The most common mimickers

Some non-neoplastic pancreatic diseases and anatomic variants can mimic pancreatic adenocarcinoma (PDA).

Pancreatitis

Focal chronic pancreatitis and autoimmune pancreatitis may have a radiologic appearance similar to PDA(focal lesion with upstream biliary or pancreatic duct dilatation).Patient symptoms can be similar:abdominal pain and weight loss.Chronic pancreatitis, with inflammation and fibrosis,can lead to irregular parenchymal enhancement on contrast CT,glandular atrophy,calcifications and pancreatic duct dilation[1-2].

MRI is useful for differential diagnosis.On MRI,PDA shows low signal intensity on unenhanced T1w sequences and an enhancement that is lower than normal pancreatic parenchyma on arterial phase sequences and becomes similar on delayed sequences [1-3].

Magnetic resonance cholangiopancreatography (MRCP) [1-3-4]:

- PDA: abrupt interruption of main pancreatic duct along the neoplastic lesion and upstream dilatation

- pancreatitis: duct-penetrating sign.

Chronic pancreatitis has an increased risk of developing pancreatic cancer (RR: 13.3) [5].

Hypervascular pancreatic lesions

Metastases

Enhancement pattern of hypervascular pancreatic metastases may be similar to other pancreatic primary tumours(i.e. NETs and microcystic serous cystadenoma),or benign lesions(i.e. intrapancreatic accessory spleen).T2-w imaging and DWI may be helpful for differential diagnosis. Metastases with hypovascular pattern may mimic pancreatic adenocarcinoma [1].

Pancreatic ductal adenocarcinoma: key points

PDA has an overall 5-year survival rate of 7% and is the 4th leading deadly cancer [6].Less than 20% of patients with PDA are diagnosed early enough to allow surgical resection,which is the only therapeutic chance to cure the neoplasm [7].

CT sensitivity in the detection of small PDA ranges from 63% to 85% [8-9]. Early PDA CT findings are usually not associated with any clinical signs or symptoms [10-11].Technical factors such as lack of a correct study protocol (i.e. lack of pancreatic phase) or inadequate image acquisition(i.e. low mA, image noise) may lead to miss early cancer lesions [12-13].

Distal parenchymal atrophy [12-14]:

- not common in early PDA;

- allows to discriminate between PDA and chronic pancreatitis (specificity 96%; sensitivity 45%);

-upstream parenchymal atrophy can allow the recognition of the hypoattenuating lesion.

Focal hypoattenuating lesion is the most common missed finding in prediagnostic exams [12-14-15] and this might be due to coexistence of hypoattenuation of distal pancreatic parenchyma.

Contour abnormality and upstream pancreatic duct dilatation are two relevant findings often encountered on prediagnostic CT which should guide the radiologist in the decision of performing a pancreatic CT/MRI study protocol [14].It’s worth remembering that these findings are not so useful in the differentiation of PDA from chronic pancreatitis [12] and that PDA and chronic pancreatitis can also coexist in the same patient [14].

Take home-message for PDA: most relevant subtle missed findings in pre-diagnostic imaging examinations that should suggest the presence of underlying pancreatic adenocarcinoma are hypoattenuating lesion,followed by contour abnormality and pancreatic duct interruption with upstream dilatation (Figures 2 and 3).

Malignant IPMN: key points

Asymptomatic pancreatic cysts are often incidentally encountered in 3-14% of routine CT scans,and their presence correlates with increasing patient age [14-15]. Pancreatic cystic lesions may be benign without malignant potential, premalignant or malignant cysts [16]. IPMN may develop malignancy with an overall incidence rate of 3.3%, 6.6%, and 15.0% at 5, 10, and 15 years, respectively [17].

The hardest challenge for both clinician and radiologist is to differentiate benign (Figures 4 and 5) from potential malignant IPMN for adequate patient management [16].

Take home-message for IPMN: according to the Revised International Consensus Fukuoka Guidelines [18], the most relevant predicting features of a malignant IPMN include thick enhancing wall and septa, presence of enhancing mural nodule of 5 mm or greater, abrupt main pancreatic duct caliber change, lymphadenopathy, large main pancreatic duct size, increasing branch-duct IPMN size, faster cyst growth rate [19]. Early signs of malignant IPMN is the presence of main pancreatic duct dilatation, with an HR of 1.47 per each 1-mm increase in size (Figures 6, 7 and 8) [17].

In our experience, this finding may be missed on prediagnostic exams. Therefore, in patients with IPMN, the diameter of the pancreatic duct should be measured by radiologists to avoid overlooking malignant IPMN.

Serous cystadenoma (SCA): key points

SCA can simulate a hypervascular pancreatic lesion, especially a neuroendocrine tumour.

SCA (Figure 9) on CT: cystic lesion with contrast-enhanced walls, possible radial calcifications [1]; on MRI, T2 hyperintensity (small cystic components of SCA) and high ADC value [1-20]. Differential diagnosis with cystic degeneration of neuroendocrine tumours or PDA may be challenging.

In our experience, we also identified a potential pitfall for the diagnosis of IPMN: the presence on precontrast CT scan of an IPMN appearing as a spontaneously hyperdense lesion in the pancreatic head with difficulty in assessment of contrast enhancement, which mimicked a serous cystadenoma (Figure 10). This radiologic appearance was due to intracystic proteinaceous content as confirmed through pancreatic EUS-FNA.