as a possible differential diagnosis.
In thinking of branch duct type IPMN, analyses of
imaging findings included the “worrisome features” of
contrast-enhancing ductal margin on CT and MRI and
mural nodules in dilated duct on EUS[17-19]. In addition,
FNA suggested intraductal-growing epithelial neoplasm
though scant cellularity. Surgery was the best choice
at that time, considering aggravated clinical symptom,
radiological findings, opinion of FNA, and patient’s
young age. However, final pathologic result revealed
interlobular and intralobular inflammation and fibrosis
associated with branch duct dilatation, compatible with
chronic pancreatitis. It was a totally unexpected one,
even though considering patient’s past medical history
of severe alcoholic pancreatitis and social history of
frequent alcohol consumption and heavy smoking.
There have been many reports for the differentiation
mass forming chronic pancreatitis from pancreatic
adenocarcinoma such as dynamic enhancement of CT
and MR imaging, Perfusion CT imaging, duel energy
A B
CBD
Figure 3 Findings from endoscopic ultrasound. A: EUS shows a few anechoic tubular structures (arrows), causing indentation of distal CBD and dilatation of
proximal bile duct; B: EUS shows small hyperechoic mural nodules (arrows) in the dilated branch pancreatic ducts. EUS: Endoscopic ultrasound; CBD: Common bile
duct.
A B
Figure 4 Macroscopic and microscopic ndings of resected specimen. A: Gross specimen shows whitish hard inltrating mass-like lesion (arrows) focally
replaced head and uncinate process of pancreas; B: Microscopy (hematoxylin and eosin, x 40) shows perilobular and intralobular brosis (asterisk) replaces normal
pancreatic acini with focal perivascular lymphocyte inltration (short arrow) and dilated branch ducts (long arrows).
*
Jee KN.
Mass forming chronic pancreatitis
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uneven fibrosis and inflammation developed in localized
area of uncinate process and head of pancreas, focal
severe perilobular and interlobular fibrosis caused
stricture and dilatation of branch pancreatic duct in
uncinate process, and the these outbreaks led to very
distinctive and peculiar radiological features of mass
forming chronic pancreatitis and clinical symptoms of
bile duct obstruction.
There has been no literature about focal fibrotic
mass forming chronic pancreatitis containing branch
duct dilatation, and incidentally this lesion showed
almost typical imaging findings of pancreatic cystic
neoplasm.
ARTICLE HIGHLIGHTS
Case characteristics
A 34-year-old man was referred to our hospital with right upper abdominal pain,
and a pancreatic solid and cystic lesion found on computed tomography (CT),
magnetic resonance (MR) image with MR cholangiography, and endoscopic
ultrasonography (EUS).
Clinical diagnosis
Branch duct type intraductal papillary mucinous neoplasm.
Differential diagnosis
Serous cystadenoma among solid and cystic pancreatic neoplasms.
Laboratory diagnosis
Abnormal laboratory results included slightly elevated level of total bilirubin (1.3
mg/dL, normal range of 0.2-1.2) and gamma-glutamyl transferase (108 IU/L,
normal range of 8-60).
Imaging diagnosis
CT and MR imaging showed a delayed contrast-enhanced solid lesion
containing pruning-pattern branch duct dilatation in uncinate process and head
of pancreas, with small hyperechoic mural nodules in the dilated branch ducts
on EUS.
Pathological diagnosis
Microscopic findings of resected specimen revealed mass forming chronic
pancreatitis including branch duct dilatation.
Treatment
The patient was treated with pylorus-preserving pancreaticoduodenectomy.
Related reports
There have been many reports for the discrimination between mass forming
chronic pancreatitis and pancreatic adenocarcinoma using various imaging
modalities.
Term explanation
There are no non-standard medical terms used in this manuscript.
Experiences and lessons
The author presents this case to share the very unusual but important
knowledge that mass forming chronic pancreatitis might include the branch duct
dilatation.
ACKNOWLEDGEMENTS
I wish to thank to Drs. Sung Ho Cho (Department of
Surgery, Dankook University Hospital) and Won-Ae
Lee (Department of Pathology, Dankook University
Hospital) for their comments and discussions about
the case.
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ARTICLE HIGHLIGHTS
Jee KN. Mass forming chronic pancreatitis
302 January 14, 2018
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Association of Pancreatology. International consensus guidelines
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P- Reviewer: Agrawal S, Tandon RK S- Editor: Chen K
L- Editor: A E- Editor: Ma YJ
Jee KN. Mass forming chronic pancreatitis
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... UPT yra reta gerybinė liga, pirmą kartą aprašyta Pack 1939 m. (plaučiuose) ir 1953 m. Baker (kepenyse) [6]. UPT gali imituoti piktybinį naviką klinikinio, radiologinio ar histologinio ištyrimo metu [7]. Nors pseudotumorai dažniausiai pažeidžia plaučius, jie gali būti aptinkami ir kituose organuose -centrinėje nervų sistemoje, pagrindinėse seilių liaukose, gerklose, krūtyse, kiaušidėse, šlapimo pūslėje, inkstuose, blužnyje, kepenyse, kasoje, akiduobės audiniuose, limfmazgiuose, taukinėje, odoje ir minkštuosiuose audiniuose [1,7]. ...
... UPT gali imituoti piktybinį naviką klinikinio, radiologinio ar histologinio ištyrimo metu [7]. Nors pseudotumorai dažniausiai pažeidžia plaučius, jie gali būti aptinkami ir kituose organuose -centrinėje nervų sistemoje, pagrindinėse seilių liaukose, gerklose, krūtyse, kiaušidėse, šlapimo pūslėje, inkstuose, blužnyje, kepenyse, kasoje, akiduobės audiniuose, limfmazgiuose, taukinėje, odoje ir minkštuosiuose audiniuose [1,7]. ...
... Uždegiminių psedudotumorų etiologija nėra aiški, tačiau manoma, kad tai gali būti susiję su infekcijomis, chemoterapija ar radiacija, intraparenchiminiu kraujavimu, autoimuniniais susirgimais ar kitomis ligomis, pavyzdžiui, cukriniu diabetu, Krono liga, Sjögren sindromu, lėtiniu kylančiuoju cholangitu, podagra, ūmine mieloblastine leukemija, autoimuniniu pankreatitu ir kt. [6,7]. Pristatytame klinikiniame atvejyje KT vaizduose buvo stebimi kasos audinio pokyčiai (nežymiai fragmentuotas audinys su gausia kalcifikacija), kurie galimai išsivystė dėl lėtinio pankreatito, be to, histologinio tyrimo atsakyme suformuluota išvada -lėtinis fibrozuojantis pankreatitas. ...
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Kasos vėžys yra viena dažniausių mirties nuo vėžio priežasčių išsivysčiusiose šalyse, tačiau yra ne viena nenavikinės kilmės būklė, kurios metu gali formuotis kasos dariniai, imituojantys šio organo vėžį. Viena jų – uždegiminis pseudotumoras. Jo dažnai nepavyksta diferencijuoti nuo kitų agresyvesnių neneoplastinės kilmės darinių, remiantis vien klinikiniais ir radio­loginiais tyrimais – diagnozei patikslinti reikalingas histologinis tyrimas. Šiame straipsnyje pristatomas uždegiminio pseudotumoro klinikinis atvejis, kai šis darinys imitavo kasos vėžį, o tiksli diagnozė buvo nustatyta tik atlikus išsamesnius radiologinius ir his­tologinį tyrimus.
... In the initial clinicopathological study, it was difficult to determine whether the original disease was IPMN or other disease, including pseudocysts, retention cysts, and mucinous non-neoplastic cysts (9). Jee reported a case of massforming pancreatitis that mimicked pancreatic cystic neoplasm (10). Kwon reported a case in which xanthogranulomatous pancreatitis mimicked a malignant tumor and speculated that cystic lesions might be originally present in the gross morphology (11). ...
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We herein report a case of a branch-duct intraductal papillary mucinous neoplasm (IPMN) with rapidly developing intracystic xanthogranulomatous nodules. A unilocular cystic lesion without a mural nodule was found in the pancreatic tail of a 69-year-old man. Ten months later, multiple mural nodules emerged unexpectedly within the cyst, and the patient underwent distal pancreatectomy. Based on immunohistochemical studies and a molecular analysis, we diagnosed him with branch-duct IPMN of the gastric immunophenotype. Fragility of the pancreatic duct mucosa and consequent exposure of the wall to pancreatic juice might have caused marked granulation nodule formation in the cyst lumen.
... Chronic pancreatitis (CP) is a disease of prolonged pancreatic inflammation, resulting in irreversible damage of the exocrine parenchyma and fibrosis of the pancreas. The most common cause of CP is alcohol use (70-80% in developed countries) [10,21]. Other etiologies include smoking, hereditary factors, autoimmune diseases, metabolic disturbances, ductal obstruction, and anatomic anomalies [22]. ...
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The discrimination of mass-forming chronic pancreatitis (MFCP) from pancreatic ductal adenocarcinoma (PDAC) is a central diagnostic dilemma. It is important to differentiate these entities since they have markedly different prognoses and management. Importantly, the appearance of these two entities significantly overlaps on a variety of imaging modalities. However, there are imaging features that may be suggestive of one entity more than the other. MFCP and PDAC may show different enhancement patterns on perfusion computed tomography (CT) and/or dynamic contrast-enhanced MRI (DCE-MRI). The duct-penetrating sign on magnetic resonance cholangiopancreatography (MRCP) is more often associated with MFCP, whereas abrupt cutoff with upstream dilatation of the main pancreatic duct and the double-duct sign (obstruction/cutoff of both the common bile duct and pancreatic duct) are more often associated with PDAC. Nevertheless, tissue sampling is the most reliable method to differentiate between these entities and is currently generally necessary for management.
... Clinically, it is hard to diagnose and the main and definite diagnosis is made by histopathology of the pancreatic mass. However, obtaining pancreatic tissue specimens from an alive individual is a therapeutic challenge when performed by puncture, resulting in limited outcomes in the diagnosis of pancreatitis due to the effects of puncture level and pancreatic fistula complications [14]. Therefore, in clinical practice, pancreatitis is usually diagnosed based on typical imaging findings, pancreatic exocrine function, pancreatic enzyme activity, and clinical manifestations at initial presentation. ...
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Objectives: To evaluate the utility of perfusion CT (PCT) in differentiating pancreatic adenocarcinoma from mass forming chronic pancreatitis (MFCP). Methods: In this ethically approved study, PCT was performed in 122 patients with pancreatic masses of which 42 patients had pancreatic adenocarcinoma and 13 had MFCP on histopathology. Perfusion parameters studied included blood flow (BF), blood volume (BV), permeability surface area product (PS), time to peak (TTP), peak enhancement intensity (PEI) and mean transit time (MTT). Twenty five controls with no pancreatic pathology were also studied. Results: Amongst the perfusion parameters BF and BV were found to be the most reliable for differentiating between adenocarcinoma and mass forming pancreatitis. Although they were reduced in both pancreatic adenocarcinoma (BF- 16.6 ± 13.1 ml/100 ml/min and BV- 5 ± 3.5 ml/100 ml) and MFCP (BF- 30.4 ± 8.7 ml/100 ml/min and BV- 8.9 ± 3.1 ml/100 ml) as compared to normal controls (BF- 94.1 ± 24 ml/100 ml/min and BV- 36 ± 10.7 ml/100 ml) but the extent of reduction was greater in pancreatic adenocarcinoma than in MFCP. Based on ROC analysis cut off values of 19.1 ml/100 ml/min for BF and 5 ml/100 ml for BV yielded optimal sensitivity and specificity for differentiating pancreatic adenocarcinoma from MFCP. Conclusions: PCT may serve as an additional paradigm for differentiating pancreatic adenocarcinoma from mass forming chronic pancreatitis and a useful tool for detecting masses which are isodense on conventional CT.
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Objective: To investigate the value of dual-energy MDCT in spectral imaging in the differential diagnosis of chronic mass-forming chronic pancreatitis (CMFP) and pancreatic ductal adenocarcinoma (PDAC) during the arterial phase (AP) and the pancreatic parenchymal phase (PP). Materials and methods: Thirty five consecutive patients with CMFP (n=15) or PDAC (n=20) underwent dual-energy MDCT in spectral imaging during AP and PP. Iodine concentrations were derived from iodine-based material-decomposition CT images and normalized to the iodine concentration in the aorta. The difference in iodine concentration between the AP and PP, contrast-to-noise ratio (CNR) and the slope K of the spectrum curve were calculated. Results: Normalized iodine concentrations (NICs) in patients with CMFP differed significantly from those in patients with PDAC during two double phases (mean NIC, 0.26±0.04mg/mL vs. 0.53±0.02mg/mL, p=0.0001; 0.07±0.02mg/mL vs. 0.28±0.04mg/mL, p=0.0002, respectively). There were significant differences in the value of the slope K of the spectrum curve in two groups during AP and PP (KCMFP=3.27±0.70 vs. KPDAC=1.35±0.41, P=0.001, and KCMFP=3.70±0.17 vs. KPDAC=2.16±0.70, p=0.003, respectively). CNRs at low energy levels (40-70keV) were higher than those at high energy levels (80-40keV). Conclusion: Individual patient CNR-optimized energy level images and the NIC can be used to improve the sensitivity and the specificity for differentiating CMFP from PDAC by use of dual-energy MDCT in spectral imaging with fast tube voltage switching.
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Objective: The purpose of this study was to identify helical CT and MR imaging features of pancreatic masses (focal enlargement) due to chronic pancreatitis and their correlation with pathologic findings. Conclusion: When histologic fibrosis is uniformly present through the pancreas in patients with chronic pancreatitis, there is no demarcation of masses due to chronic pancreatitis. When there is a greater degree of histologic fibrosis in the masslike part of the pancreas, the mass is often demarcated from the remaining pancreas, and the enhancement pattern on two-phase helical CT and dynamic gadolinium-enhanced MR imaging mimics that of pancreatic adenocarcinoma.
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The Sendai Consensus Guidelines (SCG) was formulated in 2006 to guide the management of intraductal papillary mucinous neoplasms (IPMN). The main area of controversy is the criteria for selection of branch duct (BD)-IPMN for resection. Although these guidelines have gained widespread acceptance, there is limited data to date supporting its use. This systematic review is performed to evaluate the utility of the Sendai Consensus Guidelines (SCG) for BD-IPMN. Studies evaluating the clinical utility of the SCG in surgically resected neoplasms were identified. The SCG were retrospectively applied to all resected neoplasms in these studies. BD-IPMNs which met the criteria for resection were termed SCG+ve and those for surveillance were termed SCG-ve. Twelve studies were included, of which, 9 were suitable for pooled analysis. There were 690 surgically resected BD-IPMNs, of which, 24 % were malignant. Five hundred one BD-IPMNs were classified as SCG+ve and 189 were SCG-ve. The positive predictive value (PPV) of SCG+ve neoplasms ranged from 11 to 52 % and the NPV of SCG-ve neoplasms ranged from 90 to 100 %. Overall, there were 150/501 (29.9 %) of malignant BD-IPMNs in the SCG+ve group and 171/189 (90 %) of benign BD-IPMNs in the SCG-ve group. Of the 18 reported malignant (11 invasive) BD-IPMNs in the SCG-ve group, 17 (including all 11 invasive) were from a single study. When the results from this single study were excluded, 170/171 (99 %) of SCG-ve BD-IPMNs were benign. The results of this review confirm the limitations of the SCG for BD-IPMN. The PPV of the SCG in predicting a malignant BD-IPMN was low and some malignant lesions may be missed based on these guidelines.