A 64-year-old man with a personal history of insulin-dependent diabetes mellitus, dyslipidaemia and recurrent renal colic. He reported diarrhoea, with episodes of steatorrhoea, constitutional syndrome and epigastralgia for two months. The patient was admitted through the emergency department for jaundice, choluria and progressive acholia.
Physical examination showed good general condition, afebrile, normohydrated and with cutaneous-mucosal jaundice. On abdominal examination, the gallbladder was palpable, with discomfort at that level and no signs of peritonism; the rest of the abdomen was unremarkable. Laboratory tests showed hyperbilirubinaemia of 17 mg/dl, with increased FFAA (2522 U/l) and γGT (107 U/l). No leukocytosis. Viral hepatitis markers were negative and there was an elevated CEA (7.6 ng/dl). AFP and CA19.9 were normal. Ultrasonography showed minimal dilatation of the intrahepatic bile duct and discrete dilatation of the common bile duct; the gallbladder was hydropic and without lithiasis. A rounded hypoechoic mass in the head of the pancreas of approximately 2 cm was seen, which was not confirmed by CT scan, which additionally showed dilatation of the duct of Wirsung and no adenopathy. Cholangioresonance showed similar findings with clinical suspicion of ampuloma which was not evident in the gastroscopy, which was strictly normal. With the diagnosis of obstructive jaundice of probable malignant origin, surgery was performed a week after admission, revealing a mass in the head of the pancreas with a neoplastic appearance, for which a cephalic duodenopancreatectomy with pyloric preservation and pancreatogastrostomy was performed.
In the anatomopathological study, the surgical specimen showed two clearly differentiated areas of tumour appearance. One of 1 cm and with well-defined limits in the duodenal wall, and another with undefined borders of 3 cm in the pancreatic head.

On microscopic examination, the duodenal tumour consisted of cords of polyhedral, uniform cells infiltrating the muscular fascicles of the wall. They showed nuclei with a low degree of atypicality and very low mitotic activity. The pancreatic tumour consisted of atypical glandular structures that infiltrated the duodenal wall and were lined by columnar cells with very atypical nuclei and a high mitotic index.

Once the diagnosis had been made. To confirm the different nature of the two tumours, immunohistochemical techniques were applied. The resulting immunophenotype clearly differentiated the two tumours, as the duodenal tumour was negative for CEA and positive for chromogranin, STH and glucagon and the pancreatic adenocarcinoma was only positive for CEA.
After the immediate postoperative period in the ICU, the patient was transferred to the surgery ward where he recovered favourably and was discharged 19 days after the operation to the oncology department. He was given a course of adjuvant chemotherapy based on gencitabine 1 g/m2, in four cycles, one of seven weeks and three of three weeks, with a rest period in between. She progressed well for the first few months but subsequently began to experience persistent pain in the right hypochondrium, nausea and vomiting. Given that the radiological examinations were unremarkable, he was re-intervened nine months after the first operation, confirming neoplastic recurrence, which was unresectable. The patient's general condition progressively deteriorated and he died 14 months after the first operation.

