bluuebunny/crossref_metadata_2025_split huggingface dataset:
2472 Right Ventricular Mass in a Patient With Newly Diagnosed Cirrhosis
Authors: Li Muyi , O'Brien Corey , Syed Bakhtiar 
Published: October 2019

INTRODUCTION:
While most cases of hepatocellular carcinoma (HCC) metastasis present in the lung, lymph nodes, adrenals, or bones (18%), hematogenous spread to the heart is also possible via the inferior vena cava (IVC). Worldwide prevalence of HCC is 180 million people, however only 2% present with cardiac involvement. Prognosis is typically poor due to high chance of cardiopulmonary collapse. Here we describe a patient presenting with cardiac mass concerning for HCC.

CASE DESCRIPTION/METHODS:
58-yo male with polysubstance abuse initially presented to the ED with fatigue, dyspnea on exertion, and 30 lb weight loss over a period of 6 months. On admission his labs were notable for elevated LFTs, albumin 2.7, and INR 1.28. He received an echo to rule-out endocarditis, and echo was concerning for a right ventricular mass. He also received CT chest as work-up for dyspnea, which not only revealed emphysematous changes but also a nodular liver. To better characterize the mass, he underwent cardiac MRI showing large RV mass extending into right ventricular outflow tract and the pulmonary trunk with an adjacent thrombus. Hepatitis panel was also positive for active hepatitis C. Given newly diagnosed hepatitis C and imaging/lab findings suggestive of cirrhosis, patient underwent triple phase MRI with findings of infiltrating HCC as well as extensive tumor thrombus involving both the right and left portal veins. The right ventricular mass was thought to be in setting of HCC metastasis with invasive liver disease. Patient had goals of care conversation and stated he did not want any further testing or procedures. He was discharged home with lovenox 100 mg daily for the right ventricular thrombus.

DISCUSSION:
This case highlights a rare presenting feature of HCC, as only 2% of HCC cases have cardiac involvement. Typical cardiac involvement occurs with hematogenous extension into the IVC, and while HCC with tumor extension to the portal system is quite common invasion to the IVC is rare. This patient was at risk for HCC with his untreated HCV cirrhosis, with typical 25 to 30-year latency period from exposure to development of HCC. Prognosis with cardiac involvement of HCC is poor due to high chance of cardiopulmonary collapse. Treatment considerations include systemic therapy such as sorafenib or lenvatinib in Child A patients, tyrosine kinase inhibitors that reduce angiogenesis and increases apotosis of HCC cells. Palliative cardiac surgery can also be considered in cases of obstruction.
2477 Strongyloidiasis Presenting as Isolated Hepatic Mass in an Immunocompetent Host: A Case Report
Authors: Wong Natalie Z. , Stotts Matthew J. , Daskalaki Irini , Siegelman Evan S. , Rothstein Kenneth D. 
Published: October 2019

INTRODUCTION:
Strongyloidiasis is caused by an infection with Strongyloides stercoralis. Manifestations range from absent to minimal symptoms in immunocompetent persons to a hyperinfection syndrome in immunocompromised persons. Hepatobiliary complications have been described as granulomatous hepatitis and biliary obstruction. We report a case of strongyloidiasis presenting as a solitary hepatic mass in an immunocompetent patient.

CASE DESCRIPTION/METHODS:
A 27-year-old woman with no past medical history or medications and recent travel to Costa Rica presented with intermittent right upper quadrant pain after trauma while skiing. She had no hepatomegaly, tenderness, or signs of chronic liver disease on exam. Laboratory analysis showed WBC 24.7 103/mL, absolute eosinophils 15,314 cells/mL, AST 21 U/L, ALT 35 U/L, ALP 106 IU/L, albumin 3.9 g/dL, and total bilirubin 0.3 mg/dL. Strongyloides IgG was positive. Stool was unremarkable. CEA, AFP, and CA 19-9 levels were normal. Abdominal US revealed a hepatic mass. MRI confirmed a 5 × 6 cm lesion in the inferior and anterior right lobe (Figure 1). The patient received ivermectin for strongyloidiasis. Repeat MRI at 4 weeks showed no change in lesion size. To prepare for lesion excision, the patient underwent CT imaging at 7 weeks. This showed a significant decrease in mass size to 3 × 2.5 cm (Figure 2). Surgery was deferred. MRI at 15 weeks showed continued resolution of the mass to a long axis of 2.5 cm. Marked lesion improvement with ivermectin alone was felt consistent with strongyloidiasis.

DISCUSSION:
Chronic strongyloidiasis affects 30 million people worldwide, with clinical significance mediated by equilibrium between human host and helminthic parasite. Most people are asymptomatic or have nonspecific gastrointestinal symptoms. Hepatic presentation is exceedingly rare and has been associated with immunocompromise and dissemination. To our knowledge, only one case of immunocompetent hepatic presentation has been reported.
1
In the presently described case, a large hepatic lesion in a healthy woman with marked eosinophilia was initially evaluated for a neoplastic process. Strongyloides consideration and testing was key to obtaining the diagnosis. Imaging also expanded our understanding of the range of possible radiographic findings in this disease. Physicians should be aware of chronic strongyloidiasis as they consider the differential for hepatic masses in immunocompetent patients.
2484 Intravenous Acetaminophen Associated With Hepatotoxicity in an Orthotopic Liver Transplant Patient
Authors: Khuc Thi , Selim Khaled 
Published: October 2019

INTRODUCTION:
Intravenous acetaminophen (IV APAP) is a commonly used post-operative analgesic. In adults, IV APAP administered at therapeutic doses of less than 4 g over 24 hours is considered safe. Five to ten percent of APAP is metabolized into N-acetyl-p-benzoquinone imine (NAPQI), the toxic metabolite responsible for APAP hepatotoxicity. NAPQI is inactivated when conjugated to tripeptide glutathione.

CASE DESCRIPTION/METHODS:
A 69 year old male with a history of secondary biliary liver cirrhosis status post orthotopic liver transplantation in 2006 and newly diagnosed prostate adenocarcinoma was admitted to the Urology service for planned robotic-assisted prostatectomy. He underwent uncomplicated robotic-assisted prostatectomy, requiring no fluid resuscitation, vasopressor support or blood products. Post-operatively, vital signs remained normal with no episodes of hypotension. He was started on IV APAP 1000 mg every 6 hours for 36 hours, followed by PO APAP 650 mg every 6 hours for post-operative pain. On post-operative day 2, AST was 2751 IU/L, ALT 3447 IU/L, TBili 1.9 mg/dL and INR 1.5 (Figure 1). All orders for acetaminophen were stopped. Liver Doppler ultrasound was normal. A serum acetaminophen level drawn 10 hours after the last IV APAP dose was <15 ug/mL. Work up for infectious etiologies was negative. The patient was started on IV NAC therapy. Following completion of IV NAC therapy, AST was 986 IU/L, ALT 2340 IU/L, TBili 1.9 mg/dL, and INR 1.4. The patient was discharged home on post-operative day 4. Labs during his outpatient Hepatology follow-up appointment 4 days after discharge were AST 62 IU/L, ALT 426 IU/L, TBili 1.3 mg/dL, and INR 1.1.

DISCUSSION:
This is the first case of acute liver toxicity in a post-OLT patient who received therapeutic doses of IV APAP. There was no evidence of hypotension or APAP overdose in the electronic medical records. All other etiologies for acute liver toxicity were ruled out, including shock liver, infection and vascular compromise. It is possible APAP metabolism is altered in transplant livers compared to native livers. A study on 13 liver transplant patients concluded APAP metabolism was transiently altered in orthotopic livers following liver transplantation, resulting in enhanced NAPQI production. It is possible transplant livers carry less glutathione stores due to cold storage preservation and post-transplant reperfusion, rendering them more susceptible to hepatotoxicty from NAPQI concentrations that a native liver would tolerate.
2485 An Unusual Case of a Primary Mass in the Porta Hepatis
Authors: Sidhu Simran , Gonzalez Hector , Azhar Mishah , Steinberg Stephen 
Published: October 2019

INTRODUCTION:
Burkitt's Lymphoma is an aggressive subtype of B-cell non- Hodgkin Lymphoma which can present in three forms: endemic, sporadic, and immunodeficiency- associated. It commonly presents in the pediatric population and occurs in less than 1% of adult non-Hodgkin lymphomas. It classically presents with abdominal symptoms with ascites and can commonly involve the distal ileum, stomach, cecum, and mesentery. We describe an unusual case of Burkitt's lymphoma presenting as a mass in the porta hepatis, associated with obstructive jaundice.

CASE DESCRIPTION/METHODS:
A 74 y/o male presented with a two-week history of jaundice and intermittent epigastric pain. Physical exam findings were scleral icterus, jaundiced skin, and soft nontender abdomen with normal bowel sounds. Labs were pertinent for alkaline phosphatase 1,264, AST 166, ALT 95, total bilirubin 18.8, and direct bilirubin of 15.1. Ultrasound and MRI/MRCP demonstrated a 10.3 × 6.8 × 7.2 mass infiltrating the porta hepatis, peripancreatic, and periduodenal tissues. There were no other masses or adenopathy. At ERCP there was a friable mass replacing the ampulla. Cholangiogram showed dilated intrahepatic ducts proximal to an obstruction at the level of the common bile duct and a metal expandable stent was placed. Biopsy of the ampullary mass revealed high grade, mature B-cell lymphoma. Endoscopic ultrasound revealed a heterogenous mass and fine needle aspiration yielded necrotic cells. Tumor cells were positive for CD20, PAX5, BCL6, CD10, CD20, and LEF1. Pathology was positive for Myc rearrangement and translocation t(8;14). Combination chemotherapy was then initiated.

DISCUSSION:
Primary tumors of the porta hepatitis are uncommon as it is more often the site of metastatic disease from breast, pancreas, gastric, and colon cancer. This case is particularly unusual in that the primary tumor is a Burkitt lymphoma, which did not arise from lymph nodes or from the pancreas and which presented with obstructive jaundice.
2486 Pick the Cause: Streptococcus Intermedius and Mitus/Oralis Hepatic Abscess Due to Occult Gastrointestinal Perforation
Authors: Martin Trent D. , Raymond Patricia L. 
Published: October 2019

INTRODUCTION:
Abscess bacteria identification directs both evaluation and management. In our case, identification of Strep intermedius and mitus/oralis led to identification of an unsuspected perforation.

CASE DESCRIPTION/METHODS:
A 45 y/o female presented to the ED with 5 days of fevers to 103.5 F, headache, cramping RUQ abd pain, diarrhea. CT abd revealed a 6.8 cm hypodense septated collection in the liver. Abnormal labs: WBC 32K TBili 1.3 AP 210 ALT 45. History was negative for IVDA, FH and personal hx of IBD, blood in stool, or travel. IR placed a drainage catheter on HD#1 and sent 60 cc purulent material for culture, gram stain with GPC. Culture several days later revealed sensitive Strep intermedius and Strep mitis/oralis in abscess and one anaerobic blood culture. The patient was treated with vancomycin and zosyn. Echocardiogram HD#3 showed minimal mitral calcification and no vegetations. Despite appropriate antibiotics, the RUQ pain, fevers, and WBC persisted. Repeat CT Abd on HD#7 showed a second hepatic abscess (IR placed second drain) and new pelvic abscess measuring 3.5 × 6 cm. On HD#9 we pursued occult GI causes of the persistent infection. Colonoscopy revealed a 1 cm adenoma (snared/removed) with no colon cancer, perforation, or IBD. EGD revealed a toothpick embedded in the prepyloric stomach; this was removed by snare. The patient did not recall eating food with a toothpick or swallowing one. Patient was discharged to home on HD # 11 with a PICC line to complete Unasyn course. Drainage catheters were removed 29 days after initial presentation; repeat CT scan at 52 days revealed no residual hepatic or pelvic abscess collections.

DISCUSSION:
Streptococcus intermedius is one of the members of the S. milleri group, which are normal flora in the mouth and gastrointestinal tract. S. milleri may cause liver, pelvis, and subphrenic abscess, cholangitis, peritonitis, and appendicitis. Presence of S. millerigroup bacteremia should direct attention to exclusion of occult abdominal perforation or infection, distant focal suppurative infection, and infective endocarditis. Streptococcus mitus/oralis is a common oral bacteria in the Strep viridans group; this may cause a variety of infections including cerebral, epidural, and liver abscesses and endocarditis. Upon the identification of Strep intermedius as the main abscess pathogen in our patient, prompt search for occult abdominal perforation and removal of the foreign body from the perforation tract resulted in resolution of both symptoms and infection.
2487 Primary Biliary Cholangitis With Autoimmune Hepatitis Overlap in Twin Males: A Unique Case of Related Autoimmune Diseases
Authors: Sanchez Antonio J. , Zhao Weidan 
Published: October 2019

INTRODUCTION:
Primary biliary cholangitis (PBC) and autoimmune hepatitis (AIH) are immune-mediated liver diseases with female predominance. Combined features of both, termed AIH-PBC overlap syndrome, occurs in rare instances. We present a unique case of AIH-PBC overlap syndrome in twin males.

CASE DESCRIPTION/METHODS:
Twin #1 was a 36-year-old man when he presented in 2012 with asymptomatic liver enzyme elevation. No new medications, herbals, alcohol or illicit drug use. No known family history of liver disease. Labs showed total bilirubin (TB) 0.5, alkaline phosphatase (ALP) 478, aspartate aminotransferase (AST) 81, alanine aminotransferase (ALT) 111, gamma-glutamyl transferase (GGT) 625, positive anti-mitochondrial antibody (AMA) >1:640, and hypergammaglobulinemia (2128 mg/dL). Liver biopsy showed moderate plasma rich cell infiltrate with bile duct damage and mild fibrosis, consistent with AIH-PBC overlap. Patient was treated with steroids, azathioprine (AZA), and ursodeoxycholic acid (UDCA), later switched to obeticholic acid due to refractory PBC. He subsequently experienced marked biochemical improvement without disease progression. Twin #2 presented in 2017 with elevated liver enzymes and pruritus. Labs showed TB 1.1, ALP 755, AST 81, ALT 116, GGT 838, positive ANA >1:2560, positive AMA >100, and positive ASMA >100. Liver biopsy showed moderate bile duct epithelial injury with lymphoplasmacytic infiltrate, consistent with AIH-PBC overlap, and stage II/IV hepatic fibrosis. He was treated with steroids, AZA, and UDCA. He also experienced marked biochemical improvement without disease progression.

DISCUSSION:
PBC, a rare autoimmune disorder with female preponderance, can lead to cirrhosis and liver failure. PBC-AIH overlap syndrome, described in 4.8-9.2% patients with PBC, is more likely to have rapid disease progression and hepatic decompensation. Combination of steroids, AZA and UDCA has been variably effective and can delay disease progression. To the best of our knowledge, this is the first case of AIH-PBC overlap syndrome reported in twin males and highlights the importance of inherited factors in immune mediated liver disorders. Although it is known that PBC and AIH are associated with human leukocyte antigen genes on chromosome 6, further study of the association between these disorders is limited by the paucity of patients. Early diagnosis of this condition is essential to prevent liver related complications with medical management.
2494 Rare Case of Concomitant Acute Hepatic Failure and Renal Failure Induced by Intravenous Amiodarone
Authors: Mohamed Mujtaba , Al-Hillan Alsadiq , Hossain Mohammad 
Published: October 2019

INTRODUCTION:
Hepatotoxicity caused by chronic oral amiodarone is well documented with around 15–20%. However, acute liver failure due to intravenous Amiodarone is rare clinical presentation with 3% incidence rate. Incidence of concomitant renal failure is even more rare. There is no full explanation for the underlying mechanism.

CASE DESCRIPTION/METHODS:
67-year-old male with PMH of CAD s/p coronary artery bypass graft, CKD, presented with chest pain for one week. In the ED, he was found to have atrial flutter. Due to unresponsiveness to IV beta blocker and Diltiazem, patient was loaded with IV Amiodarone and continued IV Amiodarone drip. 16 hours later patient developed acute hepatic failure with AST 4250 (10-42 IU/L), ALT 2422 (10-60 IU/L), INR 2.28 (2-3 conventional anticoagulation), acute renal failure with creatinine of 3.2 mg/dl (0.44-1.0 mg/dl), BUN of 44 mg/d (5-25 mg/dl). Patient was intubated due to acute hepatic encephalopathy. IV Amiodarone was stopped immediately. All workup for other causes of acute hepatic failure came back negative. He was started on intravenous N-Acetyl cysteine and required hemodialysis for acute renal failure. LFTs peaked 72 hours after discontinuation of Amiodarone. Kidney functions improved 5 days after discontinuation of amiodarone and hemodialysis stopped.

DISCUSSION:
Acute hepatic failure due to intravenous amiodarone is extremely rare with incidence of 3%. The underlying mechanism is still not fully understood. However, a case–control retrospective study argues that hepatotoxicity due to intravenous amiodarone cannot be differentiated from ischemic hepatitis from concomitant hypotension. Intravenous amiodarone is formulated with polysorbate 80 as a solubilizer, which has been shown to induce hypotension. In this case, patient had a stable blood pressure when amiodarone was started. Intravenous (IV) amiodarone toxicity can raise AST/ALT up to 100–200-fold (AST of 21000 and ALT of 9020 in our case) within a day of infusion which then reverses quickly after discontinuation of amiodarone. In this case, liver function tests increased after 26 hours of starting intravenous amiodarone and peaked after 72 hours of stopping the infusion. All cases of acute liver failure due amiodarone didn't survive except for one case. The most common cause of death is encephalopathy. Administration of N-Acetylcysteine was administered is associated with good outcome. Incidence of concomitant renal failure is extremely rare. It is caused by concomitant acute tubular necrosis.
2499 Idiopathic Eosinophilic Syndrome With Hepatic Involvement
Authors: Ali Ahmad , Dailey Francis , Hammoud Ghassan M. , Al-Juboori Alhareth , Rao Deepthi S. , Tahan Veysel , Tuncer Togla 
Published: October 2019

INTRODUCTION:
Hepatic involvement in hypereosinophilic syndrome is rare.

CASE DESCRIPTION/METHODS:
A 66-year-old gentleman was referred for evaluation of persistent eosinophilia, cough, wheezing, and abnormal liver chemistries. No abdominal pain, fever, weight loss, and bowel habit changes. No traveling outside the U.S. On exam his vital signs were within normal range. Eyes, scleral icterus; Lungs; wheezing the bases; Abdomen, soft, nontender, nondistended, negative for, shifting dullness, no organomegaly, no distended veins on the abdominal wall; Extremities, no edema; Skin, no icterus no bruising. His initial laboratory findings were as follows, WBC 15.3 × 109/L, Hgb of 15.3 g/dL, platelets of 438 × 109/L, absolute neutrophil count of 6.7 × 109/L, absolute lymphocyte of 2.7 × 109/L, absolute eosinophil count of 4.5 × 109/L, alkaline phosphatase of 234 U/L, AST of 51 U/L, ALT of 94 U/L, total bilirubin of 0.4 mg/dL, albumin of 4.8 g/dL. With respect to the liver related laboratory findings: negative viral hepatitis panel, ANA of 1:160, total IgG of 1010 mg/dL, IgG1 of 659 mg/dL, IgG2 of 258 mg/dL, IgG3 of 12.9 mg/dL and IgG4 of 28 mg/dL; F-actin IgG antibody 23.3 units; negative anti-smooth muscle antibodies; soluble liver antibody <20 units; negative AMA, alpha-1 antitrypsin level of 167 mg/dL; and ceruloplasmin of 27 mg/dL. Comprehensive studies for stool ova and parasites was unremarkable. Peripheral blood smear showed eosinophilia. Bone marrow biopsy, with flow cytometric analysis revealing hypereosinophilia showing aberrant expression of CD 56. Abdominal MRI revealed a 5.8 cm hemangioma in the left lobe; no hepatic steatosis. Myeloproliferative neoplasms (MPN) and platelet-derived growth factor receptor α (PDGFRA A/B) workup was negative. Liver biopsy showed many eosinophils within portal areas with foci of sinusoidal involvement compatible with idiopathic eosinophilic syndrome; chronic hepatitis (grade 2/4), with portal and periportal fibrosis (stage II/IV); no steatosis. After starting prednisone 60 mg oral daily, tapered over 4 weeks, his cough, wheezing, hepatic enzymes' elevation and eosinophilia have resolved.

DISCUSSION:
Hypereosinophilic syndrome with hepatic involvement is rare, and should be in the differential diagnosis especially when hepatic enzymes' elevation is associated with eosinophilia.
2502 Rare Hepatic Adenomatosis Diagnosed by Endoscopic Ultrasound-Guided Fine-Needle Biopsy
Authors: Banerjee Avantika , Green William C. , Soape Matthew P. 
Published: October 2019

INTRODUCTION:
While hepatic adenomas are uncommon (1:100,000), hepatic adenomatosis (HA), defined as >10 adenomas, is even more rare (1-2.4:1,000,000) and poorly understood. HA poses a significant risk of hemorrhage and progression to hepatocellular carcinoma. Diagnosis by percutaneous fine needle biopsy (FNB) poses potential risk of infection and bleeding, and can be made more safely with endoscopic ultrasound FNB (EUS-FNB). Data on safety and efficacy of EUS-FNB in diagnosis of HA is limited, however it has high efficacy in the evaluation of gastrointestinal tumors and solid pancreatic lesions. This rare case of HA highlights the scarcity and risk factors of the condition while presenting a minimally invasive approach for diagnosis.

CASE DESCRIPTION/METHODS:
A 43-year-old female presented with nausea, vomiting, diarrhea, vague epigastric pain, and unremarkable past medical history with 20-year history of oral contraceptive pill (OCP) use. Laboratory results were significant only for elevated liver function tests and quickly resolving leukocytosis and symptoms. She was diagnosed with uncomplicated gastroenteritis but an abdominal CT incidentally showed multiple hepatic lesions scattered throughout the liver. MRI confirmed diffuse hepatic steatosis and numerous liver lesions (maximum diameter 3.51 cm) (Figure 2), consistent with hepatic adenomatosis vs. metastatic cancer. EUS-FNB was performed with pathology revealing inflammatory type hepatocellular adenoma (HA-I) (Figure 3).

DISCUSSION:
Although little evidence correlates the development of HA with the use of OCP's, there is a notably higher prevalence in females, consistent with the known association of adenoma and exogenous estrogen. Our patient's female gender and 20-year OCP use are the only currently understood risk factors for her HA. They are structurally composed of an extensive sinusoidal network and have minimal connective tissue covering, expanding the risk of intralesional hemorrhage and hemoperitoneum. Continuing to diagnose this condition through minimally invasive EUS-FNB can further illuminate risk factors for progression as well as aid in the understanding of HA's pathology and risk for malignant transformation and hemorrhage.