A 63-year-old Thai man was referred to our hospital from a local government hospital in September 2018. He presented with acute intermittent epigastric pain and high-grade fever (body temperature 39°C) for 5 days. He was diagnosed with acute cholangitis and had initially been treated with intravenous ceftriaxone and metronidazole for 5 days. The symptoms slightly improved, but he still had abdominal pain and persistent fever; he was then referred to our hospital. He had a history of alcoholic chronic pancreatitisand diabetes mellitus type 2 with insulin supplementation. He had a history of heavy alcohol drinking (80 g per day for 20 years) and active smoking (10 packs per year). There was no history intravenous drug use, blood transfusion and unprotected sexual intercourse as well as no family history of viral hepatitis or liver disease.\nOn physical examination, he appeared conscious, slightly pale without icteric sclera, with vital signs body temperature 39.3°C, blood pressure 100/60 mm Hg, and pulse rate 100/min. His abdomen was soft with tenderness at the right upper abdomen. Murphy's sign was negative. The liver size was about 10 cm with a firm consistency smooth surface and blunt edge without any sign of portal hypertension or chronic liver disease.\nThe complete blood count was as follows: WBC 5,650/mm3, PMN 54%, Lymp 23%, Eos 12%; HB 11.1 g/dL, HCT 32.7%, MCV 98.5 fL, Plt 400 × 103/μL.\nThe liver biochemistry test revealed the following: total bilirubin 1.30 mg/dL (normal range 0.2–1.2 mg/dL), direct bilirubin 0.97 mg/dL (normal range 0-0.2 mg/dL), aspartate aminotransferase 185 U/L (normal range 0–32 U/L), alanine aminotransferase 70 U/L (normal range 0–33 U/L), and alkaline phosphatase 1,225 U/L (normal range 39–117 U/L).\nViral hepatitis B and C profiles were negative.\nMagnetic resonance imaging (MRI) with abdominal magnetic resonance cholangiopancreatography (MRCP) were performed; the resulting images showed abrupt change in caliber with a thickened wall of the distal common bile duct 2 cm in length caused by upstream bile duct dilatation with no obvious common bile duct stone or intra-ductal filling defect. Multiple small gallstones were detected without evidence of acute cholecystitis. Atrophic changes of pancreas with multiple pancreatic duct stones and main pancreatic dilatation were also observed (Fig. ). Initially, the diagnosis was suspected to be distal common bile duct stricture and severe cholangitis without response to initial antibiotic. He was later referred to our hospital for endoscopic management.\nEmergency ERCP was performed, which showed a dilated common bile duct 18 mm in diameter consisting of large irregular shape amorphous filling defect in the common bile duct (Fig. ). Sphincterotomy was then performed, and during the procedure a basket and balloon catheter was used to aid the extraction foreign bodies, which were observed as a dead, non-motile, leaf-shaped parasite seen in the duodenum (Fig. ). After bile duct clearance, a biliary double-pigtail plastic stent 7 Fr × 5 cm was inserted for biliary drainage.\nWe investigated the serology test for Fasciola antibody, but the result was negative. The definite diagnosis was confirmed by histopathology of dead parasite (Fig. ). The patient was treated with endoscopic removal of the dead parasite subsequent with single oral dose triclabendazole (10 mg/kg body weight/day). The clinical result was significantly improved without any relapse during the 1-year follow-up.\nThe patient came for the clinical follow-up, and an ERCP for removal of stent with complete occlusion cholangiography was done to confirm that there was no other filling defect in the extrahepatic bile duct and that the distal biliary stricture disappeared.\nLiver biochemistry returned to normal: TB 0.50 mg/dL (normal range 0.2–1.2 mg/dL); DB 0.25 mg/dL (normal range 0-0.2 mg/dl); aspartate aminotransferase 40 U/L (normal range 0–32 U/L); alanine aminotransferase 20 U/L (normal range 0–33 U/L); and alkaline phosphatase 126 U/L (normal range 39–117 U/L).
A 67-year-old woman was presented to our center at Namazi Hospital (Shiraz University of Medical Sciences, Iran) with abdominal pain, icter, nausea, and anorexia beginning two weeks prior to evaluation. Symptoms became worst progressively. She lived in the Zagros mountain area (southern Iran) consuming unsafe water and contaminated vegetables. Her past medical history was unremarkable except for a controlled hypertension with captopril. On physical examination, she was ill and icteric with right upper quadrant tenderness.\nAccording to the laboratory values upon admission, she had mild leukocytosis with prominent neutrophil without any evidence of eosinophilia. Liver biochemical tests were abnormal. Serum levels of amylase and lipase were normal. Her work up for virology markers (HAV, HBV and HCV) was negative. shows the patient’s initial laboratory results.\nIn abdominal ultrasonography, three small cysts and a dilated common bile duct were seen. Abdominal computed tomography scan showed three small cysts (<1 cm) and a dilated common bile duct, but liver parenchyma and intrahepatic bile ducts were normal ().\nERCP was performed because of the diagnosis of cholangitis. In ERCP, dilatation of common bile duct with multiple filling defects was seen, but gallbladder and intrahepatic bile ducts were normal ().\nOur primary impression for filling defects was common bile duct stones or sludge. Therefore, after sphincterotomy, we used a basket for removing the suspected stones, but surprisingly three living F. hepatica were removed by 3 times use of the basket. The F. hepaticas were alive and crawling in the basket.\nThe fluke’s samples were sent for pathology evaluation and confirmed as F. hepatica. Stool examination for detection of F. hepatica eggs was negative. In addition to antibiotics for acute cholangitis (metronidazole 500 mg/IV/q6h and ceftazidim 200 mg/IV/q8h), triclabendazole (10 mg/kg single dose) was started for therapy. After the first week, oral ciprofloxacin was replaced for IV antibiotics and continued for another week.\nClinical and laboratory condition of the patient improved after 4 weeks; leukocytosis and liver biochemical tests were completely normalized (). The patient showed no clinical and laboratory problems in favor of the liver disease after 12 months follow up.