Pancreatic ductal adenocarcinoma (PDAC) is the most common primary pancreatic malignancy, ranking fourth in cancer-related mortality in the United States. Typically, PDAC appears on images as a hypovascular mass with upstream pancreatic duct dilatation and abrupt duct cutoff, distal pancreatic atrophy, and vascular encasement, with metastatic involvement including lymphadenopathy. However, atypical manifestations that may limit detection of the underlying PDAC may also occur. Atypical PDAC features include findings related to associated conditions such as acute or chronic pancreatitis, a mass that is isointense to the parenchyma, multiplicity, diffuse tumor infiltration, associated calcifications, and cystic components. Several neoplastic and inflammatory conditions can mimic PDAC, such as paraduodenal "groove" pancreatitis, autoimmune pancreatitis, focal acute and chronic pancreatitis, neuroendocrine tumors, solid pseudopapillary neoplasms, metastases, and lymphoma. Differentiation of these conditions from PDAC can be challenging due to overlapping CT and MRI features; however, certain findings can help in differentiation. Diffusion-weighted MRI can be helpful but also can be nonspecific. Accurate diagnosis is pivotal for guiding therapeutic planning and potential outcomes in PDAC and avoiding biopsy or surgical treatment of some of these mimics. Biopsy may still be required for diagnosis in some cases. The authors describe the typical and atypical imaging findings of PDAC and features that may help to differentiate PDAC from its mimics. ©RSNA, 2023 Online supplemental material is available for this article. Quiz questions for this article are available through the Online Learning Center. See the invited commentary by Zins in this issue.

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.

Diagnosis of a focal pancreatic mass in routine clinical practice can be a challenge because patients with chronic pancreatitis may present with symptoms and imaging findings that can be difficult to distinguish from pancreatic cancer. Markers, such as cancer antigen 19-9 and carcinoembryonic antigen, are helpful if abnormal, but normal values do not rule out pancreatic cancer. One of the strongest complicating factors is that chronic pancreatitis is a risk factor for pancreatic cancer. Transition of chronic pancreatitis to pancreatic cancer is relatively rare, but it normally has a poor prognosis because diagnosis is often delayed. From a radiologic diagnosis perspective, the classic so-called double-duct sign is helpful. This sign is considered a hallmark sign of pancreatic cancer on magnetic resonance cholangiopancreatography, but it can also be identified in patients with chronic pancreatitis or with other conditions. A number of additional imaging findings or signs are, therefore, necessary. The aim of this article was to describe the strong CT and MR imaging features or integrated imaging features that can help to differentiate between pancreatic cancer and focal chronic pancreatitis.

Certain inflammatory pancreatic abnormalities may mimic pancreatic ductal adenocarcinoma at imaging, which precludes accurate preoperative diagnosis and may lead to unnecessary surgery. Inflammatory conditions that may appear masslike include mass-forming chronic pancreatitis, focal autoimmune pancreatitis, and paraduodenal pancreatitis or "groove pancreatitis." In addition, obstructive chronic pancreatitis can mimic an obstructing ampullary mass or main duct intraductal papillary mucinous neoplasm. Secondary imaging features such as the duct-penetrating sign, biliary or main pancreatic duct skip strictures, a capsulelike rim, the pancreatic duct-to-parenchyma ratio, displaced calcifications in patients with chronic calcific pancreatitis, the "double duct" sign, and vessel encasement or displacement can help to suggest the possibility of an inflammatory mass or a neoplastic process. An awareness of the secondary signs that favor a diagnosis of malignant or inflammatory lesions in the pancreas can help the radiologist to perform the differential diagnosis and determine the degree of suspicion for malignancy. Repeat biopsy or surgical resection may be necessary to achieve an accurate diagnosis and prevent unnecessary surgery for inflammatory conditions. Online supplemental material and DICOM image stacks are available for this article. ^©RSNA, 2019.

Increasing numbers of incidental pancreatic lesions are being detected each year. Accurate characterisation of pancreatic lesions into benign, precancerous, and cancer masses is crucial in deciding whether to use treatment or surveillance. Distinguishing benign lesions from precancerous and cancerous lesions can prevent patients from undergoing unnecessary major surgery. Despite the importance of accurately classifying pancreatic lesions, there is no clear algorithm for management of focal pancreatic lesions.

To determine and compare the diagnostic accuracy of various imaging modalities in detecting cancerous and precancerous lesions in people with focal pancreatic lesions.

We searched the CENTRAL, MEDLINE, Embase, and Science Citation Index until 19 July 2016. We searched the references of included studies to identify further studies. We did not restrict studies based on language or publication status, or whether data were collected prospectively or retrospectively.

We planned to include studies reporting cross-sectional information on the index test (CT (computed tomography), MRI (magnetic resonance imaging), PET (positron emission tomography), EUS (endoscopic ultrasound), EUS elastography, and EUS-guided biopsy or FNA (fine-needle aspiration)) and reference standard (confirmation of the nature of the lesion was obtained by histopathological examination of the entire lesion by surgical excision, or histopathological examination for confirmation of precancer or cancer by biopsy and clinical follow-up of at least six months in people with negative index tests) in people with pancreatic lesions irrespective of language or publication status or whether the data were collected prospectively or retrospectively.

Two review authors independently searched the references to identify relevant studies and extracted the data. We planned to use the bivariate analysis to calculate the summary sensitivity and specificity with their 95% confidence intervals and the hierarchical summary receiver operating characteristic (HSROC) to compare the tests and assess heterogeneity, but used simpler models (such as univariate random-effects model and univariate fixed-effect model) for combining studies when appropriate because of the sparse data. We were unable to compare the diagnostic performance of the tests using formal statistical methods because of sparse data.

We included 54 studies involving a total of 3,196 participants evaluating the diagnostic accuracy of various index tests. In these 54 studies, eight different target conditions were identified with different final diagnoses constituting benign, precancerous, and cancerous lesions. None of the studies was of high methodological quality. None of the comparisons in which single studies were included was of sufficiently high methodological quality to warrant highlighting of the results. For differentiation of cancerous lesions from benign or precancerous lesions, we identified only one study per index test. The second analysis, of studies differentiating cancerous versus benign lesions, provided three tests in which meta-analysis could be performed. The sensitivities and specificities for diagnosing cancer were: EUS-FNA: sensitivity 0.79 (95% confidence interval (CI) 0.07 to 1.00), specificity 1.00 (95% CI 0.91 to 1.00); EUS: sensitivity 0.95 (95% CI 0.84 to 0.99), specificity 0.53 (95% CI 0.31 to 0.74); PET: sensitivity 0.92 (95% CI 0.80 to 0.97), specificity 0.65 (95% CI 0.39 to 0.84). The third analysis, of studies differentiating precancerous or cancerous lesions from benign lesions, only provided one test (EUS-FNA) in which meta-analysis was performed. EUS-FNA had moderate sensitivity for diagnosing precancerous or cancerous lesions (sensitivity 0.73 (95% CI 0.01 to 1.00) and high specificity 0.94 (95% CI 0.15 to 1.00), the extremely wide confidence intervals reflecting the heterogeneity between the studies). The fourth analysis, of studies differentiating cancerous (invasive carcinoma) from precancerous (dysplasia) provided three tests in which meta-analysis was performed. The sensitivities and specificities for diagnosing invasive carcinoma were: CT: sensitivity 0.72 (95% CI 0.50 to 0.87), specificity 0.92 (95% CI 0.81 to 0.97); EUS: sensitivity 0.78 (95% CI 0.44 to 0.94), specificity 0.91 (95% CI 0.61 to 0.98); EUS-FNA: sensitivity 0.66 (95% CI 0.03 to 0.99), specificity 0.92 (95% CI 0.73 to 0.98). The fifth analysis, of studies differentiating cancerous (high-grade dysplasia or invasive carcinoma) versus precancerous (low- or intermediate-grade dysplasia) provided six tests in which meta-analysis was performed. The sensitivities and specificities for diagnosing cancer (high-grade dysplasia or invasive carcinoma) were: CT: sensitivity 0.87 (95% CI 0.00 to 1.00), specificity 0.96 (95% CI 0.00 to 1.00); EUS: sensitivity 0.86 (95% CI 0.74 to 0.92), specificity 0.91 (95% CI 0.83 to 0.96); EUS-FNA: sensitivity 0.47 (95% CI 0.24 to 0.70), specificity 0.91 (95% CI 0.32 to 1.00); EUS-FNA carcinoembryonic antigen 200 ng/mL: sensitivity 0.58 (95% CI 0.28 to 0.83), specificity 0.51 (95% CI 0.19 to 0.81); MRI: sensitivity 0.69 (95% CI 0.44 to 0.86), specificity 0.93 (95% CI 0.43 to 1.00); PET: sensitivity 0.90 (95% CI 0.79 to 0.96), specificity 0.94 (95% CI 0.81 to 0.99). The sixth analysis, of studies differentiating cancerous (invasive carcinoma) from precancerous (low-grade dysplasia) provided no tests in which meta-analysis was performed. The seventh analysis, of studies differentiating precancerous or cancerous (intermediate- or high-grade dysplasia or invasive carcinoma) from precancerous (low-grade dysplasia) provided two tests in which meta-analysis was performed. The sensitivity and specificity for diagnosing cancer were: CT: sensitivity 0.83 (95% CI 0.68 to 0.92), specificity 0.83 (95% CI 0.64 to 0.93) and MRI: sensitivity 0.80 (95% CI 0.58 to 0.92), specificity 0.81 (95% CI 0.53 to 0.95), respectively. The eighth analysis, of studies differentiating precancerous or cancerous (intermediate- or high-grade dysplasia or invasive carcinoma) from precancerous (low-grade dysplasia) or benign lesions provided no test in which meta-analysis was performed.There were no major alterations in the subgroup analysis of cystic pancreatic focal lesions (42 studies; 2086 participants). None of the included studies evaluated EUS elastography or sequential testing.

We were unable to arrive at any firm conclusions because of the differences in the way that study authors classified focal pancreatic lesions into cancerous, precancerous, and benign lesions; the inclusion of few studies with wide confidence intervals for each comparison; poor methodological quality in the studies; and heterogeneity in the estimates within comparisons.

In the evaluation of common pancreatic diseases, MRCP is a noninvasive alternative to ERCP. Ductal anatomy can be ascertained without risk of complications. MRCP is valuable in defining common anatomic variants, determining the state of the pancreatic duct in pancreatitis, and characterizing neoplasms, especially combined with other MR imaging sequences. With the advent of MRCP, techniques requiring endoscopy and percutaneous access are largely reserved for histologic diagnosis and treatment, or for cases in which MRCP fails to establish a diagnosis.

Acute pancreatitis is a frequent inflammatory and necrotic process of pancreas and peripancreatic field. To detect the presence of infected or sterile necrotic components and hemorrhage of the pancreatic paranchyma is important for therapeutic approach. Chronic pancreatitis is characterized by irreversible exocrine dysfunction, progressive loss of pancreatic tissue and morphological changes of the pancreatic canal. Imaging modalities play a primary role in the management of both acute and cronic pancreatitis. CT and MR imaging confirm the diagnosis and detect the severity of disease. In chronic pancreatitis, MRCP after Secretin administration, Spiral CT and endoscopic US seems to replace diagnostic ERCP. However differentiation of pseudotumor of chronic pancreatitis from the pancreatic carcinoma is difficult with either imaging modalities.

To determine if dynamic gadolinium-enhanced magnetic resonance (MR) imaging can distinguish chronic pancreatitis from pancreatic carcinoma.

A retrospective review of MR and pathology examination findings was performed for 24 patients with pancreatic ductal adenocarcinoma and seven with chronic pancreatitis who underwent dynamic gadolinium-enhanced breath-hold spoiled gradient-echo imaging. Arterial, portal, and delayed phase images were obtained after injection of gadopentatate dimeglumine. The MR images of 14 patients without clinical evidence of pancreatic disease were also reviewed as controls. Signal intensity (SI) was measured on the precontrast (pre) and gadolinium-enhanced (post) images of the area of the pancreas sampled at biopsy and of the nontumorous pancreas. Percentage enhancement was defined as SIpre/SIpost x 100.

Normal pancreas showed rapid enhancement that peaked in the arterial or portal phase. For both diseases, T1-weighted images showed hypointense masses with progressive enhancement (differences were significant [P < .05] on only delayed fat-saturated images). Differences in enhancement between either disease state and normal pancreas were significant for at least one phase. Nontumorous pancreas in patients with carcinoma showed gradual enhancement that was significantly different from that of normal pancreas.

Chronic pancreatitis and pancreatic carcinoma show abnormal pancreatic enhancement, but the two were not distinguished on the basis of degree and time of enhancement.