ORIGINAL ARTICLE

Acute Pancreatitis as a Possible Indicator of Pancreatic

Cancer: The Importance of Mass Detection

Yuto Kimura 1, Masataka Kikuyama 2 and Yuzo Kodama 1

Abstract
Objective The aims of this study were to assess the incidence of pancreatic cancer and the contributing fac-
tors for the diagnosis of tumors in patients with acute pancreatitis and to gain insight into how patients with
acute pancreatitis should be followed up.
Methods Using the electronic medical database of Shizuoka General Hospital, 177 patients admitted for
acute pancreatitis in the past 6 years were evaluated retrospectively for pancreatic cancer.
Results Twelve patients (6.8%) were newly diagnosed with pancreatic cancer. During the first hospitaliza-
tion, 5 patients (41.7%) with a detected pancreatic mass underwent surgical treatment: the final tumor stages
were IA, IIA, and IIB in 1, 2, and 2 patients, respectively. In 7 patients (58.3%) without a detected pancre-
atic mass at the first admission, a pancreatic mass was recognized on follow-up computed tomography (CT)
in 2 patients with main pancreatic duct (MPD) dilatation, and 1 patient with recurrent acute pancreatitis. The
tumor stages were IA, IIA, and IA, respectively. Among the remaining 4 patients without follow-up, the tu-
mor stage was IV. The patient gender, age, MPD dilatation, tumor marker, and serum amylase level were not
significantly associated with pancreatic cancer. The detection of a pancreatic mass on CT led to the diagnosis
of pancreatic cancer.
Conclusion Acute pancreatitis should be considered as a possible diagnostic indicator of pancreatic cancer.
Various factors associated with acute pancreatitis and pancreatic cancer were not predictive of a diagnosis of
pancreatic cancer. Only the detection of a pancreatic mass led to the early diagnosis of pancreatic cancer. Pa-
tients hospitalized for acute pancreatitis should be followed up with a diagnostic imaging modality.

Key words: acute pancreatitis, pancreatic cancer, main pancreatic duct dilatation

(Intern Med 54: 2109-2114, 2015)

(DOI: 10.2169/internalmedicine.54.4068)

with acute pancreatitis have been reported to have pancreatic

Introduction
One of the factors contributing to the poor prognosis of
patients with pancreatic cancer is that the condition is rarely
diagnosed at an early stage. The factors that interfere with
an early diagnosis include the invasive nature of examina-
tions for pancreatic disorders, incomplete identification of
risk factors associated with pancreatic cancer, and ineffective
diagnostic screening.
Pancreatic cancer is one of the causes of acute pancreati-
tis, and acute pancreatitis due to pancreatic cancer is be-
lieved to be caused by the obstruction of the main pancre-
atic duct (MPD) by the tumor (1-4). Up to 2% of patients
cancer (5-9). In another report, a history of pancreatitis was
associated with an estimated 7.2-fold increase in the risk for
pancreatic cancer (10). Furthermore, the report demonstrated
a strong association between pancreatic cancer with pancrea-
titis diagnosed within 3 years prior and the pancreatic can-
cer diagnosis (10).
In this study, we reviewed cases of pancreatic cancer in
which patients were first admitted to our hospital due to
acute pancreatitis. Our goal was to assess the incidence of
pancreatic cancer and the contributing factors for diagnosis
of the tumor in patients with acute pancreatitis, as well as to
gain insight into how patients with acute pancreatitis should
be followed up.

Department of Gastroenterology, Kyoto University Hospital, Japan and Department of Gastroenterology, Shizuoka General Hospital, Japan
Received for publication September 8, 2014; Accepted for publication January 13, 2015
Correspondence to Dr. Masataka Kikuyama, kikuyama110@yahoo.co.jp

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 Intern Med 54: 2109-2114, 2015 DOI: 10.2169/internalmedicine.54.4068
Materials and Methods
The subjects enrolled in this study consisted of 177 pa-
tients [140 males and 37 females; mean age: 57.916.78
(17-89) years] admitted to our hospital for acute pancreatitis
due to various causes (Table 1) over a 6-year period begin-
ning in 2006.
All patients underwent a blood examination, including the
determination of carbohydrate antigen 19-9 (CA19-9), carci-
noembryonic antigen (CEA), and serum amylase levels, as
well as contrast-enhanced computed tomography (CT) on
admission. CT assessments included the identification of
masses, MPD dilatation, and cystic lesions. When the di-
ameter of the MPD was 3 mm or more, MPD was defined
as dilated. If a mass compatible with pancreatic cancer was
recognized, patients were referred for surgical treatment.
In cases where CT demonstrated pancreatic abnormalities,
including MPD dilatation but no masses, the patients were
followed as outpatients and repeated CT exams were sched-
uled every 3-6 months for one year. The patients in whom a
new mass appeared on follow-up CT were re-admitted for
further examination by endoscopic retrograde cholangiopan-
creatography (ERCP). A pancreatic-duct biopsy or brush cy-
tology to reveal malignancy was conducted based on the
ERCP findings. The patients without abnormalities were not
followed up regularly by CT.
The incidence of pancreatic cancer in acute pancreatitis
cases and the factors influencing the incidence, including
findings on CT, were evaluated retrospectively. We defined
the incidence of pancreatic cancer with acute pancreatitis as
the ratio of pancreatic cancer diagnosed during the first hos-
pitalization or after discharge among all cases of acute pan-
creatitis. Tumor staging was performed using the Union for
International Cancer Control (UICC) TNM Classifica-
tion (11). In statistical analyses comparing patients with
pancreatic cancer and those without pancreatic cancer, the
factors associated with pancreatic cancer included gender,
age, CA19-9 level, CEA level, serum amylase level, and the
incidence of MPD dilatation on admission for acute pan-
creatitis. Those factors along with the tumor stage, tumor
size, and diameter of MPD were statistically compared be-
tween patients diagnosed with pancreatic cancer during hos-
pitalization and those diagnosed after discharge.
Statistical analyses were performed as follows. The pa-
tient characteristics were described using descriptive statis-
tics and expressed as the mean and standard deviation (SD).
Data comparisons between the groups were performed using
the Mann-Whitney U test (two-tailed) and Fishers exact test
(two-sided). Statistical significance was recognized at p!
0.05.
Results
Among the 177 patients with acute pancreatitis, the
causes of acute pancreatitis were idiopathic in 40 (22.6%),
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Table1.Causes of Acute Pancreatitis.
Causes n (%)
Idiopathic 40 (22.6)
Alcoholic 37 (21.0)
Gallstone 34 (19.2)
Acute exacerbation
21 (11.9 )
of chronic pancreatitis
Pancreatic cancer
Newly diagnosed 12 (6.8 )
Already known 2 (1.1 )
IPMN 7 (4.0)
Others 24 (13.6 )
Total 177
IPMN: Intraductal Papillary Mucinous Neoplasm
alcohol abuse in 37 (21.0%), gallstone in 34 (19.2%), acute
exacerbation of chronic pancreatitis in 21 (11.9%), newly di-
agnosed pancreatic cancer in 12 (6.8 %), already known
pancreatic cancer in 2 (1.1%), intraductal papillary muci-
nous neoplasm (IPMN) in 7 (4.0%), and other causes in 24
(13.6%) (Table 1). In 2 of the 14 patients with pancreatic
cancers, acute pancreatitis occurred during the course of
chemotherapy for pancreatic cancer. Of the 177 patients, 12
(6.8%) were newly diagnosed with pancreatic cancer.
For 5 patients (Table 2), representing 41.7% of the 12 pa-
tients with pancreatic cancer and 2.8% of the 177 patients
with acute pancreatitis, a pancreatic mass was recognized on
CT, and pancreatic cancer was diagnosed during the first
hospitalization. The tumors occurred at the pancreatic head
in 3 of the 5 patients and the MPD was dilated in 2. The
other patient had a tumor at the uncinate process of the pan-
creatic head, and the MPD was not dilated. The diameters of
the tumors were 48 mm, 15 mm, and 16 mm, respectively.
The remaining 2 patients had tumors at the pancreatic body
and tail and cancer at the pancreas body was accompanied
with the dilatation of the upper stream of MPD and a large
pseudocyst. The diameters of these 2 tumors were 23 mm
and 25 mm.
All of the 5 patients underwent surgical treatment and a
histopathological examination of the resected specimens,
which provided conclusive evidence of pancreatic cancer.
The average tumor diameter for these patients was 25.4 mm.
Based on the UICC standards, the final stages of tumors
were IA (1 patient), IIA (2 patients), and IIB (2 patients).
To avoid pancreatitis, ERCP was not performed in any of
these patients before surgery during the first hospitalization.
In the remaining 7 patients (Table 3), representing 58.3%
of the 12 patients with pancreatic cancer and 4.0% of the
177 patients with acute pancreatitis, CT during the first hos-
pitalization did not reveal a mass. Of these 7 patients, 2
were scheduled for CT follow-up because of a dilated MPD,
and pancreatic cancer was recognized at 7 and 12 months
 Intern Med 54: 2109-2114, 2015 DOI: 10.2169/internalmedicine.54.4068

Table2.Characteristics of the Patients Diagnosed with Pancreatic Cancer during Hospitalization.

At the Time of Diagnosis after

On Admission
Discharge

Follow-
Time CA19- MPD CA19- MPD
Age Size up CEA AMY Pseudo- CEA AMY
No Sex Location Stage of 9 Diameter 9 diameter
(years) (mm) after (ng/mL) (IU/L) cyst (ng/mL) (IU/L)
Diagnosis (U/mL) (mm) (U/mL) (mm)
Discharge

During the 1st

1 56 M Body 23 IIA NA 2 20 559 4 + NA NA NA NA
Hosp.
During the 1st
2 61 M Head 16 IA NA 2.9 163 389 1 - NA NA NA NA
Hosp.
During the 1st
3 62 M Tail 25 IIA NA 1 24 220 2 - NA NA NA NA
Hosp.
During the 1st
4 63 M Head 48 IIB NA 1 249 575 10 + NA NA NA NA
Hosp.
During the 1st
5 67 M Head 15 IIB NA 2.5 82 244 3 + NA NA NA NA
Hosp.
Normal range :
carcinoembryonic antigen (CEA) 5.0 ng/mL
carbohydrate antigen 19-9 (CA19-9) 37 U/mL

Table3.Characteristics of the Patients Diagnosed with Pancreatic Cancer after Discharge.

At the Time of Diagnosis after

OnAdmission
Discharge

Time Follow-up MPD MPD

Age Size CEA CA19-9 AMY Pseudo- CEA CA19-9 AMY
No Sex Location Stage of after Diameter Diameter
(years) (mm) (ng/mL) (U/mL) (IU/L) cyst (ng/mL) (U/mL) (IU/L)
Diagnosis Discharge (mm) (mm)

6 63 F Head 60 IV 2 Mos. Later + 1.1 19 2,882 2 - 8.3 13 32 3

7 57 F Body 22 IV 3 Mos. Later - NA 139.4 750 6 + 3.5 882 102 6

8 63 M Tail 35 IV 3 Mos. Later - NA NA 3,701 1 + 4.7 325 57 1

9 59 M Head 18 IA 7 Mos. Later + 1.1 245 1,379 5 - 4.8 46 60 9

10 69 M Head 12 IA 9 Mos. Later - 1.3 33 389 2 - 1.5 59 179 10

11 47 M Head 41 IIA 12 Mos. Later + 1.4 56 1,149 5 - 1.2 47 97 9

12 76 M Tail 30 IV 24 Mos. Later - 1.8 16 852 2 - 2.9 89 138 2

Normal range :
carcinoembryonic antigen (CEA) 5.0 ng/mL
carbohydrate antigen 19-9 (CA19-9) 37 U/mL

Table4.Factors Associated with Acute Pancreatitis and after discharge, respectively; the tumor diameter was 18 mm
Pancreatic Cancer on Admission for Acute Pancreatitis Com- in one case and 41 mm in the other case. The patients un-
pared between Two Groups with or without Pancreatic Cancer. derwent surgery, and histopathological diagnoses of pancre-
atic cancer at the final stage of IA and IIA were made. In 1
Pancreatic cancer (n=12) Control (n=165) p value
of the 7 patients, a scheduled follow-up was planned every
Gender (male/female) 10/2 130/35 0.52
Age (years) 61.9 7.19 57.69 17.24 0.40
3 months. However, a large pancreatic cancer with a diame-
CA19-9 (U/mL) 92.31 91.83 62.13 153.39 0.53
ter of 60 mm accompanied by hepatic metastasis (stage IV)
CEA (ng/mL) 1.81 0.84 2.78 2.52 0.21
was revealed subsequent to jaundice at 2 months after dis-
Serum amylase (IU/L) 1,075.5 1,110.1 992.78 1,054.69 0.79 charge. The patient underwent chemotherapy after the con-
MPD dilatation (n) 6 52 0.21 firmation of pancreatic cancer based on a percutaneous nee-
Values are n or mean SD. dle biopsy of the metastatic lesions of the liver.
Of the seven patients, 4 were not followed up because the

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 Intern Med 54: 2109-2114, 2015
Table5.Factors Associated with Acute Pancreatitis and Pancreatic Cancer
on Admission for Acute Pancreatitis Compared between Two Groups Diag-
nosed with Pancreatic Cancer during Hospitalization or after Discharge.
During hospitalization (n=5) After discharge(n=7)
Tumor stage (IA:IB:IIA:IIB/III:IV)
Tumor size (mm)
CEA (ng/mL)
CA19-9 (U/mL)
Serum amylase (IU/L)
MPD dilatation (n)
Diameter of MPD (mm)
MPD was not dilated and no mass on CT was detected at
the time of the first hospitalization (3 patients) or there was
suspicion of chronic pancreatitis with a pseudocyst (1 pa-
tient). In 3 patients, pancreatic cancers with diameters of 35
mm, 12 mm, and 30 mm were diagnosed at 3, 9, and 24
months after discharge, respectively. Two of the 3 patients
did not undergo surgery because of the tumor stage (stage
IV) and the presence of hepatic metastases; instead they re-
ceived chemotherapy after the confirmation of pancreatic
cancer based on a percutaneous needle biopsy of the metas-
tatic lesions of the liver. One of the 3 patients suffered from
recurrent acute pancreatitis at 9 months after discharge, and
a pancreatic cancer 12 mm in diameter was recognized at
the pancreatic head along with a dilated MPD. Surgery was
performed and a histopathological diagnosis of pancreatic
cancer at the final stage of IA was made. In the remaining
patient, who was not followed up because of suspicion of
chronic pancreatitis, pancreatic cancer with a diameter of 22
mm was recognized at 3 months after discharge on CT, and
a histopathological diagnosis of pancreatic cancer at the fi-
nal stage of IV was made post-surgically.
None of the factors associated with pancreatic cancer
were able to predict pancreatic cancer in patients with acute
pancreatitis (Table 4). Several factors on admission for acute
pancreatitis were compared between the patients in which
pancreatic cancer was diagnosed during hospitalization and
those diagnosed after discharge (Table 5). No factors
showed a significant difference between the two groups,
while the tumor stages in the group diagnosed during the
first hospitalization tended to be earlier and the serum amy-
lase levels in the other group tended to be higher.
Discussion
Acute pancreatitis occurs due to various causes, with idi-
opathic cases being the most common. Pancreatic cancer is
included as one of the causes (12-14). In our study, among
patients with acute pancreatitis, 12 (6.8%) had pancreatic
cancer. In cases with a diagnosis of pancreatic cancer during
the first hospitalization, the tumor stage tended to be early.
Acute pancreatitis is a favorable indicator for pancreatic
DOI: 10.2169/internalmedicine.54.4068
Diagnosis
p
1:0:2:2/0:0 2:0:1:0/0:4 0.08
25.4 13.35 31.14 16.17 0.53
1.88 0.86 1.34 0.29 0.42
107.6 97.96 84.73 90.8 0.70
397.4 167.86 1,586 1,228.63 0.06
3 3 0.19
4 3.54 3.29 1.98 0.66
Values are n or mean SD.
cancer at the early stage. However, pancreatic cancer was
not easily diagnosed because various factors, including gen-
der, age, MPD dilatation, tumor marker, and the serum amy-
lase level on admission, were not significantly associated
with pancreatic cancer. Only the detection of a pancreatic
mass enabled the early diagnosis of pancreatic cancer, al-
though the rate of pancreatic mass recognition at the onset
of acute pancreatitis among patients with pancreatic cancer
was 41.7%.
We utilized CT for diagnosing pancreatic cancer in our
study. The diameters of pancreatic cancer were larger than
15 mm in almost all cases except for 1 patient with a 12-
mm diameter tumor. The average tumor size did not differ
significantly between the patients with pancreatic cancer di-
agnosed during the first hospitalization versus after dis-
charge, probably because identifying a tumor on CT became
possible only when the tumor diameter grew to more than
15 mm. These results are consistent with previous reports
indicating that it is difficult to detect pancreatic tumors
smaller than 15 mm by CT (15-19). Nevertheless, the tumor
stages detected during the first hospitalization and in the pa-
tients followed by regular examination with CT were earlier
than those in the patients not followed. The fact that 6
(50%) and 3 (25%) of the 12 patients with pancreatic cancer
were surgically treated at stage IIA and IA, respectively,
suggests that careful observation by CT is important for the
early diagnosis of pancreatic cancer. However, the limited
sensitivity of CT for the detection of pancreatic cancer indi-
cates that other imaging modalities should be considered for
this purpose.
Endoscopic ultrasonography (EUS) is an alternative diag-
nostic method for pancreatic cancer. Several reports have de-
scribed that this modality can be used to diagnose early pan-
creatic cancers that cannot be recognized by CT (20-26). We
suggest that EUS should be selected to diagnose pancreatic
cancer at an early stage in patients with acute pancreatitis.
ERCP is also an appropriate method for examining whether
or not a tumor is occluding the MPD. However, because
acute pancreatitis is considered to be a high-risk factor for
post-ERCP pancreatitis (27-29), we chose not to proceed
with this modality during the first hospitalization.
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 Intern Med 54: 2109-2114, 2015 DOI: 10.2169/internalmedicine.54.4068
Pancreatic cancer is known to invade the MPD and ob-
struct pancreatic juice flow, which results in the dilatation of
the duct upstream of the invaded portion and induces acute
pancreatitis (1-4). MPD dilatation is an important sign of
pancreatic cancer. However, our results indicate that pancre-
atic cancer cannot be ruled out even if the MPD is not di-
lated in patients with acute pancreatitis, and the induction of
acute pancreatitis in patients with pancreatic cancer is not
limited to invasion of the MPD and obstruction of pancre-
atic juice flow. Other factors, such as chemical mediators in-
duced by pancreatic cancer, may be responsible for acute
pancreatitis in the absence of MPD obstruction. When see-
ing patients with acute pancreatitis, it is important to pay at-
tention to the presence of a pancreatic mass, and following
up patients with acute pancreatitis after discharge is neces-
sary, even though a pancreatic mass and dilatation of the
MPD may not be evident upon CT at the onset of acute
pancreatitis.
To follow up patients with acute pancreatitis post-
discharge, the interval duration and the method of monitor-
ing for tumors should be considered. We identified 1 case
with a massive pancreatic head tumor and multiple liver me-
tastases diagnosed 2 months after discharge. In another pa-
tient without planned follow-up, pancreatic cancer was diag-
nosed 24 months after discharge. However, these cases are
exceptional and in almost all patients, cancer was diagnosed
3 to 12 months after discharge. These results suggest that
performing examinations for at least 1 year after discharge
is ideal. A strong association between pancreatic cancer with
pancreatitis diagnosed within 3 years prior and the pancre-
atic cancer diagnosis was demonstrated (10). Moreover, the
risk for pancreatic cancer has been reported to be greatest in
the first year after acute pancreatitis and to decrease rapidly
thereafter (30). The suggestion to perform examinations at
3-month intervals until 1 year after discharge is not discor-
dant with the previous reports.
The incidence of pancreatic cancer in patients with acute
pancreatitis was 6.8% in our study, which is higher than that
of previous reports (5-9). Misclassification of pancreatic
cancer as pancreatitis may be responsible for the result (10).
However, a recent report indicated a 12% incidence of pan-
creatic cancer among patients with acute pancreatitis (30).
Regardless of the exact incidence, the fact remains that a
significant number of patients with acute pancreatitis will
suffer from pancreatic cancer.
In conclusion, our results suggest that acute pancreatitis is
a diagnostic indicator for pancreatic cancer, and the detec-
tion of a pancreatic mass on CT led to the diagnosis of pan-
creatic cancer, while various factors associated with acute
pancreatitis and pancreatic cancer were not predictive of a
diagnosis of pancreatic cancer. Moreover, patients hospital-
ized for acute pancreatitis should be followed up with regu-
lar examinations, including CT and EUS, if possible, for at
least 1 year, even if diagnostic images do not demonstrate
any pancreatic abnormalities suggestive of pancreatic cancer
during the first hospitalization. However, further studies are
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needed to confirm our findings due to the limited number of
patients included our study.
The authors state that they have no Conflict of Interest (COI).
References
1. Wilson C, Imrie CW. Occult pancreatic cancer with recurrent
acute pancreatitis. Postgrad Med J 62: 765-767, 1986.
2. Lin A, Feller ER. Pancreatic carcinoma as a cause of unexplained
pancreatitis: report of ten cases. Ann Intern Med 113: 166-167,
1990.
3. Li D, Xie K, Wolff R, Abbruzzese JL. Pancreatic cancer. Lancet
363: 1049-1057, 2004.
4. Tsai MJ, Liao KS, Shih PM, et al. Relapsed acute pancreatitis as
the initial presentation of pancreatic cancer in a young man: a
case report. Kaohsiung J Med Sci 26: 448-455, 2010.
5. Appelros S, Borgstrom A. Incidence, aetilogy and mortality rate of
acute pancreatitis over 10 years in a defined urban population in
Sweden. Br J Surg 86: 465-470, 1999.
6. Gullo L, Migliori M, Olh A, et al. Acute pancreatitis in five
Europian countries: etiology and mortality. Pancreas 24: 223-227,
2002.
7. Maes B, Hastier P, Buckley MJ, et al. Extensive aetilogical inves-
tigations in acute pancreatitis: results of a 1-year prospective
study. Eur J Gastroenterol Hepatol 11: 891-896, 1999.
8. Pezzili R, Billi P, Morselli-Labate AM. Severity of acute pancrea-
titis: relationship with etiology, sex and age. Hepatogastroenterol-
ogy 45: 1859-1864, 1998.
9. Thomson SR, Hendry WS, McFarlane GA, Davidson AI. Epide-
miology and outcome of acute pancreatitis. Br J Surg 74: 398-
401, 1987.
10. Bracci PM, Wang F, Hassan MM, Gupta S, Li D, Holly EA. Pan-
creatitis and pancreatic cancer in two large pooled case-control
studies. Cancer Causes Control 20: 1723-1731, 2009.
11. UICC TMN Classification of Malignant Tumours. 6th ed. Sobin
LH, Wittekind C, Eds. Wiley-Liss, New York, 2002.
12. Lin A, Feller ER. Pancreatic carcinoma as a cause of unexplained
pancreatitis: report of ten cases. Ann Intern Med 113: 166-167,
1990.
13. Gislason H, Horn A, Hoem D, et al. Acute pancreatitis in Bergen,
Norway: a study on incidence, etiology, and severity. Scand J
Surg 93: 29-33, 2004.
14. Sekimoto M, Takada T, Kawarada Y, et al. JPN Guidelines for the
management of acute pancreatitis: epidemiology, etiology, natural
history, and outcome predictors in acute pancreatitis. J Hepatobili-
ary Pancreat Surg 13: 10-24, 2006.
15. Yasuda K, Mukai H, Fujimoto S, Nakajima M, Kawai K. The di-
agnosis of pancreatic cancer by endoscopic ultrasonography. Gas-
trointest Endosc 34: 1-8, 1988.
16. Nakaizumi A, Uehara H, Iishi H, et al. Endoscopic ultrasonogra-
phy in diagnosis and staging of pancreatic cancer. Dig Dis Sci 40:
696-700, 1995.
17. Sugiyama M, Hagi H, Atomi Y, Saito M. Diagnosis of portal ve-
nous invasion by pancreatobiliary carcinoma: value of endoscopic
ultrasonography. Abdom Imaging 22: 434-438, 1997.
18. Maguchi H. The roles of endoscopic ultrasonography in the diag-
nosis of pancreatic tumors. J Hepatobiliary Pancreat Surg 11: 1-3,
2004.
19. Angelis CD, Repici A, Carucci P, et al. Pancreatic cancer imaging:
the new role of endoscopic ultrasound. JOP 8: 85-97, 2007.
20. Rsch T, Lorenz R, Braig C, et al. Endoscopic ultrasound in pan-
creatic tumor diagnosis. Gastrointest Endosc 37: 347-352, 1991.
21. Palazzo L, Roseau G, Gayet B, et al. Endoscopic ultrasonography
in the diagnosis and staging of pancreatic adenocarcinoma: results
 Intern Med 54: 2109-2114, 2015 DOI: 10.2169/internalmedicine.54.4068

of a prospective study with comparison to ultrasonography and
CT scan. Endoscopy 25: 143-150, 1993.
22. Howard TJ, Chin AC, Streib EW, Kopecky KK, Wiebke EA.
Value of helical computed tomography, angiography, and endo-
scopic ultrasound in determining resectability of periampullary
carcinoma. Am J Surg 174: 237-241, 1997.
23. Midwinter MJ, Beveridge CJ, Wilsdon JB, Bennett MK, Baudouin
CJ, Charnley RM. Correlation between spiral computed tomogra-
phy, endoscopic ultrasonography and findings at operation in pan-
creatic and ampullary tumours. Br J Surg 86: 189-193, 1999.
24. Mertz HR, Sechopoulos P, Delbeke D, Leach SD. EUS, PET, and
CT scanning for evaluation of pancreatic adenocarcinoma. Gastro-
intest Endosc 52: 367-371, 2000.
25. Dewitt J, Devereaux BM, Lehman GA, Sherman S, Imperiale TF.
Comparison of endoscopic ultrasound and computed tomography
for the preoperative evaluation of pancreatic cancer: a systematic
review. Clin Gastroenterol Hepatol 4: 717-725, 2006.
26. Papanikolaou IS, Karatzas PS, Triantafyllou K, Adler A. Role of
pancreatic endoscopic ultrasonography in 2010. World J Gastro-
intest Endosc 2: 335-343, 2010.
27. Freeman ML, DiSario JA, Nelson DB, et al. Risk factors for post-
ERCP pancreatitis: a prospective, multicenter study. Gastrointest
Endosc 54: 425-434, 2001.
28. Masci E, Mariani A, Curioni S, Testoni PA. Risk factors for pan-
creatitis following endoscopic retrograde cholangiopancreatogra-
phy: a meta-analysis. Endoscopy 35: 830-834, 2003.
29. Cheng CL, Sherman S, Watkins JL, et al. Risk factors for post-
ERCP pancreatitis: a prospective multicenter study. Am J Gastro-
enterol 101: 139-147, 2006.
30. Munigala S, Kanwal F, Xian H, Scherrer JF, Agarwai B. Increased
risk of pancreatic adenocarcinoma after acute pancreatitis. Clin
Gastroenterol Hepatol 12: 1143-1150, 2014.

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