INTRODUCTION: Peribiliary cysts are a rare entity usually found in patients with chronic liver disease and polycystic kidney disease. Patients are mostly asymptomatic therefore it is identified at times incidentally by abdominal imaging. Differential diagnosis include cholangiocarcinoma, Caroli disease and primary biliary cirrhosis. Awareness is essential to avoid misdiagnosis and unnecessary procedures including biopsies and surgeries. CASE DESCRIPTION/METHODS: A 67-year-old female with cirrhosis secondary to NASH and portal hypertension, among other comorbidities was evaluated at GI clinics. Abdominal sonogram performed for hepatocellular carcinoma surveillance showed right and left intrahepatic biliary ductal dilatation. The common bile duct measured 0.35 cm and the gallbladder showed intraluminar posterior acoustic shadows suggestive of cholelithiasis without wall thickening or pericholecystitic fluid collections. Patient denied fever, chills, abdominal pain, nausea or vomits. Abdomen was benign. Laboratories remarkable for baseline thrombocytopenia of 71, normal ALT and AST, elevation of alkaline phosphatase to 171 and hyperbilirubinemia of 3. MRCP was performed for further evaluation which showed multiple hyperintense rounded lesions tracking along the intrahepatic and extrahepatic biliary as seen with peribiliary cysts. DISCUSSION: Peribiliary cyst are usually associated to alcoholic cirrhosis with a prevalence of 9%; while in they have not been described in NASH. Pathophysiology may be due to intrahepatic circulatory disturbances of the portal venous system. Possible complications include biliary tract dilatation, obstructive jaundice and cholangitis.

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INTRODUCTION: Hypereosinophilic Syndrome (HES) is a rare disorder most commonly diagnosed in patients 20-50 years of age. It is defined as a persistent absolute eosinophil count greater than 1500 cells/microL and/or pathologic confirmation of tissue hypereosinophilia, as well as evidence of end-organ dysfunction. Prior to making a diagnosis, allergic, rheumatologic, infectious, and neoplastic etiologies should be excluded. CASE DESCRIPTION/METHODS: This is the case of an 87 -year-old male with past medical history of malaria treated with chloroquine who presented with altered mental status, dry cough and ascites de novo. Associated symptoms included unintentional weight loss of 10-15 lbs and intermittent episodes of non- bloody, watery diarrhea. He denied history of alcohol or drug use. Physical exam was remarkable for a distended abdomen with a positive fluid wave and pitting edema +1 in the lower extremities bilaterally. Labs showed a platelet count of 53,000, hypoalbuminemia (1.9 g/dl), increasing creatinine (2.1 mg/dl), alkaline phosphatase of 444 u/l, total bilirubin of 2.8 mg/dl with indirect predominance, AST of 59 u/l, ALT of 55 u/l, and eosinophilia of 72% (absolute eosinophil count of 6,048). Abdominal sonogram with doppler failed to show obstructive pathology and no evidence of hepatic vein thrombosis. Paracentesis showed absence of malignant cells, SAAG >1.1, 0.79 g/dl of protein and abundant eosinophils. Hepatitis, Iron Saturation levels, AMA, ASMA, Schistosoma and Strongyloides workup were negative. Hematology oncology service was consulted for bone marrow biopsy to asses for myeloid and lymphoid disorders. Results showed a hypercellular bone marrow with marked eosinophilia and 50% nucleated cells but C-KIT, PGFR Alpha, PGFRB, BCR/ABL, JAK 2 and TCR were all negative. A diagnosis of Hypereosinophilic Syndrome with suspected eosinophilic liver infiltration was made and the patient was started on prednisone therapy. All prior described multisystemic symptoms resolved. Eosinophilia, thrombocytopenia and all liver enzymes normalized within 24-48 hours after initiation of therapy. Ascites also resolved for which diuretic therapy was discontinued. DISCUSSION: This case is interesting as HES has an incidence of 0.36 per 100,000, and hepatic involvement accounts solely for an estimated 30% of patients. This serves to illustrate that HES should form part of the differential diagnosis when hepatic involvement and eosinophilia are concerned as prompt evaluation and treatment can lead to rapid resolution.

INTRODUCTION: TransarteriaL chemoembolization (TACE) is a widely-used treatment for unresectable hepatocellular cancer (HCC). Although TACE is minimally invasive, major complications occur in 5% of cases. These include acute cholecystitis, which is self-limiting and rarely requires surgical intervention. Liver abscess is a rare complication but can increase length-of-stay and morbidity. Our case focuses on multiple uncommon complications of TACE occurring in conjunction; gangrenous cholecystitis requiring emergent cholecystectomy, liver abscess and portal vein thrombosis. CASE DESCRIPTION/METHODS: A 67-year-old male with history of hepatitis C, cirrhosis and HCC status-post recent successful TACE who presented to the ER with right upper quadrant pain associated with fever. Physical examination with right upper quadrant tenderness and positive murphy’s sign. Laboratories showed leukocytosis and elevated alkaline phosphatase. Normal bilirubin, liver and pancreatic enzymes. Abdominopelvic CT with hydropic gallbladder with enhancing walls and pericholecystic inflammatory changes, new ill-defined hypodensities suggestive of abscess and extensive thrombus in the right portal vein. The patient received antibiotics and underwent an uneventful cholecystectomy. Post-operation findings consistent with a gangrenous gallbladder with severe adherent hepatic flexure and omentum to the gallbladder fundus. The patient was discharged on antibiotics and anticoagulation. Follow up MRI showed resolution of fluid filled lesions with almost complete resolution of the portal vein thrombosis. DISCUSSION: Cholecystitis is a complication of TACE due to reflux of the embolic material into the cystic artery. In most cases, management can be conservative. Our case is rare given that the patient developed gangrenous cholecystitis which is a serious complication that requires immediate surgical intervention. Liver abscess occurs infrequently unless there is a history of prior biliary reconstruction unlike our patient. Management includes antibiotics and percutaneous drainage for larger abscesses. In our case, our patient responded well to antibiotics. Because symptoms are non-specific, these complications may be mistaken for post embolization syndrome, which is usually self-limiting and abates by one week. Normal post-TACE CT findings can also confound the diagnosis of hepatic abscess formation. This case highlights the importance of being aware of complications of TACE as failure to recognize these may confer a higher mortality risk.

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