PMC6159167_01
(a-d) Axial arterial (a) and portal venous contrasts enhanced. (b) CT images through the pancreas obtained in 2006 using a pancreatic mass protocol show diffuse pancreatic parenchymal calcifications with mild pancreatic ductal dilatation and no discrete mass. Contrast-enhanced CT images through the pancreatic head (c) and body (d) obtained in 2015 reveal persistent parenchymal calcifications and mild pancreatic duct dilatation. Note the lack of parenchymal atrophy in 2015. Development of a new arterially enhancing mass in the pancreatic neck (arrow on c) and hypodense mass in the pancreatic tail (arrow in d) is identified.
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A multi-detector CT of the abdomen and pelvis utilizing a pancreatic mass protocol (arterial, portal venous and delayed phases) was performed which revealed a diffusely enlarged pancreas with extensive parenchymal calcifications (Figure 1). A CT of the abdomen and pelvis with pancreatic mass protocol was repeated (Figure 1), which revealed new hypoattenuating masses in the pancreatic neck and tail.
( a-e) Pre-contrast T1 weighted image with fat saturation (a) shows normal intrinsic T1 signal within the pancreas, with a T1 hypointense mass in the pancreatic tail (arrow). (b) Post-contrast arterial phase T1 weighted image reveals brisk enhancement of the pancreas with a relative hypointense mass in the pancreatic tail (arrow). Post-contrast T1 weighted image with fat saturation in portal venous phase (c) demonstrates no delayed enhancement of the pancreas, with increased irregular enhancement of the pancreatic tail mass (arrow). T2 weighted sequences with fat saturation (d) and without fat saturation (e) show the pancreatic tail mass to be T2 hyperintense (arrows). Additional T2 hyperintense masses are noted in the pancreatic neck and distal body (arrowheads in d).
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T1) was performed (Figure 2). The MRI confirmed multiple well-circumscribed masses throughout the pancreas, many of which had increased T2 signal with cystic change. The pancreatic duct was at most mildly prominent, and no lesions were identified outside of the pancreas. The largest pancreatic mass in the tail measured approximately 3.5 cm, with peripheral enhancement and central hypointense signal (Figure 2).
(a-c) Contrast-enhanced arterial phased CT image through the pancreas obtained in 2015 (a) show diffuse parenchymal calcifications with a more discrete mass in the pancreatic tail (arrow). SPECT images of the abdomen from an indium-111 Octreotide scan through the pancreas (b) show diffuse uptake of radiotracer throughout the entire pancreas (arrows). Fused SPECT-CT images from the same study (c) confirm diffuse uptake in the pancreas (arrow), including the pancreatic tail mass (arrowhead).
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Fused SPECT-CT imaging was also performed for improved uptake localization (Figure 3).
(a) 10x H&E. The nodules were comprised of trabecular cords and insular nests of fairly uniform epitheliod cells with surrounding deposition of amyloid matrix (confirmed by Congo Red special stain) and multiple calcifications (white arrow). 20x H&E. (b) Higher power view of the cords of epithelial cells with surrounding amyloid matrix. No significant pleomorphism or mitotic activity was identified on multiple representative sections. 2x IHC. (c) Immunohistochemical stain for neuroendocrine marker chromogranin A shows diffuse cytoplasmic staining of the neoplastic cells. 2x IHC. (d) Immunohistochemical stain for neuroendocrine marker synaptophysin shows diffuse cytoplasmic staining of the neoplastic cells.
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Sectioning of the pancreas revealed numerous well-circumscribed, solid and tumoural masses ranging from minute up to the largest grossly identified lesion measuring 3.5 cm in diameter (Figure 4). Many of the nodules showed numerous calcifications and localized amyloid deposition (Figure 4a,b). Immunohistochemical stains were performed and the neoplastic cells marked strongly for the neuroendocrine markers chromogranin A and synaptophysin (Figure 4c,d).