PMC5491810_01
On CECT (axial) before a steroid trial, a mass lesion about 3 cm in size detected in the pancreatic body showed low density in the early phase (a) and homogenous delayed enhancement in the portal (b) and late (c) phases.
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On CECT, a mass lesion about 3 cm in size detected in the pancreatic body showed low density in the early phase and homogenous delayed enhancement in the portal and late phases (Fig. 1).
The findings of imaging studies before a steroid trial were as follows: a: On diffusion-weighted images, the mass lesion in the pancreatic body showed a high signal. b: MRCP showed stenosis of the MPD in the pancreatic body, upstream MPD dilation 3 mm in diameter, and multiple pancreatic cysts considered to be BD-IPMNs in the pancreatic tail. c: EUS visualized a 3-cm-diameter low echoic mass with a heterogeneous internal echo structure in the body of the pancreas. d, e: On EUS, suspected BD-IPMNs were also detected in the pancreatic body and tail apart from the mass lesion. d shows small pancreatic cysts in the pancreatic body (arrowhead, cyst; arrow, main pancreatic duct) and e shows a multilocular pancreatic cyst more than 30 mm in size without a mural nodule in the pancreatic tail. f: On ERP, obstruction of the MPD in the pancreatic body was detected, and the upstream MPD could not be visualized.
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MRI, this mass lesion showed a low signal in both T1- and T2-weighted images and a high signal in the diffusion-weighted image (Fig. 2a). Magnetic resonance cholangiopancreatography (MRCP) showed a stenosis of the main pancreatic duct (MPD) in the pancreatic body, upstream MPD dilation 3 mm in diameter, and multiple pancreatic cysts a maximum of 3 cm in diameter considered to be BD-IPMNs in the pancreatic body and tail (Fig. 2b). Endoscopic ultrasonography (EUS) visualized a 3-cm low echoic mass with a heterogeneous internal echo structure in the body of the pancreas (Fig. 2c). In addition, apart from this mass lesion, suspected BD-IPMNs 30 mm in maximum size without mural nodules were detected in the tail side of the pancreas (Fig. 2d and e). On endoscopic retrograde pancreatography (ERP), obstruction of the MPD in the pancreatic body was detected, and the upstream portion of the MPD was not visualized (Fig. 2f).
a: Hematoxylin and Eosin staining (40x). The specimen was fibrotic with infiltration of many lymphocytes and plasmacytes. b: LCA staining (40x). Many LCA-positive cells diffusely infiltrated the fibrotic lesion of the specimen. c: IgG4 staining (40x). Infiltration of abundant (>=10 cells/HPF) IgG4-positive cells in the fibrotic lesion of the specimen was detected. d: Elastica-Masson staining (100x). Obliterative phlebitis was detected.
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The specimen was histopathologically fibrotic with infiltration of many lymphocytes and plasmacytes, and obliterative phlebitis was also detected (Fig. 3).
a-c: CECT (axial) after the initial administration of prednisolone (a: 2 weeks after, b: 2 months after, c: 5 months after) showed the mass lesion in the pancreatic body to be notably reduced in size, and the enhancement patterns of this mass lesion on CECT returned to those of the normal pancreas. d: ERP after a steroid trial revealed improvement of the MPD obstruction in the pancreatic body, visualization of the MPD up to the pancreatic tail and communication of the MPD with the 30-mm BD-IPMN in the pancreatic tail.
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Two weeks after the initial administration of prednisolone, CECT revealed the mass lesion in the pancreatic body to be notably reduced in size, and the enhancement patterns of this mass lesion on CECT returned to those of the normal pancreas five months after the initial administration of prednisolone (Fig. 4a-c). ERP three weeks after the initial administration of prednisolone showed improvement of the MPD obstruction in the pancreatic body, visualization of the MPD up to the pancreatic tail, and communication of the MPD with the 30-mm BD-IPMN in the pancreatic tail (Fig. 4d), which definitively revealed this pancreatic cyst to be BD-IPMN.