A 60-year-old male was admitted to the gastrointestinal medical clinic of Severance Hospital to undergo an operation for duodenal cancer.
The patient had developed renal tuberculosis 30 years previously, received medical treatment for several months, and was completely cured. In June 2009, he visited a local clinic after experiencing general weakness and melena over a period of 1 month, was diagnosed with duodenal cancer with multiple liver metastases (Fig. 1A and 1B), and was transferred to our hospital.
Esophagogastroduodenoscopy (EGD) (Fig. 1C) confirmed an ulcerofungating mass with poorly differentiated neuroendocrine carcinoma at the superior duodenal angle of the duodenum (Fig. 2A and 2B). Initial computed tomography (CT) showed multiple liver metastases. From November 2009 to January 2010, six cycles of palliative chemotherapy comprising 5-fluorouracil (5-FU) at 1,000 mg/m2 (days 1 to 3), etoposide at 100 mg/m2 (days 1 to 3), and cisplatin at 70 mg/m2 (day 1) were performed. After these treatments, fludeoxyglucose uptake was no longer seen on positron emission tomography (PET)-CT. There was no remnant malignant lesion on EGD, and the patient had only pathologically confirmed chronic gastritis. Two more cycles of chemotherapy were performed. He was subsequently confirmed to have no evidence of disease in February 2010.
In June 2010, a polyp was detected in the former lesion site and was confirmed to be chronic inflammation by EGD biopsy. There were no abnormal findings on CT. In February 2011, a polyp was detected by EGD at the same site as that of the former polyp (Fig. 3A). This was pathologically confirmed to be adenocarcinoma by immunohistochemical staining. Chromogranin A and synaptophysin, which are neuroendocrine markers, were negative. Carcinoembryonic antigen (CEA), which is usually detected in cases of adenocarcinoma, was positive (Fig. 3B). The patient was admitted for an operation. Upon examination, his vital signs were normal. He reported no symptoms, and there was no palpable mass, organs, or tenderness in the abdomen. The results of a complete blood count were normal, as were the plasma levels of routine chemistry and tumor markers (CEA and CA 19-9). Magnetic resonance imaging (MRI) and PET-CT showed no abnormal findings at the site of the duodenal lesion, which was detected by EGD. However, there were suspicious metastatic lesions at segments 6/7 and segment 7 of the liver, so intraoperative radiofrequency ablation was planned and performed on 28 February 2011. The duodenal adenocarcinoma was not invading the mesentery. Pylorus-preserving pancreaticoduodenectomy was performed. A definite lesion was not found by intraoperative sonography, but a lesion was found attached to the right margin of the right hepatic vein on preoperative MRI. Thus, right posterior segmental curative resection of the liver was performed.
The surgical pathology results showed moderately differentiated duodenal adenocarcinoma at the site of the primary lesion, and mild nonspecific reactive hepatitis was confirmed in the liver via immunohistochemical staining (Fig. 4). At the site of the primary lesion, there were no neuroendocrine cells; only pure adenocarcinoma cells were present. Therefore, the final stage was T1N0M0, and the patient underwent no further adjuvant chemotherapy. The patient is undergoing follow-up in the outpatient department without recurrence.