PMC9755655_01
Radiological evaluation before and after surgery. (A) Irregularly shaped pancreas seen on contrast-enhanced computed tomography (CT) at the first admission. (B) Enlarged pancreas on contrast-enhanced CT before surgery. (C) Head of the pancreas protruding into the duodenum on contrast-enhanced CT before surgery. (D-F) Axial T1-weighted in-phase and out-of-phase images obtained during follow-up (D, 1.5 years after surgery; E, 2 years after surgery; F, 2.5 years after surgery). There were several patchy and nodular high-signal lesions in the right lobe of the liver on the in-phase image. Note a significant signal drop in these lesions on the opposed-phase image. The lesions gradually enlarged during follow-up. A nodule inside the largest lesion was detected in the last follow-up scan.
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No abnormality was apparent in the liver or other organs ( Figure 1A ). A CT examination showed a more enlarged pancreas, part of which was protruding into the duodenum ( Figures 1B, C ). At 1.5 years postoperatively, multiple small patchy and nodular lesions with opposite signals on axial T1-weighted in-phase and out-of-phase MRI were detected in the liver for the first time ( Figure 1D ). The volumes of the lesions continued to increase after a further 6 months and 1 year ( Figures 1E, F ).
Pathological results. (A) Hematoxylin-eosin staining of the pancreatic neuroendocrine neoplasm. (B) Somatostatin immunostaining. (C) Biopsy of the liver metastases.
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Immunostaining of chromogranin A, synaptophysin, and somatostatin was positive, but immunostaining of insulin, gastrin, and glucagon was negative ( Figures 2A, B ). Histologic evaluation showed a small number of NEN cells and peritumoral liver cells with fatty change ( Figure 2C ).
Contrast-enhanced ultrasonography of lesions in the liver. (A) B-mode ultrasound examination revealed several lesions with an inner hypoechoic area and outer hyperechoic area. (B-D) Contrast-enhanced ultrasonographic scans [(B), 13 s in the arterial phase; (C), 68 s in the portal venous phase; (D), 152 s in the delayed phase] showed rapid enhancement in the arterial phase, early washout in the portal venous phase, and hypo-enhancement in the delayed phase in the inner hypoechoic area. However, the peripheral area was continuously iso-enhancing or hypo-enhancing.
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A hypoechoic area with a diameter of 2.2 cm was observed inside this hyperechoic lesion ( Figure 3A ). However, continuous iso-enhancement or hypo-enhancement was seen in the peripheral area ( Figures 3B-D ).
Timeline showing the course of the disease.
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Timeline showing the course of the disease is in  Figure 4 .