A 64-year-old female with epigastric and right upper quadrant pain was referred to Taleghani Hospital in Tehran, Iran. She complained of intermittent pain attacks radiating to the back, exacerbated after eating. There had been 3–4 episodes of pain on most days, lasting about 1 h and then decreasing gradually for at least 6 month before presentation.\nShe also stated weight loss of about 3 kg (from 66 to 63 kg) within 6 months without fever, icterus or any change in bowel habit. In her past medical history, there were no important medical problems.\nHer previous laboratory evaluation revealed an increased erythrocyte sedimentation rate (64 mm/h), while total bilirubin was 3.2 mg/dl (normal <2 mg/dl), aspartate aminotransferase 31 IU/l (normal <30 IU/l), alanine aminotransferase 37 IU/l (normal <30 IU/l), alkaline phosphatase 473 IU/l (normal <306 IU/l) and γ-glutamyltranspeptidase 82 IU/l (normal <60 IU/l). Complete blood count showed hemoglobin 12.1 g/dl, platelets 190,000/mm3 (normal 100,000–450,000/mm3) and white blood cells 4,030/mm3 (normal 4,000–10,000/mm3) with 12% eosinophils (484/mm3) on peripheral smear. Blood chemistry tests were in the normal range. Hydatid antibody titer was requested and was within normal limits. The results of stool examinations at three different times for detecting ova and parasites as well as occult blood were normal.\nAfter admission, ultrasonography and abdominopelvic computed tomography (CT) scan showed normal intrahepatic bile ducts, but an ill-defined large heterogeneous mass lesion which contained multiple hypodense portions in the right and caudate lobes of the liver was noted (fig. ). There were no other remarkable findings on ultrasonography and CT imaging. After that, the patient underwent evaluation to rule out possible malignant and non-malignant etiologies as follows: Endoscopy and colonoscopy were performed to rule out probable sources of liver metastasis, which were both unremarkable. The patient also underwent CT-guided core needle biopsy for pathologic and microbiological evaluation, which showed predominant eosinophil infiltration of liver sections with microabscess (eosinophilic abscess) formation without neoplastic or granulomatous process. Microbiological cultures of aspiration fluid of the liver mass showed no growth after 72 h.\nEmpirically, initial treatment with intravenous ceftriaxone and metronidazole was initiated, followed by oral ciprofloxacin and metronidazole. Following antibiotic therapy, the patient's symptoms alleviated gradually, and erythrocyte sedimentation rate decreased to 10 mm/h within 3 weeks. The patient was discharged from hospital and on follow-up visits mentioned improvement in her general condition. Ultrasonography performed 2 months after discharge showed resolution of the liver mass with normal intra- and extrahepatic biliary ducts, but second follow-up ultrasonography revealed a small (8 × 10 mm) cystic lesion in the right lobe of the liver with dilation of the common bile duct (CBD) (9 mm) that was confirmed by magnetic resonance imaging (fig. ). Magnetic resonance cholangiopancreatography showed a slightly dilated CBD (9.5 mm) and normal intrahepatic bile ducts, with irregularity of the wall of the distal third of the CBD with suspicious filling defect (fig. ). Finally, EUS with a linear echoendoscope showed a 10 mm CBD with long, linear, hyperechogenic structures, moving freely in the lower third of the CBD, in favor of F. hepatica (fig. ). After diagnosis of F. hepatica by EUS, ERCP was performed, and after sphincterotomy, an extraction balloon was passed and removed a live Fasciola (fig. ).
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).