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 73-year-old man, farmer from Gorgan, a city in the north of Iran, who came because of fever and icterus since 1 week before presentation. He had no obvious symptoms since 1 week before admission when he developed progressive jaundice and episodic right upper quadrant pain especially after meal but unrelated to position or respiration. He also reported mild fever, anorexia, and generalized body pain during this period. To analyze his problem, abdominal sonography was performed in outpatient setting, which showed an increased liver echogenesity without the dilation of bile ducts and gall stone. Based oh the abovementioned symptoms, his primary care physician made a diagnosis of viral hepatitis, but the patient eventually developed constant high-grade fever and right upper quadrant pain. Therefore, he was referred to our hospital and was admitted. At the time of hospitalization, the temperature was 39.5°C, the pulse was 90 beats/min, and the respiratory rate was 18 breaths/min. The blood pressure was 110/65 mm Hg. On physical examination, the patient did not appear to be in severe pain, and there was mild jaundice. The lungs and heart sounds were normal. The abdomen was flat, and the bowel sounds were present. There was tenderness in the right upper and quadrant, with mild guarding but without rebound tenderness. No mass or hernia was detected. The arms and legs were well perfused. No abnormalities were found on rectal examination. His sonography at admission revealed minimal intrahepatic and mild extrahepatic biliary dilation, while other organs were normal and no stones were observed. Blood tests revealed mild normocytic normochromic anemia, while white blood cell and absolute eosinophil count were normal in the patient. The erythrocyte sedimentation rates were high (90 mm/h) and serum chemical analysis revealed the following values: albumin, 3.4 g/dl; alkaline phosphatase, 170 U/l (normal range, 53–128); alanine aminotransferase, 73 U/l (normal range, 10–35); aspartate aminotransferase, 54 U/l (normal range, 14–50); and total bilirubin, 8.9 mg/dl (normal range 0.3–1.2), with a direct bilirubin level of 5.7 mg/dl (normal,< 0.2). The white-cell count was 11 400/mm3, with 84% neutrophils and 1% eosinophils. The urine was orange and was positive for bile (++), protein (+), and urobilinogen (+). Because of the endemicity of leptospirosis, serologic test (indirect hemagglutination test) was done, which revealed negative result. A urine culture and multiple blood cultures were negative. Assays for the presence of hepatitis B antigen and antibody, hepatitis C antibody, and antimitochondrial antibodies were negative. Chest radiographs showed no abnormalities. Endoscopic retrograde cholangiopancreatography (ERCP) demonstrated extrahepatic biliary dilatation; the common bile ducts (CBDs) were about 12–15 mm in diameter, with a small filling defect in the distal part [].\nSerologic test for showed high titer against that (positive titer 1/80), and the detection of ova in stool documented infestation with this liver fluke. After diagnosis, triclabendazole was administered at a dose of 10–12 mg/kg for 1 or 2 days, after which the symptoms disappeared and biochemical values soon returned to normal, and the patient was discharged with good condition. During the follow-up, her jaundice subsided, and ultrasonography revealed an almost normal CBD in our patient.