AJR 2002; 178:79-86
© American Roentgen Ray Society
Spectrum of Causes of Pancreatic Calcifications
Robert J. Lesniak1,
Mark D. Hohenwalter1 and
Andrew J. Taylor2
1
Department of Radiology, Medical College of Wisconsin, 9200 W. Wisconsin Ave.,
Milwaukee, WI 53226-3596.
2
Department of Radiology, University of Wisconsin Medical School, 600 Highland
Ave., Madison, WI 53792-3252.
Received December 21, 2000;
accepted after revision August 2, 2001.
Address correspondence to A. J. Taylor.
Introduction
The discovery of pancreatic calcifications has long been used in the
diagnosis of pancreatic disease, and for many years imaging of the pancreas
was largely limited to the radiographic identification of these
calcifications. Today, our ability to image the pancreas has greatly advanced
with modalities including CT, sonography, endoscopic retrograde
cholangiopancreatography, and MR imaging. This improved visualization of the
pancreas allows better identification of pancreatic calcifications and their
underlying cause.
Traditionally, pancreatic calcifications have been largely associated with
chronic calcific pancreatitis from alcohol abuse. Although alcohol abuse
remains the predominant cause of pancreatic calcifications, many other causes
also deserve attention. Knowing what entities cause calcifications and their
typical appearance can help in an accurate diagnosis. However, imaging alone
cannot be trusted for a definitive diagnosis because many of these entities
overlap in their appearance
[1]. We report a spectrum of
causes and imaging appearances related to calcification of the pancreas.
Inflammatory
Chronic alcoholic pancreatitis is the most common cause of pancreatic
calcifications in the United States. Although the exact mechanism of chronic
alcoholic pancreatitis has not been clearly elucidated, the characteristic
pathologic changes are well known. The ducts become obstructed by
proteinaceous plugs that can eventually accumulate calcium carbonate. This
obstruction results in ductal ectasia and periductal fibrosis. The calculi
occur in ducts of all sizes and vary from microscopic to greater than 1 cm in
diameter.
The radiographic appearance is generally that of numerous irregular small
calcifications throughout the pancreas (Fig.
1A,1B,1C,1D).
The head of the pancreas is usually involved more prominently than the tail.
The degree of calcification appears to parallel the course of the disease
[2]. Although these
intraductal, calcified concretions generally progress, the stone load
occasionally will decrease. Calcifications related to chronic alcoholic
pancreatitis may rarely be appreciated when mural calcification develops in a
chronic pseudocyst.
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Fig. 1A. —Calcifications associated with chronic alcoholic
pancreatitis. Radiograph of abdomen of 57-year-old man with chronic abdominal
pain shows numerous dense calcifications over pancreatic area. Subsequently,
history of chronic alcohol abuse was obtained.
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Fig. 1B. —Calcifications associated with chronic alcoholic
pancreatitis. Contrast-enhanced CT of abdomen in 58-year-old man with history
of alcohol abuse who presented with jaundice. In this case, calcifications in
enlarged pancreatic head and biliary tree dilatation are due to pancreatitis.
Rarely, pancreatic adenocarcinoma can be associated with ductal
calcifications. However, pancreatitis is more common.
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Fig. 1C. —Calcifications associated with chronic alcoholic
pancreatitis. Contrast-enhanced CT of abdomen in 58-year-old man with history
of alcohol abuse who presented with jaundice. In this case, calcifications in
enlarged pancreatic head and biliary tree dilatation are due to pancreatitis.
Rarely, pancreatic adenocarcinoma can be associated with ductal
calcifications. However, pancreatitis is more common.
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Fig. 1D. —Calcifications associated with chronic alcoholic
pancreatitis. Transverse sonogram of pancreas in 52-year-old man with chronic
alcoholic pancreatitis displays some large concretions that shadow (curved
arrow). However, many smaller stones are represented as bright reflectors
but without accompanying sonic shadow (arrowhead). This is a common
finding. Also present are segments of abnormally dilated pancreatic duct
(arrow).
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Chronic pancreatitis caused by hyperparathyroidism, tropical pancreatitis,
and idiopathic pancreatitis can also result in intraductal calculi. Notably,
other causes of pancreatitis, including gallstones, drugs, trauma, and
viruses, do not characteristically cause pancreatic calcifications.
Developmental
Although hereditary pancreatitis is rare, it is a well-known cause of
pancreatic calcifications in the pediatric population. Hereditary pancreatitis
has an autosomal dominant pattern of inheritance with an estimated 80%
penetrance [3]. It generally
manifests itself during childhood with a peak incidence at 5 years old.
However, a second peak at 17 years old may be attributable to the introduction
of alcohol in the diet. Intraductal calcifications occur in approximately 50%
of patients. These stones have a characteristic large, rounded appearance
(Fig.
2A,2B).
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Fig. 2A. —Hereditary pancreatitis in 18-year-old man with abdominal
pain and distended abdomen. His brother was previously diagnosed with
hereditary pancreatitis. On endoscopic retrograde pancreatogram, large
intraductal concretions (arrows) are present.
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Fig. 2B. —Hereditary pancreatitis in 18-year-old man with abdominal
pain and distended abdomen. His brother was previously diagnosed with
hereditary pancreatitis. On subsequent contrast-enhanced CT, calcified
concretions in pancreatic body and tail are seen. Massive ascites is
pancreatic in origin.
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Along with hereditary pancreatitis, cystic fibrosis accounts for most of
the pancreatic calcifications in children. Cystic fibrosis is an autosomal
recessive disease affecting one in 3000 children in the United States. The
most common finding on CT is fatty replacement of the pancreas. Intraductal
calcifications occur in a minority of patients and are generally limited to
patients with advanced pancreatic fibrosis. These fine granular calcifications
occur in the smaller pancreatic duct radicals
[4] (Fig.
3A,3B).
Neoplasms
The most common primary pancreatic tumor, ductal adenocarcinoma,
characteristically does not calcify. However, pancreatic carcinoma may develop
in a pancreas with underlying chronic calcific pancreatitis (Fig.
4A,4B).
Or, calcifications may develop in the setting of chronic pancreatitis from an
obstructing ductal adenocarcinoma (Fig.
5A,5B).
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Fig. 4A. —Adenocarcinoma superimposed on chronic calcific pancreatitis
in 71-year-old woman with history of alcohol abuse who presented with
jaundice. On CT scan, pancreatic head contains calcifications displaced by
poorly defined mass (arrows).
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Fig. 4B. —Adenocarcinoma superimposed on chronic calcific pancreatitis
in 71-year-old woman with history of alcohol abuse who presented with
jaundice. Radiograph of pancreatic head obtained before injection on
endoscopic retrograde pancreatogram shows these calcifications to be in form
of ducts (arrow). Subsequent biopsy reveals carcinoma in head of
pancreas.
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Fig. 5A. —Calcifications develop upstream from malignant obstruction in
81-year-old woman who presented with epigastric pain. Patient had no history
of alcohol abuse. On CT scan, small calcification is present in dilated main
pancreatic duct (arrow). Also note dilated intrahepatic biliary
ducts.
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Fig. 5B. —Calcifications develop upstream from malignant obstruction in
81-year-old woman who presented with epigastric pain. Patient had no history
of alcohol abuse. On endoscopic retrograde pancreatogram, ductal concretion
(arrow) is present behind malignant stricture. Pancreatic carcinoma
was found at surgery.
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A number of less common tumors have associated calcifications. Islet cell
tumors are known for the presence of tumoral calcifications. Islet cell tumors
are classified as functional or nonhyperfunctional. Functional tumors are
typically detected early because of their symptoms and thus are frequently
less than 2 cm in diameter. Nonhyperfunctioning tumors tend to be larger at
the time of diagnosis, measuring over 8 cm in diameter
[5]. A direct correlation
exists between islet cell tumor size and the increasing likelihood of cystic
necrosis with subsequent dystrophic calcification in the mass. A greater
percentage of the nonhyperfunctioning variety develop tumoral calcifications.
These calcifications tend to be focal, coarse, irregular, and located
relatively centrally in a large pancreatic mass
(Fig 6). However, insulinoma,
which is the most common functioning islet cell tumor, may contain
calcifications in up to 20% of cases (Fig.
7A,7B).
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Fig. 6. —Nonhyperfunctioning islet cell tumor in 41-year-old woman who
presented with vague epigastric pain. Complex mass is found on
contrast-enhanced CT scan. Note central calcifications and low-attenuation
areas of necrosis in mass. Absence of biliary ductal dilatation is unusual for
pancreatic adenocarcinoma in this location. Subsequent biopsy confirmed
diagnosis of non-hyperfunctioning islet cell tumor.
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Fig. 7A. —Insulinoma in 24-year-old woman who presented with
hypoglycemia. Because of clinical likelihood of insulinoma, noncontrast CT
scan was initially obtained. Subtle 2.0 x 3.0 cm area of high
attenuation in pancreas (arrow) is found to represent calcified
insulinoma at surgical pathology.
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Intraductal papillary mucinous neoplasms consist of abnormal ductal
epithelium, which ranges from hyperplasia to carcinoma, and usually produce a
large amount of mucin. The abnormal epithelial cells may be located in the
main pancreatic duct or a side branch. The mucin distends the local duct
system and frequently extends downstream to widen the papillary orifice.
Intraductal papillary neoplasms may produce a multilocular mass in the
pancreatic head or occasionally distend the main pancreatic duct, resulting in
a unilocular cystic mass. Although not commonly seen, dystrophic
calcifications may develop in the mucus
[6] (Fig.
8A,8B).
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Fig. 8A. —Intraductal papillary neoplasm in 52-year-old woman with
pancreatic stent recently placed for pancreatitis outside our institution.
Radiograph obtained before endoscopic retrograde pancreatogram shows
pancreatic stent adjacent to moderate-sized focus of calcification with
smaller calcifications (arrows) also visualized.
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Fig. 8B. —Intraductal papillary neoplasm in 52-year-old woman with
pancreatic stent recently placed for pancreatitis outside our institution.
Contrast-enhanced CT scan depicts dominant calcification in pancreatic head
(arrow) and smaller flecks of calcium (arrowheads). On
endoscopic retrograde pancreatogram (not shown), other, noncalcified, mucinous
filling defects were seen.
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Mucinous cystic neoplasms have been previously referred to as mucinous or
macrocystic cystadenomas or cystadenocarcinomas
[7]. They are most commonly
found in women in their sixth decade. The tumors may be unilocular or
multilocular cystic lesions with individual loculi of at least 2 cm. The
mucinous cystic neoplasm consists of a thick outer capsule with its inner
portion characteristically composed of ovarian stroma. Mucus fills the cyst,
but septations and polypoid excrescences may also be present. Calcifications
occur in the cyst wall or septa and tend to be curvilinear (Fig.
9A,9B).
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Fig. 9A. —Mucinous cystic neoplasm in 79-year-old woman with pancreatic
mass found during imaging workup for lower back pain. Noncontrast CT scan was
obtained because of renal compromise. Mucinous cystic neoplasm has small
linear focus of calcification in its wall (arrow).
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Fig. 9B. —Mucinous cystic neoplasm in 79-year-old woman with pancreatic
mass found during imaging workup for lower back pain. Fast spin-echo
T2-weighted MR image better displays internal network of septations. However,
as is common with MR imaging, mural calcification is not seen.
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Serous cystadenomas, also called microcystic adenomas, are considered a
benign pancreatic neoplasm. These tend to occur in patients more than 60 years
old [8]. They are slow growing
and frequently have grown to 10 cm in diameter. Serous cystadenomas are made
up of numerous, small, thin-walled cysts. These characteristics give the tumor
an overall nodular border with a honeycomb internal architecture. The tumors
commonly calcify (Fig. 10).
The pattern of calcification is characteristic of a central calcified scar
with calcified septations radiating outward, resulting in a sunburst
pattern.
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Fig. 10. —Serous cystadenoma in 65-year-old woman with mass in
pancreatic head. Delayed contrast-enhanced CT scan shows nodular pancreatic
mass with honeycombed appearance (arrow). Central scar is only
faintly calcified.
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Solid and pseudopapillary epithelial neoplasms are rare tumors found almost
exclusively in young women. They are considered to be a low-grade malignant
tumor and are usually large at the time of diagnosis, measuring an average of
9 cm [9]. Most commonly, solid
and pseudopapillary neoplasms are found in the pancreatic tail and are
composed of solid and cystic areas that are separated by pseudopapillary
epithelium. Calcification of these tumors (Fig.
11A,11B,11C)
is common [9]. The
calcification is characteristically peripheral and frequently punctate.
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Fig. 11B. —Solid and pseudopapillary epithelial neoplasm in 34-year-old
woman with back pain. Subsequent contrast-enhanced CT scans define
calcification as part of pancreatic mass. Portion of this mass is soft tissue
(arrow), whereas second component appears as peripherally calcified
cyst (arrowhead).
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Fig. 11C. —Solid and pseudopapillary epithelial neoplasm in 34-year-old
woman with back pain. Subsequent contrast-enhanced CT scans define
calcification as part of pancreatic mass. Portion of this mass is soft tissue
(arrow), whereas second component appears as peripherally calcified
cyst (arrowhead).
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Metastases to the pancreas are uncommon. The most common sources are
breast, lung, kidney, melanoma, and colon cancer. Calcifications have been
reported in cases of metastatic renal cell carcinoma and metastatic colon
carcinoma [10]
(Fig. 12). Another uncommon
pancreatic tumor, the pancreatoblastoma, can develop calcifications in 20% of
cases [11].
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Fig. 12. —Pancreatic metastases in 63-year-old man with mucinous colon
carcinoma. Contrast-enhanced CT scan shows pancreatic mass with calcification
(straight arrow) present with similar calcifications in liver
(curved arrows). Biopsies showed both liver and pancreatic lesions
were metastatic.
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Senescent
Occasionally, intraductal calculi occur in the older population with no
identifiable cause (Fig.
13A,13B).
These idiopathic calculi are rarely seen in patients less than 70 years old,
with their incidence increasing with age
[12]. The calculi occur in the
peripheral ducts and are generally 1-3 mm. They can cause atrophy and fibrosis
of the pancreas as a result of duct obstruction.
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Fig. 13A. —Senescent pancreatic calcifications in 77-year-old man
without significant medical history who presented with steatorrhea. CT section
through body and tail of pancreas shows tiny peripheral calcifications
(arrowheads). Also apparent is glandular atrophy and main duct
dilatation.
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Fig. 13B. —Senescent pancreatic calcifications in 77-year-old man
without significant medical history who presented with steatorrhea. CT scan on
slightly more caudad section shows that large intraductal calculus
(arrow) is cause of ductal obstruction.
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Mimics
Several potential mimics of pancreatic calcification exist. Calcification
of the splenic artery is generally identifiable by its characteristic linear,
tram-track appearance. However, in some cases it can be difficult to
distinguish from pancreatic calcification (Fig.
14A,14B).
On CT, dense arterial contrast enhancement in the pancreas can simulate
calcifications (Fig.
15A,15B).
Calcified gallstones in the distal common bile duct are a potential mimic
(Fig. 16). Retained contrast
in duodenal diverticula can also be mistaken for calcification in the
pancreas.
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Fig. 14A. —Splenic artery mimic in 51-year-old woman with no symptoms
relating to her pancreas. Portal venous phase contrast-enhanced CT scan shows
ring-like area of high attenuation in pancreas (arrow). Question of
small islet cell tumor with peripheral calcification was raised. At least one
area is definitely calcified (arrowhead).
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Fig. 14B. —Splenic artery mimic in 51-year-old woman with no symptoms
relating to her pancreas. Patient was brought back for double-helical CT scan
using thinner slice section. Sections during arterial phase of this
examination better show tortuous splenic artery that indents into normal
pancreas.
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Fig. 15A. —Contrast-enhanced intrapancreatic artery mimicking
calcification in 5-year-old girl who presented with pancreatitis. On
contrast-enhanced CT scan, small focus of increased attenuation was thought to
be pancreatic calcification (arrow). Possibility of hereditary
pancreatitis was raised. Normal endoscopic retrograde cholangiopancreatogram
followed (not shown).
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Fig. 15B. —Contrast-enhanced intrapancreatic artery mimicking
calcification in 5-year-old girl who presented with pancreatitis. Subsequent
unenhanced CT scan was obtained that showed normal-appearing pancreas and
failed to visualize any pancreatic calcification verifying that area of
increased attenuation on initial examination was intrapancreatic vessel.
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Introduction
Inflammatory
