A 33 year old male was admitted to our hospital presenting with six-month history of intermittent right epigastric vague pain, and having lost 5 kg in weight over a 2-month period. According to the patient's history, he had had no coughing, fever, jaundice, diarrhea, hematemesis and melena. He had never received a BCG vaccine, but there was no prior history of tuberculosis, or any family history. One month ago, an abdominal computed tomography (CT) performed at another affiliated hospital of our University showed a pancreatic cystic mass, and diagnosed as pancreatic cystadenocarcinoma. On admission, the physical examination revealed no abnormalities.
Initial laboratory values revealed a WBC count of 7.54 x 109/L (85.4% neutrophils, 9% lymphocytes, and 4.9% monocytes), Hb 8.7 g/L, ALT 96 U/L (normal 5-45 U/L), AST 161 U/L (normal 5-45 U/L), GGT 705 U/L (normal 4-50 U/L), and ALP 593 U/L (normal 42-128 U/L), Albumin 37.6 g/L and Globulin 34 g/L, Bilirubin, serum CEA, and amylase in serum and urine were all within normal limits; oral glucose tolerance test was normal, the detection of HBV, HCV and HIV were all negative. A chest X-ray film and hypotonic duodenography showed normal. Abdominal ultrasound (US) examination revealed an irregular hypoechoic lesion of 6.6 cm x 4.4 cm in the head of pancreas, and with a calcification at the edge of the mass, and without dilation of bile duct system and pancreatic duct (Fig 1); color Doppler flow imaging did not demonstrate blood stream in the mass. The above-mentioned contrast enhanced CT scan showed a inhomogeneous cystic mass in the head and uncinate process of the pancreas with peripheral rim enhancement, the body and tail of pancreas were normal; the head of pancreas, spleen were enlarged, and mild dilation of main pancreatic duct was also demonstrated (Fig 2). It was clinically suspected as pancreatic cystadenocarcinoma. Two attempts of US-guided percutaneous fine needle aspiration (FNA) failed due to tough tissue not permitting the needle to penetrate.
An exploratory laparotomy revealed 300 ml yellow ascite in abdominal cavity, lymphadenopathies around the hepatoduodenal ligament, and a few miliary nodules on pevic visceral peritoneum; omentum, liver and gall bladder were normal, serosal layer of the porta hepatis and the enlarged head of pancreas were edema without nodules. The head of pancreas was elastic hard to palpate. Incisional biopsy of the mass yielded a caseous material, and the wall of abscess cavity was about 1.2 cm in thickness. The cavity, mainly locating at pancreatic head, uncus and peri-pancreas, was separated by fibrotic septa and approximately contained 60 ml milk-like pus. The abscess wall revealed diffuse adipocyte vacuoles together with fibrocytes and lymphocytes suggestive of chronic inflammation on frozen section, but acid-fast stain was positive. After lavaging cavity, applying streptomycin 2.0 g in it, and placing a peripancreatic pigtail drainage, the laparotomy ended. Postoperative recovery was uneventful. Histopathology still confirmed chronic inflammation, without typical changes of tuberculous granuloma such as Langhan's giant cells or epithelioid histiocytes. Patient was started on 3-drug antitubercular regime and at follow up thereafter, patient was asymptomatic. The pancreas demonstrated normal in the CT scan after 7-month duration of antituberculous therapy, but the size of enlarged spleen remained invariable (Fig. 3). One year later, further examinations were performed for the patient to learn whether he has the potential risk of variceal bleeding. Moderate stenosis, not occlusion of splenic vein was confirmed by Doppler ultrasound; no esophageal or fundus varices was also found by gastroscopy.