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Gastrointestinal Imaging |
1 From the Departments of Radiology (D.V.S., S.P.K., M.M.M., S.S., P.R.M., J.F.S.), Endoscopy (J.F.), Pathology (G.Y.L.), and Surgery (C.D.F., A.L.W.), Massachusetts General Hospital, White Bldg 270F, 55 Fruit St, Boston MA 02114. Received September 5, 2003; revision requested November 4; final revision received March 26, 2004; accepted April 15. Address correspondence to D.V.S. (e-mail: dsahani@partners.org).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Twenty-nine patients (25 male and four female; mean age, 56 years; range, 15–82 years) with histopathologic diagnosis of autoimmune pancreatitis were examined. Data were reviewed by two radiologists in consensus. Imaging findings for review included those from helical computed tomography (CT), 25 patients; magnetic resonance (MR) imaging with MR cholangiopancreatography (MRCP), four patients; endoscopic ultrasonography (US), 21 patients; endoscopic retrograde cholangiopancreatography (ERCP), 19 patients; and percutaneous transhepatic cholangiography, one patient. Images were analyzed for appearances of pancreas, biliary and pancreatic ducts, and other findings, such as peripancreatic inflammation, encasement of vessels, mass effect, pancreatic calcification, peripancreatic nodes, and peripancreatic fluid collection. Follow-up images were available in nine patients. Serologic markers such as serum immunoglobulin G (IgG) and antinuclear antibody levels were available in 12 patients.
RESULTS: CT showed diffuse (n = 14) and focal (n = 7) enlargement of pancreas. Seven patients had minimal peripancreatic stranding, with lack of vascular encasement, calcification, or peripancreatic fluid collection. Nine patients had enlarged peripancreatic lymph nodes. MR imaging showed focal (n = 2) and diffuse (n = 2) enlargement with rimlike enhancement in one. MRCP revealed pancreatic duct strictures in two and sclerosing cholangitis–like appearance in one. Endoscopic US showed diffuse enlargement of pancreas with altered echotexture in 13 patients and focal mass in the head in six. ERCP showed stricture of distal common bile duct in 12 patients, irregular narrowing of intrahepatic ducts in six, diffuse irregular narrowing of pancreatic duct in nine, and focal stricture of proximal pancreatic duct in six. Serologic markers showed increased IgG and antinuclear antibody levels in seven of 12 patients. At follow-up, CT abnormalities and common bile duct strictures resolved after steroid therapy in three patients.
CONCLUSION: Features that suggest autoimmune pancreatitis include focal or diffuse pancreatic enlargement, with minimal peripancreatic inflammation and absence of vascular encasement or calcification at CT and endoscopic US, and diffuse irregular narrowing of main pancreatic duct, with associated multiple biliary strictures at ERCP.
© RSNA, 2004
Index terms: Magnetic resonance (MR), cholangiopancreatography, 77.121411, 77.121415 • Pancreas, CT, 77.12115 • Pancreas, MR, 77.121411, 77.121415 • Pancreas, US, 77.1298 • Pancreatitis, 77.291
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Several authors have described patients with chronic pancreatitis that is associated with autoimmune diseases. Sarles et al (2) described a type of chronic pancreatitis that might be caused by an autoimmune mechanism and termed it "primary inflammatory sclerosis of the pancreas." Yoshida and colleagues (3) reported a similar case and proposed that pancreatitis with these characteristics be referred to as autoimmune pancreatitis. Current accepted terminology for this condition is lymphoplasmacytic sclerosing pancreatitis or autoimmune pancreatitis (3).
Autoimmune pancreatitis should be distinguished from alcoholic chronic pancreatitis, because steroid therapy for the former type is effective, morphologic changes are reversible, and pancreatic function can return to normal levels. The incidence and prevalence of this disease are not well documented in the literature; however, 150 cases have been reported in the Japanese literature (4). Similarly, the association with autoimmune diseases has been reported (4–10), but the exact incidence of this association is lacking. Though response to steroids is documented in the literature (11), the dosage and duration of such therapy is not standardized. In addition, the usual course of this disease is not known.
Indeed, features of autoimmune pancreatitis, which include hypergammaglobulinemia, were recognized more than 35 years ago; furthermore, autoimmune pancreatitis may occur alone or occasionally with other immune-mediated disorders (4–10). Because it is a distinct disease and is different from acute or chronic pancreatitis on the basis of clinical, pathologic, and imaging findings, it has been defined as a special form of chronic pancreatitis caused by an autoimmune disease mechanism or associated with autoimmune-related diseases. The purpose of our study was to retrospectively determine imaging findings in patients with autoimmune pancreatitis.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Eighteen patients had undergone surgery: The Whipple procedure was performed in 10 patients; pylorus-sparing pancreaticoduodenectomy, in one patient; distal subtotal pancreatectomy, in one patient; and laparotomy with pancreatic biopsy and associated choledochojejunostomy, in six patients. In the remaining 11 patients, diagnosis was based on pancreatic biopsy. Endoscopic ultrasonography (US)–guided biopsy was performed in nine patients, and computed tomography (CT)–guided biopsy was performed in two. One patient with mediastinal nodes and another patient with submandibular nodes underwent lymph nodal biopsies, as well.
In all patients who had undergone surgery, the detailed gross and histopathologic evaluation reports were available. The clinical data, which included symptoms at presentation, history of previous attacks of pancreatitis, alcohol abuse, associated symptoms involving other systems, history of autoimmune diseases, and laboratory findings, were reviewed by one author (D.V.S.).
Imaging
Helical CT images were available in 25 of 29 patients. Examination was performed with either single–detector row helical CT (n = 18) (HiSpeed; GE Medical Systems, Milwaukee, Wis) or multi–detector row helical CT (n = 7) (LightSpeed; GE Medical Systems), with a maximum section thickness of 5 mm. (Information about all scanners was not available.) Results of precontrast and postcontrast examinations of the pancreas were available in 10 patients, and results of postcontrast examinations alone were available in 15 patients. In 20 patients, postcontrast CT was performed after the administration of 130–150 mL of nonionic contrast medium at the rate of 3–5 mL/sec with a power injector. In five patients, the exact volume and the rate of contrast medium administered were not available. In nine patients, CT was performed after endoscopic retrograde cholangiopancreatography and stent placement in the common bile duct. Six patients underwent follow-up CT.
Magnetic resonance (MR) imaging and MR cholangiopancreatography were performed in four patients, and images were available for evaluation. Imaging was performed with a 1.5-T MR imaging system (Signa Advantage; GE Medical Systems) with a standard phased-array torso coil. Precontrast T1-weighted MR imaging (repetition time msec/echo time msec, 150–200/2.1, 4.2) with and without fat saturation and respiratory-triggered T2-weighted MR imaging (5000–8000/80–135) were performed, followed by dynamic fat-suppressed T1-weighted MR imaging (150–200/2.1) after administration of a gadolinium-based contrast agent (Magnevist; Berlex Laboratories, Wayne, NJ). MR cholangiopancreatography was performed with a single-shot fast spin-echo thick-slab technique (25 000–30 000/800–1000).
Transabdominal US images were available in nine patients. All examinations were performed by experienced technologists with the supervision of subspecialty-trained radiologists who had a minimum of 5 years of experience. All the scans were obtained with a US unit (Logic 500; GE Medical Systems) and a 3–5-MHz probe. Color Doppler imaging was not performed. Endoscopic US was performed in 21 patients with another US unit (Pentax Linear Array Endoscopic Ultrasound; Precision Instruments, Orangeburg, NY) and a 7.5-MHz probe. Endoscopic US was performed by three gastroenterologists with a minimum of 5 years of experience in endoscopic US.
Endoscopic retrograde cholangiopancreatographic images were available in 19 patients. In three patients, a pancreatogram was not obtained. In addition, one patient underwent percutaneous transhepatic cholangiography after unsuccessful endoscopic retrograde cholangiopancreatography. Six patients had undergone follow-up endoscopic retrograde cholangiopancreatography after steroid therapy. All imaging was performed by three endoscopists with a minimum of 5 years of experience.
Follow-up Imaging
Nine patients underwent follow-up imaging: Three patients underwent both CT and endoscopic retrograde cholangiopancreatography; one patient underwent endoscopic US, CT, and endoscopic retrograde cholangiopancreatography; two patients underwent endoscopic retrograde cholangiopancreatography; and three patients underwent CT.
Image Analysis
CT, MR imaging, and endoscopic retrograde cholangiopancreatographic imaging findings were evaluated in consensus by two radiologists (D.V.S., S.P.K.) who had a minimum of 6 years of experience in radiology. Reports of endoscopic US generated by gastroenterologists were used. All the imaging studies were analyzed for the following: focal or diffuse enlargement of the pancreas, peripancreatic inflammation, pancreatic duct morphology, intraductal calculi or calcification, parenchymal calcification, peripancreatic fluid collection, vascular encasement, regional lymphadenopathy, intra- and extrahepatic biliary ductal dilatation, and additional findings such as gallbladder abnormality or liver or peritoneal abnormalities.
Serologic Evaluation
Serologic markers were available in 12 patients. These included serum immunoglobulin G (IgG) and antinuclear antibody levels. In addition, other laboratory values that included the tumor marker CA 19-9 and serum amylase, lipase, alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase levels were available in 12 patients. These were evaluated for abnormal increases.
Histopathologic Evaluation
Histopathologic evaluation was performed by one author (G.Y.L.) with more than 8 years of experience in pathology. The pathologic reports were used for this study. Pathologic data were reviewed for gross or microscopic evidence of malignancy, extent of inflammation and fibrosis, ductal changes, presence of atrophy, peripancreatic inflammation, vascular involvement, and lymph node changes.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Imaging Findings
Helical CT.—Diffuse enlargement of the pancreas was seen in 14 of 25 patients. In all these patients, the pancreas appeared uniformly enlarged (Fig 1), with absence of pancreatic clefts and with a sharp outline. In three patients with diffuse enlargement, focal enlargement was noted in the pancreatic head, which was isoattenuating to the pancreas in two patients and hypoattenuating to the pancreas in one patient. Minimal peripancreatic stranding that suggested inflammation was seen in six patients. The inflammatory thickening was confined to the peripancreatic region and did not involve the mesentery, the anterior pararenal fascia, or the lateroconal fascia. A peripheral rim of low attenuation was seen in three patients. In one patient with focal enlargement, the main pancreatic duct was dilated. There was no substantial mass effect or parenchymal calcification.
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Peripancreatic nodes were seen in nine patients; in seven of these nine patients, the nodes were more than 1 cm in diameter on the short axis. The diameter of the nodes varied from 6 to 30 mm (mean, 14 mm), and the number of these nodes ranged from two to 10 (mean, 4.5).
Dilated intrahepatic biliary ducts were observed in six patients, and a dilated common bile duct was seen in two patients. The dilated common bile duct was 11–16 mm (mean, 12.2 mm) in diameter. Other associated findings that occurred in one patient each were stricture of the common bile duct, thickening of the distal ileum, retroperitoneal fibrosis (Fig 1), bilateral renal hypoattenuating lesions that were inflammatory pseudotumors (Fig 1), bilateral pleural effusions, and mediastinal nodes (Fig 1) with lung nodules. One patient had thickening of the common bile duct that showed moderate enhancement.
MR imaging and MR cholangiopancreatography.—Diffuse pancreatic enlargement with minimal high signal intensity on T2-weighted MR images was seen in two of four patients. These two patients had heterogeneous enhancement, and associated rimlike enhancement in the body and the tail of the pancreas was observed in one of these two patients. Peripancreatic inflammation was seen in one patient with diffuse enlargement. Two patients had a focal mass in the head of the pancreas. Homogeneous enhancement of the pancreas was seen in these two patients. MR cholangiopancreatography revealed primary sclerosing cholangitis–like findings with multiple intrahepatic strictures and dilated intrahepatic ducts in one patient and stricture of the common bile duct in another patient. Diffuse narrowing of the main pancreatic duct was observed in two patients with diffuse enlargement.
Transabdominal US.—A focal hypoechoic mass at the pancreatic head and the uncinate process was present in one of nine patients. One patient had diffuse enlargement of the pancreas (Fig 1). In seven patients, the pancreas had no abnormalities. Other findings included intrahepatic biliary ductal dilatation in five patients and a dilated common bile duct in four patients. The common bile duct was 9–14 mm in diameter (mean diameter, 11 mm). A distended gallbladder with sludge was noted in three patients. Two patients had a thickened gallbladder wall, with thickness of the wall that was 4–6 mm (mean, 5 mm).
Endoscopic US.—The predominant finding in 21 patients who underwent this examination was pancreatic swelling with altered echotexture. Diffuse altered echotexture with enlargement was seen in 13 patients. Additionally, two patients with diffuse disease also had ill-defined focal enlargement—one focal mass in the head in one patient and two focal masses in the head and in the tail in the other patient. Six patients had focal enlargement of the head of the pancreas (Fig 2). In one patient, the pancreas appeared normal at endoscopic US, with a focal mass in the medial wall of the duodenum. However, at surgery, this was found to be the enlarged head of the pancreas. In one patient, the pancreas appeared normal, with a diffusely dilated main pancreatic duct. Peripancreatic enlarged nodes (>1 cm in diameter on the short axis) were seen in eight patients. Thickened extrahepatic bile ducts were observed in two patients. There was no evidence of parenchymal calcification, vascular encasement, peripancreatic fluid collection, or peripancreatic inflammatory changes.
Endoscopic retrograde cholangiopancreatography and percutaneous transhepatic cholangiography.—Biliary ductal abnormalities were seen in 17 of 20 patients (19 who underwent endoscopic retrograde cholangiopancreatography and one who underwent percutaneous transhepatic cholangiography). The commonest finding was stricture of the distal common bile duct, which was present in 12 patients (Figs 1, 3). Multiple short intrahepatic duct strictures (Fig 1) that resembled primary sclerosing cholangitis were present in six patients, and one of these six patients had concomitant common bile duct stricture. In two patients, endoscopic retrograde cholangiopancreatography did not disclose any abnormalities. Endoscopic retrograde cholangiopancreatography was performed in 16 of 19 patients. Diffuse irregularity and narrowing of the pancreatic duct was observed in nine patients (Fig 1). Focal stricture in the proximal pancreatic duct was seen in six patients (Fig 3). One patient had a normal pancreatic duct, with concomitant pancreatic divisum (a congenital anomaly of the pancreatic duct).
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One patient who had a focal mass at prior endoscopic US developed diffuse enlargement with altered echotexture at follow-up endoscopic US performed after 2 months.
At follow-up endoscopic retrograde cholangiopancreatography within 6 months, results indicated resolution of the stricture in the common bile duct in three patients. Of these three patients, two developed new intrahepatic duct strictures. One patient developed intrahepatic duct strictures similar to those observed in primary sclerosing cholangitis within 3 months of initial presentation. One patient developed focal stricture of the proximal main pancreatic duct after 12 months. In one patient in whom an initial attempt at endoscopic retrograde cholangiopancreatography was unsuccessful, follow-up with this modality within 2 months showed diffuse irregular narrowing of the main pancreatic duct. In one patient with initial focal proximal main pancreatic duct stricture, follow-up endoscopic retrograde cholangiopancreatography within 2 months revealed diffuse narrowing of the main pancreatic duct.
Histopathologic Findings
During surgery, the pancreas was "rock-hard" at palpation, which was reflected at gross pathologic examination as a fleshy fibrotic masslike pancreas (Fig 2). Uniformly thickened and dilated bile ducts were noted with smooth and glistening mucosal surfaces. Lithiasis, inspissated bile, and mucosal erosions were absent.
The microscopic examination revealed the cardinal histopathologic features in all patients. The most conspicuous findings were a dense lymphoplasmacytic inflammatory infiltrate and scattered eosinophils. When residual pancreatic tissue was present, the inflammatory cells aggregated around medium and large interlobular ducts. Clusters of inflammatory cells were also present in the walls of small veins and nerves at the periphery of the masses. Whenever vessels were involved in the inflammatory process, the inflammation was strikingly limited to medium and large vessels. This was characterized by a polymorphous infiltrate that extended transmurally into the vein, with characteristic eccentric involvement of the wall. Microscopic examination of the bile duct wall revealed expansion of the wall that resulted from a fibroinflammatory process. In some cases, the walls of both the pancreatic duct and intrapancreatic portion of the common pancreatic duct were surrounded by a variable degree of fibrosis. Various degrees of pancreatic parenchymal atrophy were noted. The atrophy ranged from minimal acinar destruction to complete obliteration of the pancreatic parenchyma caused by a dense fibrosis, with marked collagen deposition and a dense inflammatory infiltrate.
In patients who underwent endoscopic US–guided biopsy or CT-guided biopsy, the histopathologic features were not entirely conclusive. There were a predominant lymphocytic infiltrate, a varying number of plasma cells, fibrosis, and an absence of malignant cells. However, at initial experience with this entity, a prospective diagnosis of autoimmune pancreatitis was established on the basis of clinical, radiologic, and serologic findings.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Most of the patients with these diseases have serum markers of autoimmune disorders, such as increased IgG and antinuclear antibody levels. This was observed in our study, wherein seven of 12 tested patients had increased IgG and antinuclear antibody levels. Similar findings were also observed in other studies (9,12). The pathologic features of this disease have been described in the literature (13,14), but the imaging features have not been well described. A good response to steroid therapy also has been described in the literature (15,16). To our knowledge, our study included one of the largest series of patients with autoimmune pancreatitis, with detailed documentation of clinical features, cross-sectional imaging findings, and correlation of imaging findings with histopathologic findings.
Clinical features are nonspecific and include upper abdominal pain, easy fatigability, and jaundice. Imaging is usually performed to determine the cause of jaundice. As reported in the literature, there is a strong male preponderance. In our study, 25 of 29 patients were men. The elderly age group is predominantly affected, which has been reported in previous studies (12).
The association with other autoimmune disorders has been well described (4–10). Remarkably, these patients do not have prior attacks of acute pancreatitis or alcohol abuse. This probably suggests a slow progression of disease, with no acute exacerbation. Remission of the disease with steroid therapy is also remarkable, but a few cases of recurrence have been described even after surgery (13,17).
In our study, three patients had resolution of enlargement at CT after corticosteroid therapy. Patients with an autoimmune disorder with involvement of other organs also responded well with corticosteroids in our study.
In our study, imaging features consistently indicated focal or diffuse enlargement of the pancreas at endoscopic US, CT, and MR imaging. Though the diffuse form is the most commonly reported in the literature, focal forms have been described by a few researchers (16). In our study, the diffuse form, as seen at CT and endoscopic US, was more common than was the focal form. Findings at CT and at endoscopic US (in 19 patients) were in agreement in the identification of the type of pancreatic involvement in nine patients with the diffuse form and in one patient with the focal form.
In three patients, endoscopic US helped to identify the diffuse altered echotexture (n = 1) or focal disease (n = 2) when CT findings were normal. In three patients with focal disease at endoscopic US, the diffuse nature of the disease was evident at CT. This discrepancy can be explained by the limited view with endoscopic US for visualization of the entire pancreas. Another reason could be the interval between the two imaging sessions. In these patients, endoscopic US was performed 2–4 weeks prior to CT (average, 9 days). Similarly, in two cases where CT showed focal disease, endoscopic US depicted diffuse altered echotexture of the entire pancreas. This can be explained by higher sensitivity of endoscopic US for tissue textural alterations. In one patient in whom endoscopic US showed a normal pancreas, CT showed focal enlargement of the head; however, this was an apparent error in which endoscopic US depicted a duodenal mass but at surgery the finding was observed as a pancreatic head mass.
The focal form that involved the head and the uncinate process was difficult to differentiate from pancreatic carcinoma. This is evident from the findings in our study, as most of the patients with the focal form underwent surgery, with a clinical diagnosis of pancreatic carcinoma. The diagnosis of pancreatic cancer was also considered preoperatively, which indicated the difficulty in the differentiation of the focal form of autoimmune pancreatitis from pancreatic carcinoma at gross examination. This is also reported in a few studies (18). A diffusely enlarged pancreas can be present in malignant lymphoma, plasmacytoma, metastases, and diffuse infiltrative pancreatic carcinoma. However, in most of these conditions, heterogeneous attenuation of the pancreas and an irregular pancreatic contour are observed, findings that are in contrast to those observed in autoimmune pancreatitis.
Peripancreatic fat stranding was seen in seven patients at CT, but this was minimal. This finding probably suggests a low-grade inflammatory reaction in patients with this entity. The classic appearance of the pancreas in most of the patients with diffuse forms was a mildly enlarged pancreas (sausage shaped), with homogeneous attenuation, moderate enhancement, and sharp borders, with the absence of normal pancreatic clefts (featureless) and a peripheral rim of hypoattenuation that possibly represented inflammatory exudates. Also in our study, three patients had rimlike hypoattenuation in the periphery of the pancreas that corresponded to inflammation and fibrosis at pathologic analysis.
Irie et al (19) reported a capsulelike smooth rim of contrast enhancement at CT and MR imaging examination of patients with autoimmune pancreatitis that was presumed to represent fluid collection, phlegmon, or fibrosis. We did not observe such a finding at CT, but at MR imaging, one patient had peripheral rim enhancement. This corresponded to peripheral inflammation and fibrosis. Homogeneous enhancement of the pancreas was seen in all patients except one who had a focal hypoattenuating mass in the head at CT in our study. This can be used to differentiate the focal form from pancreatic carcinoma, as most of the carcinomas show less enhancement than does the normal pancreas at imaging in the arterial phase. However, in one series of cases, 11% of pancreatic tumors were isoattenuating to pancreatic parenchyma at contrast-enhanced CT (20). Invasion of vessels, vascular encasement, mass effect, and fluid collections were conspicuously absent in all cases. This is also reported in the literature (19).
Biliary and pancreatic ductal abnormalities are well described in the literature. Yoshida et al (3) have described endoscopic retrograde cholangiopancreatographic criteria for diagnosis of autoimmune pancreatitis. These criteria included diffuse irregular narrowing of the main pancreatic duct and abnormalities noted at endoscopic retrograde cholangiopancreatography that normalized after steroid therapy. Most of the patients in our study had biliary and pancreatic ductal strictures at endoscopic retrograde cholangiopancreatography or MR cholangiopancreatography, with minimal thickening and irregularity of the ducts. The involvement of the main pancreatic duct is very characteristic of this entity and is seen at endoscopic retrograde cholangiopancreatography.
Kamisawa et al (21) reported similar findings of diffuse swelling of the pancreas with irregular narrowing of the main pancreatic duct in five patients with autoimmune pancreatitis. Biliary strictures resemble those observed in primary sclerosing cholangitis (22). Resolution of the ductal abnormality has been well described in the literature and was also observed in our study in three patients with biliary strictures. However, in two of these patients, new biliary strictures appeared at different sites at follow-up.
There were a few limitations in our study. Given its retrospective nature, all the patients did not undergo all the imaging tests, and serologic tests for autoimmune diseases, such as IgG4 level, were not available in all patients. Likewise, surgical confirmation was not available in all subjects. Finally, follow-up imaging after treatment with corticosteroids was available in a selected number of patients, which limits our understanding of the natural course of this disease.
In summary, our study findings show that serologic and clinical findings, such as the IgG level and a history of autoimmune disease, should alert the radiologist to the rare diagnosis of autoimmune pancreatitis. In an appropriate clinical setting, a constellation of imaging features at CT and endoscopic retrograde cholangiopancreatography is helpful in the diagnosis of autoimmune pancreatitis. Features at CT that can help distinguish autoimmune pancreatitis from pancreatic cancer include homogeneous enhancement of the pancreas, absence of encasement of mesenteric vessels or substantial parenchymal atrophy, and the absence of metastatic disease in the liver or the peritoneum, which are all characteristic of autoimmune pancreatitis. Concomitant diffuse pancreatic ductal narrowing and common bile duct and intrahepatic biliary strictures that resemble primary sclerosing cholangitis should also raise the probability of a diagnosis of autoimmune pancreatitis. A trial of corticosteroid therapy may be beneficial. However, in the absence of supporting history and serologic marker levels, a focal form of autoimmune pancreatitis may be extremely difficult to differentiate from pancreatic cancer on the basis of imaging features alone.
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FOOTNOTES |
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Authors stated no financial relationship to disclose.
Author contributions: Guarantors of integrity of entire study, D.V.S., J.F.S.; study concepts, D.V.S., J.F.; study design, D.V.S., S.S.; literature research, D.V.S., S.P.K., J.F.; clinical studies, D.V.S., S.P.K.; data acquisition, D.V.S., G.Y.L., C.D.F., J.F.; data analysis/interpretation, D.V.S., S.P.K., G.Y.L.; manuscript preparation, D.V.S., S.P.K., J.F., P.R.M.; manuscript definition of intellectual content, D.V.S., J.F.; manuscript editing, S.S., C.D.F., A.L.W., P.R.M., M.M.M.; manuscript revision/review, S.P.K., D.V.S.; manuscript final version approval, D.V.S.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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