A 34 year old male was hospitalized because of severe abdominal pain and diarrhea. An abdominal X-ray revealed multiple calculi in the head of pancreas and blood tests showed his serum calcium level to be high. He underwent surgery of the parathyroid gland and a parathyroid tumor was removed. Two months later, resection of the head of the pancreas was also performed. Eighteen months after his operation there has been no recurrence of abdominal pain or diarrhea and his serum calcium level is within the normal range. We report this case herein and also discuss the possible cause and effect relationship between primary hyperparathyroidism and pancreatitis, and the appropriate management, in relation to a review of the literature.

We report a male patient aged 45 years, who in 1993 had been diagnosed as having middle bile duct cancer and had received a pancreatoduodenectomy. Histopathology showed a nodular tumor with the main lesion in the middle bile duct and superficial spreading in both proximal and distal directions (which was not observed macroscopically), and residual tumor in the epithelium of the cut edge near the liver. The patient underwent follow-up without postoperative adjuvant therapy. In 2002, 9 years after the operation, the patient developed jaundice and was diagnosed with recurrence of bile duct cancer in the anastomotic site, based on cholangiographic results. He underwent resection of the right hepatic and caudate lobes and the anastomotic region of the bile duct and jejunum. Pathological findings showed an invasive tumor in the anastomotic region, with continuous intraepithelial spread in the direction of the bile duct, which suggested that the residual tumor in the epithelium had grown to become an invasive cancer. In this patient, the recurrence required 9 years after resection. This case provides evidence for the clinical course that might be anticipated for a patient with a residual tumor in the epithelium of the bile duct stump and subsequent superficial spreading bile duct cancer.

Three cases of bleeding esophageal varices associated with arteriovenous malformation of the pancreas have been observed over the last 7 years. In 1 case, arteriovenous malformation (AVM) was the cause of the portal hypertension; thus, it was considered to be a "primary lesion." In the other cases, liver cirrhosis was the cause of the portal hypertension, and the AVM, which originally was a minor pathology, became significant as the portal hypertension progressed, thus making it a "secondary lesion." In the case of a "primary lesion," resection of the lesion is the preferred treatment for bleeding varices, but our case had multiple lesions, and excision was problematic. In the case of bleeding varices caused by liver cirrhosis, if liver function is normal, surgical treatment of both the varices and the AVM is recommended, while if the liver function is abnormal, repeated sclerotherapy is the best mode of therapy.

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